DiseaseName	Regulator	Target	RegulationDiretion	Experimental.method.for.lncRNA.target	ExpressionPattern	Experimental.method.for.lncRNA.expression	Data.accession	Data.accession2	influencedFunction	regulatoryMechanism	regulatoryType	levelOfRegulation	Drugs	cancerStemCell	hallmark	diseaseCategory	DiseaseName2	RegulatorType	TargetType	RegulatorEnsembleID	lncRegulatorPosition	TargetEnsembleID	lncTargetPosition	RegulatorEntrezID	TargetEntrezID	RegulatorAliases	TargetAliases	Evidence	PubMedID	RID	SearchregulatoryMechanism
Papillary thyroid carcinoma	LINC00313	miR-4429	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000185186	GRCh38_21:43461960-43479534	NA	NA	114038	NA	C21orf84|CH507-42P11.5|NCRNA00313	NA	Long noncoding RNA LINC00313 modulates papillary thyroid cancer tumorigenesis via sponging miR-4429	29940766	RID00001	ceRNA or sponge
Malignant glioma	FAM83H-AS1	CDKN1A	negatively-E	RIP;RNA pull-down assay;western blot;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734140-143746337	ENSG00000124762	NA	100128338	1026	onco-lncRNA-3	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21).FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A;thereby influencing the cell cycle and proliferation	29870057	RID00002	epigenetic regulation
Hepatocellular carcinoma	NEAT1	TGFB1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-139-5p)	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105329	NA	283131	7040	LINC00084|NCRNA00084|TncRNA|VINC	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NEAT1 upregulates TGF-beta1 to induce hepatocellular carcinoma progression by sponging hsa-mir-139-5p.	29797561	RID00003	ceRNA or sponge
Breast cancer	NEAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-448)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000148516	NA	283131	6935	LINC00084|NCRNA00084|TncRNA|VINC	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1.Overexpression of NEAT1 can induce breast cancer cell growth, migration, and invasion by inhibiting miR-448 and upregulating ZEB1	29323713	RID00004	ceRNA or sponge
Gastric cancer	ZFPM2-AS1	MIF	positively-F	mass spectrometry;western blot;RNA pull-down assay;RIP	upregulation	qPCR;microarray;sequencing	GSE1279;TCGA	GSE1279.zip;STAD.zip	cancer progression(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251003	GRCh38_8:105546089-106060524	ENSG00000240972	NA	102723356	4282	SCAT3	GIF|GLIF|MMIF	ZFPM2-AS1, a novel lncRNA, attenuates the p53 pathway and promotes gastric carcinogenesis by stabilizing MIF;tumor-activated ZFPM2-AS1 could bind to and protect the degradation of macrophage migration inhibitory factor (MIF);Knockdown of MIF expression diminished ZFPM2-AS1's impact on p53 expression in gastric cancer cells.	29985481	RID00005	interact with protein
Breast cancer	SNHG1	miR-448	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+);immune evasion(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Evading Immune Detection	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.SNHG1 directly contacted with miR-448, which could negatively regulate IDO;Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.	29886172	RID00006	transcriptional regulation
Breast cancer	SNHG1	IDO1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+);immune evasion(+)	ceRNA(miR-448)	regulation	NA	NA	NA	Evading Immune Detection	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000131203	NA	23642	3620	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	IDO|IDO-1|INDO	LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.SNHG1 directly contacted with miR-448, which could negatively regulate IDO;Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.	29886172	RID00007	ceRNA or sponge
Lung adenocarcinoma	LINC00222	GSK3B	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+);WNT signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203801	GRCh38_6:108751654-108769942	ENSG00000082701	NA	387111	2932	C6orf181|NCRNA00222|dJ354J5.2	NA	Long non-coding RNA LINC00222 regulates GSK3beta activity and promotes cell apoptosis in lung adenocarcinoma;overexpression of LINC00222 enhanced the activity of glycogen synthase kinase-3beta(GSK3beta), which is a key element of the Wnt signaling pathway;Enforced expression of LINC00222 significantly inhibited the proliferation, migration and invasive ability of lung adenocarcinoma cells	29990868	RID00008	expression association
Cholangiocarcinoma	TP73-AS1	CASP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000164305	NA	57212	836	KIAA0495|PDAM	CPP32|CPP32B|SCA-1	Enhanced expression of lncRNA TP73-AS1 predicts adverse phenotypes for cholangiocarcinoma and exerts oncogenic properties in vitro and in vivo.silencing of TP73-AS1 facilitates apoptosis via activating caspase-3 and caspase-9;TP73-AS1 could also facilitate migration and invasion potential of CCA cells;TP73-AS1 transcription is enhanced in both CCA tissue samples and cell lines, and this upregulation is closely associated with larger tumor size (p=0.008) and advanced TNM stage	29966969	RID00009	expression association
Cholangiocarcinoma	TP73-AS1	CASP9	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000132906	NA	57212	842	KIAA0495|PDAM	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Enhanced expression of lncRNA TP73-AS1 predicts adverse phenotypes for cholangiocarcinoma and exerts oncogenic properties in vitro and in vivo.silencing of TP73-AS1 facilitates apoptosis via activating caspase-3 and caspase-9;TP73-AS1 could also facilitate migration and invasion potential of CCA cells;TP73-AS1 transcription is enhanced in both CCA tissue samples and cell lines, and this upregulation is closely associated with larger tumor size (p=0.008) and advanced TNM stage	29966969	RID00010	expression association
Ovarian cancer	PVT1	miR-133a	negatively-F	qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long non-coding RNA PVT1 promotes cell proliferation and invasion through regulating miR-133a in ovarian cancer;qRT-PCR and luciferase reporter assays demonstrated PVT1 regulated miR-133a expression;Knockdown of PVT1 inhibited cell proliferation, migration and invasion through negative regulating miR-133a in OC cells	29957467	RID00011	ceRNA or sponge
Colorectal cancer	FEZF1-AS1	PKM	positively-F	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	qRT-PCR;microarray	NA	NA	STAT3 signaling pathway(+);cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000067225	NA	154860	5315	NA	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	LncRNA-FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling.FEZF1-AS1 could bind and increase the stability of the pyruvate kinase 2 (PKM2) protein;these data provide mechanistic insights into the regulation of FEZF1-AS1 on both STAT3 signaling and glycolysis by binding PKM2 and increasing its stability;LncRNA-FEZF1-AS1 Promotes Tumor proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling	29914894	RID00012	interact with protein
Retinoblastoma	DANCR	MMP9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-34c;miR-613)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000100985	NA	57291	4318	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA DANCR aggravates retinoblastoma through miR-34c and miR-613 by targeting MMP-9.our results reveal that DANCR function as competing endogenous RNA (ceRNA) for miR-34c and miR-613 to modulate progression and metastasis in RB oncogenesis via targeting MMP-9	29744877	RID00013	ceRNA or sponge
Prostate cancer	HOTTIP	miR-216a-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Long non-coding RNA HOTTIP promotes prostate cancer cells proliferation and migration by sponging miR-216a-5p;Bioinformatics online programs predicted that HOTTIP sponge miR-216a-5p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOTTIP could negatively regulate the expression of miR-216a-5p in PCa cells	29884766	RID00014	ceRNA or sponge
Gastric cancer	PEG10	miR-3200	negatively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000242265	GRCh38_7:94656325-94669695	NA	NA	NA	NA	EDR|HB-1|MEF3L|Mar2|Mart2|RGAG3|RTL2|SIRH1	NA	Knockdown of long non-coding RNA PEG10 inhibits growth, migration and invasion of gastric carcinoma cells via up-regulating miR-3200;	29940767	RID00015	expression association
Gastric cancer	CCAT1	BMI1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000168283	NA	100507056	648	CARLO5|CARLo-5|onco-lncRNA-40	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Knockdown of long noncoding RNA CCAT1 inhibits cell growth, invasion and peritoneal metastasis via downregulation of Bmi-1 in gastric cancer;The results showed that CCAT1 knockdown markedly inhibited cell proliferation, migration and invasion, arrested the cell cycle at G0/G1 phase in vitro, and inhibited peritoneal metastasis in nude mice, along with the downregulation of Bmi-1	29940756	RID00016	expression association
Esophageal cancer	GAS5	miR-301a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Promotes proliferation, Migration, and Invasion by Regulation of miR-301a in Esophageal Cancer;miR-301a appeared to be directly sponged by GAS5	29386089	RID00017	ceRNA or sponge
Malignant glioma	CCDC26	miR-203	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR;northern blot	NA	NA	cell growth(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229140	GRCh38_8:128634199-129683770	NA	NA	137196	NA	RAM	NA	Silencing of lncRNA CCDC26 Restrains the Growth and Migration of Glioma Cells In Vitro and In Vivo via Targeting miR-203; miR-203 is a direct target of CCDC26	28600863	RID00018	ceRNA or sponge
Lung adenocarcinoma	CRNDE	CDKN1A	negatively-E	RNAi;ChIP	upregulation	qRT-PCR	NA	NA	radioresistance(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000124762	NA	NA	1026	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression;the mechanistic investigations showed that CRNDE could interact with PRC2 and recruit its core component EZH2 to p21 (CDKN1A) promoter regions and repress its transcription;	28550688	RID00019	epigenetic regulation
Osteosarcoma	LINC00858	CDK14	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-139)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229404	GRCh38_10:84267747-84294659	ENSG00000058091	NA	170425	5218	CRCAL-2	PFTAIRE1|PFTK1	Long noncoding RNA LINC00858 promotes osteosarcoma through regulating miR-139-CDK14 axis;LINC00858 was identified to sponge miR-139 to form RNA-induced silencing complex (RISC) using luciferase reporter assay and RNA immunoprecipitation;these data prove that LINC00858/miR-139/CDK14 axis promotes the tumorigenesis of osteosarcoma	29944887	RID00020	ceRNA or sponge
Hepatocellular carcinoma	HOTAIR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell migration(+)	ceRNA(miR-23b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000148516	NA	100124700	6935	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA HOTAIR contributes to the malignancy of hepatocellular carcinoma by enhancing epithelial-mesenchymal transition via sponging miR-23b-3p from ZEB1;Our in vitro experiments suggested that HOTAIR promoted invasion and migration of HCC cells through enhancing EMT via sponging miR-23b-3p from ZEB1. Finally, the in vivo experiments indicated that HOTAIR could promote metastasis of HCC by enhancing EMT in vivo.	29778425	RID00021	ceRNA or sponge
Cervical cancer	HAGLR	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-130a-3p)	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000148516	NA	401022	6935	HOXD-AS1|MIR7704HG|Mdgt	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	HOXD-AS1 Exerts Oncogenic Functions and Promotes Chemoresistance in Cisplatin-Resistant Cervical Cancer Cells;These results collectively show that HOXD-AS1 can act as a competing endogenous RNA to upregulate ZEB1 expression via miR-130a-3p	29896986	RID00022	ceRNA or sponge
Endometrial cancer	TDRG1	VEGFA	positively-F	RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000112715	NA	732253	7422	LINC00532|lincRNA-NR_024015	MVCD1|VEGF|VPF	LncRNA TDRG1 enhances tumorigenicity in endometrial carcinoma by binding and targeting VEGF-A protein;RNA binding protein immunoprecipitation (RIP) assays confirmed that lncRNA TDRG1 directly binds to VEGF-A protein;knockdown of VEGFA in lncRNA TDRG1-overexpressing endometrial carcinoma cells reversed the effects of lncRNA TDRG1 on cell proliferation, invasion, migration and apoptosis	29920344	RID00023	interact with protein
Colorectal cancer	LIFR-AS1	TNFAIP3	positively-E	RNA pull-down assay;RIP;luciferase reporter assay;	upregulation	microarray;qRT-PCR	NA	NA	photodynamic therapy resistance(+);cell proliferation(+);apoptosis process(-)	ceRNA(miR-29a)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000244968	GRCh38_5:38556765-38671216	ENSG00000118503	NA	100506495	7128	NA	A20|AISBL|OTUD7C|TNFA1P2	Functional role of a long non-coding RNA LIFR-AS1/miR-29a/TNFAIP3 axis incolorectal cancer resistance to pohotodynamic therapy;LIFR-AS1 serves as a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of CRC to PDT	29807108	RID00024	ceRNA or sponge
Nasopharynx carcinoma	THORLNC	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(-);cell stemness(+)	transcriptional regulation	binding/interaction	RNA-RNA	cisplatin	NA	Limitless Replicative Potential	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000137693	NA	100506797	10413	NA	COB1|YAP|YAP2|YAP65|YKI	LncRNA THOR attenuates cisplatin sensitivity of nasopharyngeal carcinoma cells via enhancing cells stemness;THOR could enhance YAP transcriptional activity via directly binding to YAP and suppressing its translocation from nuclear to cytoplasm	29959065	RID00025	transcriptional regulation
Non-small cell lung cancer	LINC00339	FOXM1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000218510	GRCh38_1:22024558-22031223	ENSG00000111206	NA	29092	2305	HSPC157|NCRNA00339	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long non-coding RNA LINC00339 facilitates the tumorigenesis of non-small cell lung cancer by sponging miR-145 through targeting FOXM1;Luciferase reporter assay and RNA immunoprecipitation (RIP) revealed that LINC00339 promoted the NSCLC progression via FOXM1 via targeting miR-145	29906749	RID00026	ceRNA or sponge
Lung adenocarcinoma	NNT-AS1	miR-129-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR;sequencing	TCGA	LUAD.zip	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000248092	GRCh38_5:43571594-43603230	NA	NA	100652772	NA	NA	NA	LncRNA NNT-AS1 promotes the proliferation, and invasion of lung cancer cells via regulating miR-129-5p expression;we identified that NNT-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-129-5p in lung cancer	29857296	RID00027	ceRNA or sponge
Breast cancer	CBR3-AS1	TGFB1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000105329	NA	100506428	7040	PlncRNA-1|PlncRNA1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-beta1 and downregulating PHGDH;Upregulation of PlncRNA-1 promoted the expression of TGF-beta1, but inhibited the expression of PHGDH;LncRNA PlncRNA-1 overexpression reduced the proliferation rate, but increased the apoptosis rate of breast cancer cells, while treatment with TGF-beta inhibitor reduced those effects of PlncRNA-1 overexpression	29626321	RID00028	expression association
Breast cancer	CBR3-AS1	PHGDH	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell growth(-);cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000092621	NA	100506428	26227	PlncRNA-1|PlncRNA1	3-PGDH|3PGDH|HEL-S-113|NLS|NLS1|PDG|PGAD|PGD|PGDH|PHGDHD|SERA	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-beta1 and downregulating PHGDH;Upregulation of PlncRNA-1 promoted the expression of TGF-beta1, but inhibited the expression of PHGDH;LncRNA PlncRNA-1 overexpression reduced the proliferation rate, but increased the apoptosis rate of breast cancer cells, while treatment with TGF-beta inhibitor reduced those effects of PlncRNA-1 overexpression	29626321	RID00029	expression association
Colorectal cancer	HOTAIR	CDKN1A	negatively-E	RT-qPCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Down-Regulated LncRNA-HOTAIR Suppressed Colorectal Cancer Cell proliferation,Invasion, and Migration by Mediating p21	29808247	RID00030	expression association
Gastric cancer	HOTAIR	RUNX3	negatively-F	RPI-Seq;RIP;RNA pull-down assay	NA	NA	NA	NA	cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000020633	NA	100124700	864	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AML2|CBFA3|PEBP2aC	HOTAIR induces the ubiquitination of Runx3 by interacting with Mex3b and enhances the invasion of gastric cancer cells;We found that HOTAIR was bound to Runx3 protein and identified the fragment of HOTAIR spanning 1951-2100 bp as the specific binding site;Inhibition of HOTAIR significantly suppressed gastric cancer cell migration and invasion through upregulating claudin1, which could be reversed by co-deficiency of Runx3.	29417297	RID00031	interact with protein
Pancreatic cancer	ZEB2-AS1	HMGB1	positively-E	RIP;luciferase reporter assay	upregulation	microarray	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000189403	NA	100303491	3146	ZEB2-AS|ZEB2AS|ZEB2NAT	HMG-1|HMG1|HMG3|SBP-1	LncRNA ZEB2-AS1 promotes pancreatic cancer cell growth and invasion through regulating the miR-204/HMGB1 axis; ZEB2-AS1 exerted as a ceRNA and negatively regulated miR-204 expression;HMGB1 was identified as a down-stream target of miR-204	29753015	RID00032	ceRNA or sponge
Hepatocellular carcinoma	FUNDC2P4	CDH1	positively-E	western blot	downregulation	microarray;qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227009	GRCh38_22:39155525-39155945	ENSG00000039068	NA	100127979	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA FUNDC2P4 down-regulation promotes epithelial-mesenchymal transition by reducing E-cadherin expression in residual hepatocellular carcinoma after insufficient radiofrequency ablation;overexpression of FUNDC2P4 inhibited proliferation, invasion and migration potential and up-regulated E-cadherin expression in SMMC-7721 cells, whereas silencing FUNDC2P4 promoted these potentials	29295626	RID00033	expression association
Malignant glioma	SNHG12	ELAVL1	interact	RIP;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000066044	NA	85028	1994	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	ELAV1|HUR|Hua|MelG	Long non-coding RNA SNHG12 promotes the proliferation and migration of glioma cells by binding to HuR;RIP and RNA pull-down assays demonstrated that SNHG12 was associated with and was stabilized by HuR	30015836	RID00034	interact with protein
Melanoma	LNCRNA-ATB	YAP1	positively-E	RNA pull-down assay;RT-qPCR;western blot	upregulation	microarray;qRT-PCR	GSE3189	GSE3189.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-590-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000137693	NA	114004396	10413	NA	COB1|YAP|YAP2|YAP65|YKI	lncRNA-ATB functions as a competing endogenous RNA to promote YAP1 by sponging miR-590-5p in malignant melanoma;lncRNA-ATB functions as a competing endogenous RNA (ceRNA) to enhance Yes associated protein 1 expression by competitively sponging microRNA miR-590-5p;lncRNA-ATB functions as a ceRNA to promote MM proliferation and invasion	29956757	RID00035	ceRNA or sponge
Colorectal cancer	CYTOR	NRP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+);cell growth(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000099250	NA	112597	8829	C2orf59|LINC00152|NCRNA00152	BDCA4|CD304|NP1|NRP|VEGF165R	Long non-coding RNA 00152 functions as a competing endogenous RNA to regulate NRP1 expression by sponging with miRNA-206 in colorectal cancer;lnc00152 overexpression promoted epithelial-mesenchymal transition (EMT) and increased neuropilin-1 (NRP1) expression in the CRC cells;the critical role of lnc00152 in tumor growth and progression in CRC	29956750	RID00036	ceRNA or sponge
Colon cancer	MALAT1	HMGB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	LncRNA MALAT1 induces colon cancer development by regulating miR-129-5p/HMGB1 axis;miR-129-5p was identified and confirmed as a direct regulator of MALAT1;MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer;miR-129-5p mimics were able to restrain the progression of colon cancer cells;Inhibition of MALAT1 can inhibit the proliferation of colon cancer	29226325	RID00037	ceRNA or sponge
Hepatocellular carcinoma	NEAT1	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-485)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|NCRNA00084|TncRNA|VINC	ADMIO|ADMIO1|APRF|HIES	The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR-485 and enhancing the expression of the STAT3;sh-STAT3 was able to restrain HCC cell migration and invasion process;NEAT1 inhibiton can repress HCC growth, migration, and invasion. NEAT1 paraspeckle promotes human hepatocellular carcinoma progression by strengthening IL-6/STAT3 signaling.Destruction of paraspeckle formation by silencing the paraspeckle essential components NEAT1_2 or NONO could suppress IL-6-induced STAT3 phosphorylation in HCC cells.Our results demonstrate that paraspeckle can nuclear entrap the inhibitors of IL-6/STAT3 signaling as well as DNA damage, and then strengthen the promoting effect on HCC progression by IL-6. Mechanistically, paraspeckle promotes IL-6-induced STAT3 phosphorylation by binding and trapping peroxiredoxin-5 (PRDX5) mRNA in nucleus, decreasing protein level of PRDX5 which can directly interact with STAT3 and inhibit STAT3 phosphorylation.	29219178;30377567	RID00038	ceRNA or sponge
Non-small cell lung cancer	MALAT1	STAT3	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-124)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168610	NA	378938	6774	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ADMIO|ADMIO1|APRF|HIES	The lncRNA MALAT1 contributes to non-small cell lung cancer development via modulating miR-124/STAT3 axis;Downregulation of MALAT1 can inhibit NSCLC development by enhancing miR-124 and decreasing STAT3 expression;shMALAT1 can inhibit NSCLC cell proliferation, colony formation and apoptosis	29215698	RID00039	ceRNA or sponge
Lung adenocarcinoma	SNHG5	CASP1	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	ceRNA(miR-377)	regulation	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000137752	NA	387066	834	C6orf160|LINC00044|NCRNA00044|U50HG	ICE|IL1BC|P45	The long non-coding RNA SNHG5 regulates gefitinib resistance in lung adenocarcinoma cells by targetting miR-377/CASP1 axis;SNHG5 overexpression sensitized gefitinib resistant; Overexpression of SNHG5 suppressed the expression of miR-377, while the knockdown of SNHG5 increased the miR-377 expression;CASP1 was predicted as a downstream target of miR-377	29592872	RID00040	ceRNA or sponge
Osteosarcoma	FOXP4-AS1	LATS1	negatively-E	RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000131023	NA	101060264	9113	NA	WARTS|wts	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID00041	epigenetic regulation
Urinary bladder cancer	TUG1	miR-29c	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Upregulation of Long Noncoding RNA TUG1 Promotes Bladder Cancer Cell proliferation, Migration, and Invasion by Inhibiting miR-29c;There were direct interactions between miR-29c and the binding sites of TUG1	29321088	RID00042	ceRNA or sponge
Urinary bladder cancer	LNCRNA-ATB	miR-126	negatively-F	qRT-PCR;luciferase reporter assay	NA	NA	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	NA	GRCh38_14:19126530-19128974	NA	NA	114004396	NA	NA	NA	Long Noncoding RNA ATB Promotes proliferation, Migration, and Invasion in Bladder Cancer by Suppressing MicroRNA-126;lncRNA-ATB overexpression significantly promoted cell viability, migration, and invasion in T24 cells;lncRNA-ATB was a molecular sponge of miR-126 and exerted tumor-promoting effects by downregulation of miR-126	29321082	RID00043	ceRNA or sponge
Retinoblastoma	SP1	PANDAR	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	Sustained Angiogenesis	Cancer	Retinoblastoma	TF	lncRNA	ENSG00000185591	NA	ENSG00000281450	GRCh38_6:36673621-36675126	6667	101154753	NA	PANDA	SP1-induced upregulation of lncRNA PANDAR predicts adverse phenotypes in retinoblastoma and regulates cell growth and apoptosis in vitro and in vivo;SP1 could bind directly to the PANDAR promoter region and activate its transcription;PANDAR was increased in RB tissues and cells, and this upregulation was associated with advanced IIRC stage, positive optic nerve invasion, and lower differentiation grade in RB patients	29778422	RID00044	transcriptional regulation
Colorectal cancer	STAT1	LINC00174	positively-E	luciferase reporter assay;RNA pull-down assay;RNAi;JARSPAR	upregulation	sequencing	TCGA	COAD.zip	cancer progression(+);prognosis(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000115415	NA	ENSG00000179406	GRCh38_7:66376044-66493566	6772	285908	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	NCRNA00174	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ;the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients;transcription factor STAT1 mediated LINC00174 expression in CRC	29729381	RID00045	transcriptional regulation
Colorectal cancer	LINC00174	TAZ	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis(+)	ceRNA(miR-1910-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000179406	GRCh38_7:66376044-66493566	ENSG00000102125	NA	285908	6901	NCRNA00174	BTHS|CMD3A|EFE|EFE2|G4.5|LVNCX|Taz1	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ;the aberrant overexpression of LINC00175 indicated the poor prognosis of CRC patients;LINC00174 contributed to CRC progression by regulating miR-1910-3p/TAZ signal pathway	29729381	RID00046	ceRNA or sponge
Non-small cell lung cancer	TP73-AS1	EZH2	positively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	epigenetic regulation;ceRNA(miR-449a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000106462	NA	57212	2146	KIAA0495|PDAM	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA TP73-AS1 promotes non-small cell lung cancer progression by competitively sponging miR-449a/EZH2;miR-449a both targeted the 3'-UTR of TP73-AS1 and EZH2;the knockdown of TP73-AS1 inhibited NSCLC cell proliferation, tumor growth and cycle progression in vivo and in vitro	29803931	RID00047	epigenetic regulation;ceRNA or sponge
Triple-receptor negative breast cancer	GAS5	miR-196a-5p	negatively-F	qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA GAS5 suppresses triple negative breast cancer progression through inhibition of proliferation and invasion by competitively binding miR-196a-5p;GAS5 can bind to miR-196a-5p and there is a negative relationship between GAS5 and miR-196a-5p expression;GAS5 functioned as a competing endogenous RNA (ceRNA) antagonizing tumor promotion of miR-196a-5p-expressing TNBC cells	29793177	RID00048	ceRNA or sponge
Endometrial cancer	MIR22HG	DAPK1	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-141-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000196730	NA	84981	1612	C17orf91	DAPK|ROCO3	LncRNA MIR22HG negatively regulates miR-141-3p to enhance DAPK1 expression and inhibits endometrial carcinoma cells proliferation;miR-141-3p was identified and confirmed to be the target of MIR22HG;DAPK1 was confirmed to be regulated by MIR22HG and miR-141-3p	29775889	RID00049	ceRNA or sponge
Chronic myeloid leukemia	MEG3	miR-21	negatively-E	RNA pull-down assay;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	epigenetic regulation;sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long noncoding RNA MEG3 inhibits proliferation of chronic myeloid leukemia cells by sponging microRNA21;Overexpression of MEG3 and silencing the expression of miR-21 inhibited proliferation and induced apoptosis.lncRNA MEG3 and its target miR21 may serve as novel therapeutic targets for CML blast crisis; and demethylation drugs might also have potential clinical application in treating CML blast crisis.	29772439	RID00050	epigenetic regulation;ceRNA or sponge
Pancreatic cancer	MIAT	miR-133a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	The interaction of long non-coding RNA MIAT and miR-133 play a role in the proliferation and metastasis of pancreatic carcinoma;Bioinformatics analysis and luciferase reporter assay validated that miR-133 may target MIAT 3'-UTR;	29772434	RID00051	ceRNA or sponge
Hepatocellular carcinoma	SOX21-AS1	CDKN1A	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000124762	NA	100507533	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA SOX21-AS1 is associated with progression of hepatocellular carcinoma and predicts prognosis through epigenetically silencing p21;SOX21-AS1 epigenetically silenced p21 via recruiting EZH2 to the promoter of p21;SOX21-AS1 can interact with p21 to affect hepatocellular carcinoma progression	29772433	RID00052	epigenetic regulation
Osteosarcoma	DICER1-AS1	ATG5	positively-E	luciferase reporter assay;RIP;western blot	upregulation	microarray;RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell autophagy(+)	ceRNA(miR-30b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000235706	GRCh38_14:95157645-95181475	ENSG00000057663	NA	400242	9474	DICER1-AS	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	LncRNA DICER1-AS1 promotes the proliferation, invasion and autophagy of osteosarcoma cells via miR-30b/ATG5;miR-30b was verified to target 3'-UTR of DICER1-AS1 and ATG5	29772430	RID00053	ceRNA or sponge
Tongue squamous cell carcinoma	CASC15	miR-33a-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000272168	GRCh38_6:21664185-22654455	NA	NA	401237	NA	CANT|LINC00340|lnc-SOX4-1	NA	Long non-coding RNA CASC15 promotes tongue squamous carcinoma progression through targeting miR-33a-5p; Moreover, we showed that the expression of CASC15 was negatively related with miR-33a-5p expression in TSCC tissues.Ectopic expression of CASC15 promoted TSCC cell proliferation, cycle, and migration through targeting miR-33a-5p	29804249	RID00054	expression association
Non-small cell lung cancer	FOXO1	RP11-838N2.4	negatively-E	ChIP	upregulation	microarray;RT-PCR	NA	NA	chemoresistance(+)	histone modification	binding/interaction	RNA-RNA	erlotinib	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000150907	NA	ENSG00000266835	GRCh38_18:3466250-3478978	2308	NA	FKH1|FKHR|FOXO1A	NA	Exosome-mediated transfer of lncRNA RP11-838N2.4 promotes erlotinib resistance in non-small cell lung cancer.forkhead box protein O1 (FOXO1) could bind to the promoter region of lncRNA RP11-838N2.4, resulting in its silencing through the recruitment of histone deacetylase.	29845246	RID00055	epigenetic regulation
Hepatocellular carcinoma	FTX	PPARG	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+);cancer progression(+)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	TF	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000132170	NA	100302692	5468	LINC00182|MIR374AHG|NCRNA00182	CIMT1|GLM1|NR1C3|PPARG1|PPARG2|PPARgamma	lncRNA Ftx promotes aerobic glycolysis and tumor progression through the PPARgamma pathway in hepatocellular carcinoma;peroxisome proliferator-activated receptor gamma (PPARgamma) expression in human HCC tissues and cell lines was positively correlated with lncRNA Ftx	29845188	RID00056	expression association
Laryngeal squamous cell carcinoma	MIR31HG	miR-31	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);cell cycle(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long non-coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR-31;LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR-31 expression.Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues.	29737563	RID00057	expression association
Osteosarcoma	BTG3-AS1	miR-21	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000280594	GRCh38_21:17611744-17633199	NA	NA	110806272	NA	NA	NA	Long non-coding RNA ASBEL promotes osteosarcoma cell proliferation, migration,and invasion by regulating microRNA-21;Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR-21;PP2A was a direct target of miR-21;we verified that ASBEL-miR-21-PP2A pathway might play critical regulatory effects on the pathogenesis of osteosarcoma	29323740	RID00058	expression association
Hepatocellular carcinoma	CASC2	miR-24-3p	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell viability(-);apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR-24-3p;the expression of CASC2 was negatively related to miR-24-3p expression in the HCC tissues;CASC2 could negatively regulate the expression of miR-24-3p in vitro	29091305	RID00059	expression association
Gastric cancer	TFAP4	TRERNA1	positively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000090447	NA	ENSG00000231265	GRCh38_20:50040716-50041504	7023	100887755	AP-4|bHLHc41	LINC00651|treRNA	Elevated TFAP4 regulates lncRNA TRERNA1 to promote cell migration and invasion in gastric cancer;TFAP4 specifically regulated the transcriptional activity of TRERNA1 by binding to the E box motifs in the TRERNA1 promoter;TRERNA1 was upregulation in gastric carcinogenesis and promoted cell migration and invasion in GC	29845218	RID00061	transcriptional regulation
Pancreatic cancer	PVT1	TGFB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000105329	NA	5820	7040	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00062	expression association
Pancreatic cancer	PVT1	SMAD2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000175387	NA	5820	4087	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00063	expression association
Pancreatic cancer	PVT1	SMAD3	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000166949	NA	5820	4088	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HSPC193|HsT17436|JV15-2|LDS1C|LDS3|MADH3	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00064	expression association
Pancreatic cancer	PVT1	SMAD4	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);TGF-beta/SMAD signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000141646	NA	5820	4089	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	DPC4|JIP|MADH4|MYHRS	PVT1 promoted the growth and the epithelial mesenchymal transition;knockdown of PVT1 inhibited the TGF-beta/Smad signaling, including p-Smad2/3 and TGF-beta1 but enhanced the expression of Smad4	29845201	RID00065	expression association
Lung cancer	OIP5-AS1	miR-378a-3p	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000247556	GRCh38_15:41283990-41309737	NA	NA	729082	NA	cyrano|linc-OIP5	NA	Long non-coding RNA OIP5-AS1 promotes proliferation of lung cancer cells and leads to poor prognosis by targeting miR-378a-3p;OIP5-AS1 functions as a competing endogenous RNA of miR-378a-3p;the speed of tumor growth was increased and decreased when OIP5-AS1 was upregulation and downregulated	29897167	RID00066	ceRNA or sponge
Colon cancer	XIST	WNT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000125084	NA	7503	7471	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	BMND16|INT1|OI15	Long non-coding RNA XIST sponges miR-34a to promotes colon cancer progression via WNT/beta-catenin signaling pathway;the growth rate of cells transfected with si-XIST was significantly decreased compared to that with si-NC, which was reversed by miR-34a targeted with 3'-UTR;Moreover, miR-34a suppressed the expression of WNT1 by binding with the 3'-UTR	29679755	RID00067	ceRNA or sponge
Urinary bladder cancer	LSINCT5	MYCNOS-01	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENST00000641263	GRCh38_2:15936265-15941582	101234261	NA	NA	NA	LSINCT5 activates Wnt/beta-catenin signaling by interacting with NCYM to promote bladder cancer progression;LSINCT5 could physically interact with NCYM, a de novo gene product from the MYCN cis-antisense RNA and inhibit GSK3beta activity leading to enhanced Wnt/beta-catenin signaling activation and epithelial mesenchymal transition.	29772237	RID00068	interact with protein
Prostate cancer	PCSEAT	EZH2	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	PRAD.zip	cell proliferation(+)	ceRNA(miR-143-3p;miR-24-2-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	NA	GRCh38.p13:41576148-41581634	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA PCSEAT exhibits an oncogenic property in prostate cancer and functions as a competing endogenous RNA that associates with EZH2;PCSEAT promotes cell proliferation, at least in part by affecting miR-143-3p- and miR-24-2-5p-mediated regulation of EZH2, suggesting that PCSEAT and EZH2 competitively sponge miR-143-3p and miR-24-2-5p	29803673	RID00069	ceRNA or sponge
Pancreatic ductal adenocarcinoma	PVT1	ULK1	positively-E	RNA pull-down assay;RIP	upregulation	qRT-PCR;ISH	GSE15471;GSE16515	GSE15471.zip;GSE16515.zip	cell autophagy(+);cancer progression(+)	ceRNA(miR-20a-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000177169	NA	5820	8408	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG1|ATG1A|UNC51|Unc51.1|hATG1	LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis;PVT1 promoted cyto-protective autophagy and cell growth by targeting ULK1;PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression	30001707	RID00070	ceRNA or sponge
Cervical cancer	MALAT1	miR-142-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	metformin	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Metformin, a first-line drug for type 2 diabetes mellitus, disrupts the MALAT1/miR-142-3p sponge to decrease invasion and migration in cervical cancer cells;the direct interaction between miR-142-3p and MALAT1 were located in the 3'untranslated region (3'UTR) of lncRNA MATAL1	29704494	RID00071	ceRNA or sponge
Cholangiocarcinoma	NEAT1	CDH1	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000039068	NA	283131	999	LINC00084|NCRNA00084|TncRNA|VINC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells;NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression	29970216	RID00072	epigenetic regulation
Tongue cancer	KCNQ1OT1	EZR	positively-E	luciferase reporter assay	upregulation	microarray;RT-PCR	NA	NA	chemoresistance(+);cell proliferation(+);Ezrin/Fak/Src signaling pathway(-)	ceRNA(miR-211-5p)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000092820	NA	10984	7430	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CVIL|CVL|HEL-S-105|VIL2	LncRNA KCNQ1OT1 regulates proliferation and cisplatin resistance in tongue cancer via miR-211-5p mediated Ezrin/Fak/Src signaling;miR-211-5p harbor binding sites for the 3'-UTRof Ezrin Mrna;KCNQ1OT1 facilitates tumor growth and chemo-resistance by acting as a competing endogenous RNA (ceRNA) to modulate the expression of miR-211-5p	29970910	RID00073	ceRNA or sponge
Cholangiocarcinoma	SNHG1	CDKN1A	negatively-E	RIP;RNA pull-down assay	upregulation	microarray;RT-PCR	TCGA;GSE76297	CHOL.zip;GSE76297.zip	cell proliferation(+);cell migration(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000124762	NA	23642	1026	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma;SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A;SNHG1 knockdown extensively inhibited CCA cell migration as well as proliferation in vitro and in vivo	29970899	RID00074	epigenetic regulation
Gastric cancer	linc-UFC1	LIN28B	negatively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-498)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:161152776-161158856	ENSG00000187772	NA	NA	389421	NA	NA	Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b; UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression	29970131	RID00075	ceRNA or sponge
Colorectal cancer	SNHG7	GALNT7	positively-E	RNAi;luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+);cancer progression(+);cell proliferation(+);cell metastasis(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000109586	NA	84973	51809	NCRNA00061	GALNAC-T7|GalNAcT7	Long non-coding RNA-SNHG7 acts as a target of miR-34a to increase GALNT7 level and regulate PI3K/Akt/mTOR pathway in colorectal cancer progression;Further results indicated that SNHG7 facilitated the proliferation and metastasis as a competing endogenous RNA to regulate GALNT7 expression by sponging miR-34a in CRC cell lines.SNHG7 also played the oncogenic role in regulating PI3K/Akt/mTOR pathway by competing endogenous miR-34a and GALNT7.	29970122	RID00076	ceRNA or sponge
Ovarian cancer	UCA1	ABCB1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-129)	regulation	NA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000085563	NA	652995	5243	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	UCA1 confers paclitaxel resistance to ovarian cancer through miR-129/ABCB1 axis;UCA1 silencing induced PTX sensitivity of SKOV3/PTX and HeyA-8/PTX cells by de-repressing ABCB1 through sponging miR-129	29777711	RID00077	ceRNA or sponge
Prostate cancer	FENDRR	RUNX1	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+);cell invasion(-);cell migration(-)	ceRNA(miR-18a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000159216	NA	400550	861	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	Long non-coding RNA FENDRR reduces prostate cancer malignancy by competitively binding miR-18a-5p with RUNX1;FENDRR and RUNX1 contain potential target sites for miR-18a-5p;The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1	29465000	RID00078	ceRNA or sponge
Multiple myeloma	FEZF1-AS1	AKT3	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-610)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Myeloma	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000117020	NA	154860	10000	NA	MPPH|MPPH2|PKB-GAMMA|PKBG|PRKBG|RAC-PK-gamma|RAC-gamma|STK-2	Long non-coding RNA FEZF1-AS1 promotes cell growth in multiple myeloma via miR-610/Akt3 axis;our data indicated that FEZF1-AS1 functioned as a competing endogenous RNA in MM cells that regulated miR-610 expression, which suppressed Akt3;FEZF1-AS1 promoted MM cells proliferation through regulating miR-610/Akt3 axis.Akt3 acted a target of miR-610 and positively related to FEZF1-AS1	29864963	RID00079	ceRNA or sponge
Non-small cell lung cancer	NEAT1	IGF2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell metastasis(+)	ceRNA(let-7a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000167244	NA	283131	3481	LINC00084|NCRNA00084|TncRNA|VINC	C11orf43|GRDF|IGF-II|PP9974	lncRNA NEAT1 competes against let-7a to contribute to non-small cell lung cancer proliferation and metastasis;Luciferase reporter assay validated direct binding of NEAT1/let-7a and let-7a/IGF-2;NEAT1 regulates lung cancer cell progression by competing endogenous RNA network of NEAT1/let-7a/IGF2	29864936	RID00080	ceRNA or sponge
Cervical cancer	BCYRN1	miR-138	negatively-F	luciferase reporter assay	upregulation	qRT-PCR;northern blot	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000236824	GRCh38_2:47335315-47335514	NA	NA	618	NA	BC200|BC200a|LINC00004|NCRNA00004	NA	Long non-coding RNA BCYRN1 promotes the proliferation and metastasis of cervical cancer via targeting microRNA-138 in vitro and in vivo.	29552212	RID00081	ceRNA or sponge
Chondrosarcoma	BCAR4	MTOR	positively-E	western blot;RNAi;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);mTOR signaling pathway(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000198793	NA	400500	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long non-coding RNA BCAR4 promotes chondrosarcoma cell proliferation and migration through activation of mTOR signaling pathway.Impact statement LncRNA BCAR4 promoted chondrosarcoma cell proliferation and migration through activation of mTOR signaling pathway, and thus contributed to chondrosarcoma progression.mTOR signaling pathway was epigenetically activated by BCAR4-induced hyperacetylation of histone H3.	28399646	RID00082	epigenetic regulation
Non-small cell lung cancer	BCAR4	VIM	negatively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000026025	NA	400500	7431	NA	NA	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00083	expression association
Non-small cell lung cancer	BCAR4	CDH2	positively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000170558	NA	400500	1000	NA	CD325|CDHN|CDw325|NCAD	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00084	expression association
Non-small cell lung cancer	BCAR4	CDH1	positively-E	RNAi;western blot;immunofluorescence assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000039068	NA	400500	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition.BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).	28537678	RID00085	expression association
Gastric cancer	BLACAT1	ABCB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	ceRNA(miR-361)	regulation	NA	oxaliplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000085563	NA	101669762	5243	LINC00912|linc-UBC1|onco-lncRNA-30	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long noncoding RNA BLACAT1 modulates ABCB1 to promote oxaliplatin resistance of gastric cancer via sponging miR-361.	29710482	RID00087	ceRNA or sponge
Non-small cell lung cancer	TUG1	MKI67	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148773	NA	55000	4288	LINC00080|NCRNA00080|TI-227H	KIA|MIB-|MIB-1|PPP1R105	Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC. Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	29277771	RID00088	expression association
Non-small cell lung cancer	TUG1	HOXB7	negatively-E	RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000260027	NA	55000	3217	LINC00080|NCRNA00080|TI-227H	HHO.C1|HOX2|HOX2C|Hox-2.3	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421;29277771	RID00089	epigenetic regulation
Non-small cell lung cancer	TUG1	EZH2	interact	RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421;27485439	RID00090	interact with protein
Non-small cell lung cancer	TP53	TUG1	positively-E	ChIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000253352	GRCh38_22:30969245-30979395	7157	55000	BCC7|BMFS5|LFS1|P53|TRP53	LINC00080|NCRNA00080|TI-227H	P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. Here we report that taurine-upregulated gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in non-small cell lung carcinoma (NSCLC) tissues. ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy.Silencing of TUG1 inhibited both tumor growth and expression of the proliferation marker Ki67 and HOX-gene family HOXB7 in the PDX model of NSCLC.	24853421	RID00091	transcriptional regulation
Acute myeloid leukemia	CASC15	SOX4	positively-E	luciferase reporter assay	upregulation	qRT-PCR;microarray	GSE75461;GSE17459	GSE75461.zip;GSE17459.zip	cell survival(+);cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000124766	NA	401237	6659	CANT|LINC00340|lnc-SOX4-1	EVI16	The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia; At the cellular level, CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4. we found that CASC15 enhances YY1-mediated regulation of the SOX4 promoter;CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4.	28724437	RID00093	transcriptional regulation
Melanoma	CASC2	PLXNC1	positively-E	luciferase reporter assay	downregulation	microarray	GSE86373	GSE86373.zip	tumorigenesis(-)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000136040	NA	255082	10154	C10orf5	CD232|PLXN-C1|VESPR	Long non-coding RNA CASC2 inhibits tumorigenesis via the miR-181a/PLXNC1 axis in melanoma.Our results demonstrated that lncRNA CASC2 can promote PLXNC1 expression by sponging miR-181a, thereby inhibiting the proliferation and invasion of melanoma cells, indicating that lncRNA CASC2 functions via the miR-181a/PLXNC1 axis in melanoma.	29514220	RID00094	ceRNA or sponge
Renal cell carcinoma	miR-21	CASC2	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	255082	NA	C10orf5	Downregulation of lncRNA CASC2 by microRNA-21 increases the proliferation and migration of renal cell carcinoma cells.The present study provides evidence indicating that CASC2 targeted by miR-21 acts as a tumor suppressor in RCC. Therefore, CASC2 may be considered a novel target for the diagnosis and treatment of RCC.	27222255	RID00095	ceRNA or sponge
Osteosarcoma	CASC2	miR-181a	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a;ectopic expression of CASC2 suppressed miR-181a expression and enhanced the expression of Ras association domain family member 6 (RASSF6), PTEN and ATM in osteosarcoma cell, which were the direct target gene of miR-181a	29194827	RID00096	expression association
Osteosarcoma	CASC2	RASSF6	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000169435	NA	255082	166824	C10orf5	NA	Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a.Ectopic expression of CASC2 suppressed the osteosarcoma cell proliferation,colony formation and invasion through regulating RASSF6 expression;the expression of RASSF6 was positively correlated with the expression of CASC2 in osteosarcoma tissues	29194827	RID00097	expression association
Colorectal cancer	CASC2	PIAS3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	ceRNA(miR-18a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000131788	NA	255082	10401	C10orf5	ZMIZ5	Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a.This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth	27198161	RID00098	ceRNA or sponge
Colorectal cancer	CASC2	STAT3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell growth(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000168610	NA	255082	6774	C10orf5	ADMIO|ADMIO1|APRF|HIES	The long noncoding RNA CASC2 functions as a competing endogenous RNA by sponging miR-18a in colorectal cancer. In this study, CASC2 expression was significantly decreased in CRC tissues and CRC cell lines.Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a. This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth in vitro and in vivo by extending the G0/G1-S phase transition.	27198161	RID00099	expression association
Hepatocellular carcinoma	CASC2	FBXW7	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-)	ceRNA(miR-367)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000109670	NA	255082	55294	C10orf5	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	Long non-coding RNA CASC2 suppresses epithelial-mesenchymal transition of hepatocellular carcinoma cells through CASC2/miR-367/FBXW7 axis;Further studies demonstrated that CASC2 could function as a competing endogenous RNA (ceRNA) by sponging miR-367 in HCC cells;further investigations disclosed that FBXW7 was a downstream target of miR-367 and CASC2 prohibited EMT progression and subsequently exerted its anti-metastatic effects via CASC2/miR-367/FBXW7 axis in HCC cells	28716020	RID00100	ceRNA or sponge
Hepatocellular carcinoma	CASC2	miR-362-5p	negatively-F	luciferase reporter assay;qRT-PCR	downregulation	qRT-PCR	NA	NA	NF-kB signaling pathway(-);tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR-362-5p/Nf-kB axis.we determined that CASC2 regulates HCC cell activity by targeting miR-362-5p and thus inhibiting the NF-kB pathway.we identified the microRNA miR-362-5p as an endogenous target of CASC2	29319182	RID00101	ceRNA or sponge
Epithelial ovarian cancer	CASC2	EIF4A3	negatively-F	RIP	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);cancer progression(-)	interact with protein	binding/interaction	RNA-protein	sanguinarine	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000141543	NA	255082	9775	C10orf5	DDX48|Fal1|MUK34|NMP265|NUK34|RCPS|eIF-4A-III|eIF4A-III|eIF4AIII	Sanguinarine inhibits epithelial ovarian cancer development via regulating long non-coding RNA CASC2-EIF4A3 axis and/or inhibiting NF-kB signaling or PI3K/AKT/mTOR pathway. Our findings reveal that sanguinarine exhibits antitumor effects in epithelial ovarian cancer cells possible via regulating CASC2-EIF4A3 axis and/or inhibiting NF-kB signaling or PI3K/AKT/mTOR pathway.EIF4A3 was identified as a CASC2 binding protein.	29571014	RID00102	interact with protein
Colorectal cancer	CASC7	ING3	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000259758	GRCh38_8:140520156-140529501	ENSG00000071243	NA	NA	54556	NA	Eaf4|ING2|MEAF4|p47ING3	Long non-coding RNA CASC7 inhibits the proliferation and migration of colon cancer cells via inhibiting microRNA-21;CASC7 and ING3 were both a target of miR-21 in CRC cells, and CASC7 could control ING3 expression by regulating miR-21. Moreover, we have found that CASC7 inhibited colon cancer cell proliferation and migration via miR-21/ING3 axis. These observations suggested that CASC7 played an important role in CRC pathogenesis and may be considered as a novel diagnostic marker of CRC.	28954383	RID00103	ceRNA or sponge
Urinary bladder cancer	CASC8	FGFR1	interact	western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);glucose metabolic process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000246228	GRCh38_8:127289817-127482139	ENSG00000077782	NA	727677	2260	CARLO1|CARLo-1|LINC00860	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Long Noncoding RNA Cancer Susceptibility Candidate 8 Suppresses the Proliferation of Bladder Cancer Cells via Regulating Glycolysis.Overexpression of CASC8 remarkably suppressed the bladder cancer cell proliferation. Mechanistically, we illustrated that CASC8 reduced the glycolysis of bladder cancer cells via interacting with the fibroblast growth factor receptor 1 (FGFR1).	28759252	RID00104	interact with protein
Esophagus squamous cell carcinoma	CASC9	PDCD4	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000150593	NA	101805492	27250	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	H731	Up-regulation of lncRNA CASC9 promotes esophageal squamous cell carcinoma growth by negatively regulating PDCD4 expression through EZH2.Our study firstly demonstrates that lncRNA CASC9 functions as an oncogene by negatively regulating PDCD4 expression through recruiting EZH2 and subsequently altering H3K27me3 level.Furthermore interfering CASC9 decreased cell proliferation and blocked cell cycle G1/S transition.	28854977	RID00105	epigenetic regulation
Esophagus squamous cell carcinoma	CASC9	EZH2	interact	RIP;RNA pull-down assay;ChIP	upregulation	microarray;qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000106462	NA	101805492	2146	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Up-regulation of lncRNA CASC9 promotes esophageal squamous cell carcinoma growth by negatively regulating PDCD4 expression through EZH2;enhancer of zeste homolog2 (EZH2) could bind to both CASC9 and PDCD4 promoter region. Interfering CASC9 reduced the enrichment of EZH2 and H3K27me3 in the PDCD4 promoter region	28854977	RID00106	interact with protein
Gastric cancer	CASC9	ABCB1	positively-E	RNAi;western blot	upregulation	microarray;qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	paclitaxel;adriamycin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000085563	NA	101805492	5243	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Silence of cancer susceptibility candidate 9 inhibits gastric cancer and reverses chemoresistance.In addition, CASC9 knockdown in BGC823/DR and SGC7901/DR cells restored chemosensitivity to paclitaxel and adriamycin. This was associated with decreased expression of multidrug resistance 1 (MDR1) protein	28146436	RID00107	expression association
Gastric cancer	CAT104	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	ceRNA(miR-381)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:148879196-148879701	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Noncoding RNA CAT104 Promotes Cell Viability, Migration, and Invasion in Gastric Carcinoma Cells Through Activation of MicroRNA-381-Inhibiting Zinc Finger E-box-Binding Homeobox 1 (ZEB1) Expression.Bioinformatics analysis found that CAT104 was negatively bound to miR-381. Zinc finger E-box-binding homeobox 1 (ZEB1) was identified as a direct target of miR-381.	29295724	RID00108	ceRNA or sponge
Melanoma	CCAT1	miR-33a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	The lncRNA CCAT1 Upregulates proliferation and Invasion in Melanoma Cells via Suppressing miR-33a.Bioinformatics analysis predicted that miR-33a acted as a target of CCAT1, which was confirmed by dual-luciferase reporter assay.CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma	28409554	RID00110	ceRNA or sponge
Renal cell carcinoma	CCAT1	BIRC7	positively-F	RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000101197	NA	100507056	79444	CARLO5|CARLo-5|onco-lncRNA-40	KIAP|LIVIN|ML-IAP|MLIAP|RNF50	LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein.RNA pulldown and RIP assays showed that CCAT1 was physically associated with Livin protein. Livin was significantly inhibited by CCAT1 silencing;CCAT1 silencing could inhibit the growth of RCC in vivo that was accompanied by the reduction of Livin in RCC tissues. CCAT1 inhibits RCC cell apoptosis and increases cell viability through up-regulation of Livin	28470345	RID00111	interact with protein
Nasopharynx carcinoma	CCAT1	CPEB2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemosensitivity(-)	ceRNA(miR-181a)	regulation	NA	paclitaxel	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000137449	NA	100507056	132864	CARLO5|CARLo-5|onco-lncRNA-40	CPE-BP2|CPEB-2|hCPEB-2	LncRNA CCAT1 modulates the sensitivity of paclitaxel in nasopharynx cancers cells via miR-181a/CPEB2 axis.Bioinformatics analysis and luciferase reporter assay indicated that the upregulation CCAT1 sponges miR-181a in NPC cells. Furthermore, RNA immuno-precipitation assays showed that miR-181a could directly bind to CCAT1 mRNA in NPC cells. We restored miR-181a in NPC cells, and found restoration of miR-181a re-sensitized the NPC cells to paclitaxel in vitro. In addition, our results also showed that miR-181a was a modulator of paclitaxel sensitivity due to its regulative effect on cell apoptosis via targeting CPEB2 in NPC cells.	28358263	RID00112	ceRNA or sponge
Lung adenocarcinoma	CCAT1	BCL2L1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(let-7c)	regulation	NA	docetaxel	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000171552	NA	100507056	598	CARLO5|CARLo-5|onco-lncRNA-40	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells.the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells.	27566568	RID00113	ceRNA or sponge
Laryngeal squamous cell carcinoma	CCAT1	ZFX	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000005889	NA	100507056	7543	CARLO5|CARLo-5|onco-lncRNA-40	ZNF926	Long non-coding RNA CCAT1/miR-218/ZFX axis modulates the progression of laryngeal squamous cell cancer.colon cancer-associated transcript-1 knockdown inhibits proliferation and invasion of laryngeal squamous cell cancer cells through enhancing zinc finger protein, X-linked by sponging microRNA-218	28631575	RID00114	ceRNA or sponge
Epithelial ovarian cancer	CCAT1	ADAM17	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-152)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000151694	NA	100507056	6868	CARLO5|CARLo-5|onco-lncRNA-40	ADAM18|CD156B|CSVP|NISBD|NISBD1|TACE	Long non-coding RNA CCAT1 promotes metastasis and poor prognosis in epithelial ovarian cancer.We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion. our study first revealed a critical role of CCAT1-miR-152/miR-130b-ADAM17/WNT1/STAT3/ZEB1 regulatory network in EOC cell metastasis.	28754469	RID00115	ceRNA or sponge
Epithelial ovarian cancer	CCAT1	WNT1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-152)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000125084	NA	100507056	7471	CARLO5|CARLo-5|onco-lncRNA-40	BMND16|INT1|OI15	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00116	ceRNA or sponge
Epithelial ovarian cancer	CCAT1	STAT3	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-130b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000168610	NA	100507056	6774	CARLO5|CARLo-5|onco-lncRNA-40	ADMIO|ADMIO1|APRF|HIES	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00117	ceRNA or sponge
Epithelial ovarian cancer	CCAT1	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);prognosis	ceRNA(miR-130b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000148516	NA	100507056	6935	CARLO5|CARLo-5|onco-lncRNA-40	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b,Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion.	28754469	RID00118	ceRNA or sponge
Hepatocellular carcinoma	CCAT1	CDK1	positively-E	luciferase reporter assay;RNA pull-down assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000170312	NA	100507056	983	CARLO5|CARLo-5|onco-lncRNA-40	CDC2|CDC28A|P34CDC2	Long non-coding RNA colon cancer-associated transcript 1 functions as a competing endogenous RNA to regulate cyclin-dependent kinase 1 expression by sponging miR-490-3p in hepatocellular carcinoma progression.	28381168	RID00119	ceRNA or sponge
Colon cancer	CCAT2	miR-145	negatively-E	CRISPR/Cas9	upregulation	qRT-PCR	NA	NA	cell differentiation(+);cell proliferation(+)	maturation process	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	A novel mechanism of lncRNA and miRNA interaction: CCAT2 regulates miR-145 expression by suppressing its maturation process in colon cancer cells; We have observed that modulated expression of CCAT2 regulates the expression of miR-145 in colon cancer HCT-116 and HT-29 cells. In contrast, stable up-regulation of CCAT2 decreases mature miR-145 and increases the expression of several CSC markers in colon cancer cells. These results indicate CCAT2 selectively blocks miR-145 maturation by inhibiting pre-miR-145 export to cytoplasm;Knockout of CCAT2 increases miR-145 and negatively regulates miR-21 in HCT-116 cells, impairs proliferation and differentiation	28964256	RID00120	expression association
Epithelial ovarian cancer	CCAT2	miR-424	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	Long Noncoding RNA CCAT2 Knockdown Suppresses Tumorous Progression by Sponging miR-424 in Epithelial Ovarian Cancer.	28550684	RID00121	ceRNA or sponge
Lung adenocarcinoma	LINC00460	FOXA1	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	LUAD.zip	cell growth(+)	ceRNA(miR-302c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000129514	NA	728192	3169	NA	HNF3A|TCF3A	LncRNA LINC00460 promotes tumor growth of human lung adenocarcinoma by targeting miR-302c-5p/FOXA1 axis. LINC00460 promotes LC progression by competitively binding miR-302c-5p and regulating FOXA1 signal pathway.	30359741	RID00122	ceRNA or sponge
Hepatocellular carcinoma	THORLNC	CTNNB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000168036	NA	100506797	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA THOR promotes liver cancer stem cells expansion via beta-catenin pathway.THOR was upregulation in liver CSCs and could promote HCC cells dedifferentiation and liver CSCs expansion by targeting beta-catenin signaling.the self-renewal capacity between THOR knockdown HCC cells and control cells, which further confirmed that beta-catenin was required in THOR promoted liver CSCs expansion.	30359743	RID00123	expression association
Nasopharynx carcinoma	LINC00319	KLF12	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	sequencing;qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-1207-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000188660	GRCh38_21:43446601-43453902	ENSG00000118922	NA	284836	11278	C21orf125|NCRNA00319|PRED49	AP-2rep|AP2REP|HSPC122	Long non-coding RNA 319 facilitates nasopharyngeal carcinoma carcinogenesis through regulation of miR-1207-5p/KLF12 axis. Rescue assay was performed to further confirm that LINC00319 contributed to NPC progression by regulating miR-1207-5p/KLF12 signal pathway. LINC00319 acts as a ceRNA for miR-1207-5p in NPC	30243935	RID00124	ceRNA or sponge
Retinoblastoma	H19	miR-143	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Knockdown of lncRNA-H19 inhibits cell viability, migration and invasion while promotes apoptosis via microRNA-143/RUNX2 axis in retinoblastoma.Knockdown of lncRNA-H19 acted a tumor suppressive role in Y79 cells through up-regulating miR-143. Moreover, miR-143 exerted tumor suppressive effects on Y79 cells by targeting RUNX2, along with inhibition of the PI3K/AKT/mTOR pathways.	30551533	RID00125	expression association
Retinoblastoma	H19	RUNX2	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000124813	NA	283120	860	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	Knockdown of lncRNA-H19 inhibits cell viability, migration and invasion while promotes apoptosis via microRNA-143/RUNX2 axis in retinoblastoma.Knockdown of lncRNA-H19 acted a tumor suppressive role in Y79 cells through up-regulating miR-143. Moreover, miR-143 exerted tumor suppressive effects on Y79 cells by targeting RUNX2, along with inhibition of the PI3K/AKT/mTOR pathways.	30551533	RID00126	expression association
Colon cancer	HULC	RTKN	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000114993	NA	728655	6242	HCCAT1|LINC00078|NCRNA00078	NA	Long non-coding RNA HULC interacts with miR-613 to regulate colon cancer growth and metastasis through targeting RTKN.	30551459	RID00127	ceRNA or sponge
Acute lymphocytic leukemia	HOXA-AS2	HOXA3	positively-E	RNAi;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+);EGFR/Ras/Raf/MEK/ERK signaling pathway(+)	transcriptional regulation	regulation	NA	glucocorticoid	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000105997	NA	285943	3200	HOXA3as	HOX1|HOX1E	TCF7L2 activated HOXA-AS2 decreased the glucocorticoid sensitivity in acute lymphoblastic leukemia through regulating HOXA3/EGFR/Ras/Raf/MEK/ERK pathway. we found that lncRNA HOXA-AS2 was highly expressed both in prednisone insensitive ALL cell lines and patient samples. Gain or loss-of-function assays revealed that HOXA-AS2 enhanced GC resistance via promoting cell proliferation and inhibiting cell apoptosis. Furthermore, we validated that HOXA-AS2 upregulation HOXA3, thereby activating EGFR/Ras/Raf/MEK/ERK signaling pathway. HOXA3 is a target of HOXA-AS2	30551418	RID00128	transcriptional regulation
Hepatocellular carcinoma	MIAT	EPHA2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-520d-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000142627	NA	440823	1969	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	ARCC2|CTPA|CTPP1|CTRCT6|ECK	Deregulation of miR-520d-3p promotes hepatocellular carcinoma development via lncRNA MIAT regulation and EPHA2 signaling activation.We also demonstrated that MIAT may function as a sponge competitive endogenous RNA for miR-520d-3p, and thus regulate the molecular expression of EPHA2.Decreased level of miR-520d-3p was relevant to poor overall survival,whereas miR-520d-3p up-regulation resulted in a marked inhibition of cell growth,migration and invasion.	30551417	RID00129	ceRNA or sponge
Non-small cell lung cancer	LINC01510	CDK14	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	prognosis(-);cancer progression(+)	ceRNA(miR-339-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000231210	GRCh38_7:116563594-116663829	ENSG00000058091	NA	100996266	5218	NA	PFTAIRE1|PFTK1	Increased expression of LINC01510 predicts poor prognosis and promotes malignant progression in human non-small cell lung cancer.mechanistic studies revealed that LINC01510 exerted its oncogenic functions in NSCLC through miR-339-5p-mediated regulation of CDK14.LINC01510 positively regulates CDK14 expression through sponging miR-339-5p in NSCLC cells	30399588	RID00130	ceRNA or sponge
Non-small cell lung cancer	SNHG16	MUC5AC	positively-E	luciferase reporter assay;qRT-PCR;ELISA	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	ceRNA(miR-146a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000215182	NA	100507246	4586	Nbla10727|Nbla12061|ncRAN	MUC5|TBM|leB|mucin	Increased expression of long non-coding RNA SNHG16 correlates with tumor progression and poor prognosis in non-small cell lung cancer.miR-146a is further identified and confirmed to be the target of SNHG16, and SNHG16 functions by targeting miR-146a. Subsequently, MUC5AC, a major mucin in the human respiratory tract correlated with post-operative metastasis and recurrence of NSCLC, is confirmed to be regulated by SNHG16 and miR-146a, and plays a positive role in promoting cell proliferation, migration and invasion	30287374	RID00131	ceRNA or sponge
Non-small cell lung cancer	EGFR-AS1	miR-223	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224057	GRCh38_7:55179750-55188934	NA	NA	100507500	NA	NA	NA	Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.Bioinformatics analysis and a luciferase reporter assay confirmed that EGFR-AS1 mediated cell proliferation and chemoresistance through directly binding to microRNA-223. Overexpression of lncRNA EGFR-AS1 is associated with a poor prognosis and promotes chemotherapy resistance in non-small cell lung cancer.	30431074	RID00132	ceRNA or sponge
Acute lymphocytic leukemia	SNHG16	miR-124-3p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor-suppressive function(+)	epigenetic regulation;sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000163597	GRCh38_17:76557764-76565348	NA	NA	100507246	NA	Nbla10727|Nbla12061|ncRAN	NA	Long non-coding RNA SNHG16 has Tumor suppressing effect in acute lymphoblastic leukemia by inverse interaction on hsa-miR-124-3p.SNHG16 is upregulation in ALL, and its inhibition has tumor suppressive effect in ALL, likely through epigenetic interaction on hsa-miR-124-3p.	30380185	RID00133	epigenetic regulation;ceRNA or sponge
Hepatocellular carcinoma	DGCR5	CTNNB1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000168036	NA	26220	1499	LINC00037|NCRNA00037	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00134	expression association
Hepatocellular carcinoma	DGCR5	CCND1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000110092	NA	26220	595	LINC00037|NCRNA00037	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00135	expression association
Hepatocellular carcinoma	DGCR5	GSK3B	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cancer progression(-);WNT signaling pathway(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000082701	NA	26220	2932	LINC00037|NCRNA00037	NA	Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting beta-catenin, cyclin D1 and increasing GSK-3beta levels	30230592	RID00136	expression association
Urinary bladder cancer	HIF1A-AS2	TP53	negatively-E	luciferase reporter assay;immunoprecipitation	upregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	transcriptional regulation	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000141510	NA	100750247	7157	3'aHIF-1A|aHIF	BCC7|BMFS5|LFS1|P53|TRP53	The long noncoding RNA HIF1A-AS2 facilitates cisplatin resistance in bladder cancer.Mechanically, we found that HIF1A-AS2 suppressed the transcription activity of p53 family proteins by promoting the expression of high-mobility group A1 (HMGA1).This study suggests that upregulation HIF1A-AS2 hampers the p53 family proteins dependent apoptotic pathway to promote Cis resistance in bladder cancer.	30216500	RID00137	transcriptional regulation
Urinary bladder cancer	SNHG6	SNAI1	interact	western blot;immunofluorescence assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124216	NA	641638	6615	HBII-276HG|NCRNA00058|U87HG	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer. SNHG6 is involved in regulation of EMT in BC, whichmay be mediated by Snail1/2	30168179	RID00138	interact with protein
Urinary bladder cancer	SNHG6	SNAI2	interact	western blot;immunofluorescence assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000019549	NA	641638	6591	HBII-276HG|NCRNA00058|U87HG	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer.SNHG6 is involved in regulation of EMT in BC, whichmay be mediated by Snail1/2	30168179	RID00139	interact with protein
Urinary bladder cancer	SNHG6	NUAK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000074590	NA	641638	9891	HBII-276HG|NCRNA00058|U87HG	ARK5	Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1-like kinase-1 expression by competitively binding microRNA-125b and interacting with Snail1/2 in bladder cancer. SNHG6 may partly regulate themigration and invasion of BC cells through the hsa-miR-125b-NUAK1 pathway	30168179	RID00140	ceRNA or sponge
Malignant glioma	LOC728196	TCF7	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	GSE83511	GSE83511.zip	tumorigenesis(+)	ceRNA(miR-513c)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENST00000651138	GRCh38.p13:111510602-111513888	ENSG00000081059	NA	728196	6932	NA	TCF-1	LncRNA LOC728196/miR-513c axis facilitates glioma carcinogenesis by targeting TCF7.Mechanistic studies further demonstrated that LOC728196 acts as the sponge for miR-513c to upregulate TCF7 expression.	30179681	RID00141	ceRNA or sponge
Hepatocellular carcinoma	LINC00052	SOX9	negatively-E	luciferase reporter assay	downregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000125398	NA	145978	6662	NCRNA00052|TMEM83	CMD1|CMPD1|SRA1|SRXX2|SRXY10	LINC00052/miR-101-3p axis inhibits cell proliferation and metastasis by targeting SOX9 in hepatocellular carcinoma.LINC00052 downgulated SOX9 to inhibit HCC cells proliferation and metastasis by interacting with miR-101-3p.	30098428	RID00142	ceRNA or sponge
Breast cancer	MEG3	NFKB1	positively-E	immunofluorescence staining	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000109320	NA	55384	4790	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-kB and p53.these results suggest that MEG3 inhibits breast cancer growth and induces breast cancer apoptosis, partially via the activation of the ER stress, NF-kB and p53 pathways, and that NF-kB signaling is required for MEG3-induced p53 activation in breast cancer cells.	30556250	RID00143	expression association
Breast cancer	MEG3	TP53	positively-E	RNAi;western blot	downregulation	qRT-PCR;ISH	NA	NA	cell growth(-);apoptosis process(+);cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-kB and p53.these results suggest that MEG3 inhibits breast cancer growth and induces breast cancer apoptosis, partially via the activation of the ER stress, NF-kB and p53 pathways, and that NF-kB signaling is required for MEG3-induced p53 activation in breast cancer cells.Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation,migration and invasion by depending on p53's transcriptional activity.Surprisingly,overexpression of MEG3 activates p53's transcriptional activity by decreasing MDM2's transcription level, and thus stabilizes and accumulates P53.	30556250;27166155	RID00144	expression association
Non-small cell lung cancer	BABAM2-AS1	NR4A3	positively-E	RIP;RNA pull-down assay;western blot;ChIP	downregulation	microarray;qRT-PCR	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(-);cell survival(-)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_2:27889456-27891114	ENSG00000119508	NA	100302650	8013	NA	CHN|CSMF|MINOR|NOR1|TEC	BRE-AS1 reduces NSCLC cell viability, represses NSCLC cell proliferation, and induces NSCLC cell apoptosis in vitro, and represses NSCLC tumor growth in vivo. our data demonstrate that BRE-AS1 represses NSCLC cell growth and survival via up-regulating NR4A3.Mechanistic investigation revealed that BRE-AS1 physically binds STAT3, reduces the binding of STAT3 to the promoter of NR4A3, relieves the repression of NR4A3 caused by STAT3, and up-regulates NR4A3 expression.	30227111	RID00145	transcriptional regulation
Breast cancer	ZFHX4-AS1	FAT4	negatively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	GSE33447;GSE26910	GSE33447.zip;GSE26910.zip	cell migration(+);cell invasion(+);Hippo signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253661	GRCh38_8:76491200-76683308	ENSG00000196159	NA	100192378	79633	NA	CDHF14|CDHR11|FAT-J|FATJ|HKLLS2|NBLA00548|VMLDS2	Down-regulated long non-coding RNA RNAZFHX4-AS1 suppresses invasion and migration of breast cancer cells via FAT4-dependent Hippo signaling pathway. FAT4 was the target gene of lncRNA ZFHX4-AS1, and lncRNA ZFHX4-AS1 silencing increased FAT4 expressions	30546116	RID00146	transcriptional regulation
Hemangioma	MEG3	miR-494	negatively-F	luciferase reporter assay;RIP;western blot	downregulation	qRT-PCR	NA	NA	PTEN/PI3K/AKT signaling pathway(-);tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Hemangioma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	lncRNA MEG3 Suppresses the Tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway.	30562741	RID00147	ceRNA or sponge
Liver fibrosis	HOTTIP	TGFBR1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106799	NA	100316868	7046	HOXA-AS6|HOXA13-AS1|NCRNA00213	AAT5|ACVRLK4|ALK-5|ALK5|ESS1|LDS1|LDS1A|LDS2A|MSSE|SKR4|TBR-i|TBRI|TGFR-1|tbetaR-I	Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a.Dual-Luciferase Reporter Assay was performed to validate the interaction between miR-148a and HOTTIP, TGFBR1, or TGFBR2.	30562760	RID00148	ceRNA or sponge
Liver fibrosis	HOTTIP	TGFBR2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000163513	NA	100316868	7048	HOXA-AS6|HOXA13-AS1|NCRNA00213	AAT3|FAA3|LDS1B|LDS2|LDS2B|MFS2|RIIC|TAAD2|TBR-ii|TBRII|TGFR-2|TGFbeta-RII	Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a.Dual-Luciferase Reporter Assay was performed to validate the interaction between miR-148a and HOTTIP, TGFBR1, or TGFBR2.	30562760	RID00149	ceRNA or sponge
Laryngeal carcinoma	DGCR5	miR-195	negatively-F	RIP	upregulation	qRT-PCR	NA	NA	radiosensitivity(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000237517	GRCh38_22:18970514-18994628	NA	NA	26220	NA	LINC00037|NCRNA00037	NA	Knockdown of DGCR5 enhances the radiosensitivity of human laryngeal carcinoma cells via inducing miR-195.microRNA (miR)-195 was predicted as a direct downstream target of DGCR5.	30549038	RID00150	ceRNA or sponge
Pre-eclampsia	WDR86-AS1	LITAF	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);cell proliferation(+);cell migration(+)	ceRNA(miR-10b-3p)	regulation	NA	NA	NA	Tumor Promoting Inflammation;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000243836	GRCh38_7:151409161-151413354	ENSG00000189067	NA	100131176	9516	NA	PIG7|SIMPLE|TP53I7	A potential regulatory network among WDR86-AS1, miR-10b-3p, and LITAF is possibly involved in preeclampsia pathogenesis.WDR86-AS1 and LITAF mRNA were confirmed as targets of miR-10b-3p. WDR86-AS1 downregulated miR-10b-3p but promoted LITAF expression. Microarray analyses revealed that LITAF controlled the inflammatory responses and migration and proliferation of HTR-8/SVneo cells under hypoxia.	30552989	RID00151	ceRNA or sponge
Retinoblastoma	CDKN2B-AS1	ATM	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149311	NA	100048912	472	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AT1|ATA|ATC|ATD|ATDC|ATE|TEL1|TELO1	The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway.The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB.	30355646	RID00152	expression association
Retinoblastoma	CDKN2B-AS1	E2F1	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000101412	NA	100048912	1869	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	E2F-1|RBAP1|RBBP3|RBP3	The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway.The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB.	30355646	RID00153	expression association
Retinoblastoma	OIP5-AS1	AGPAT2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-340-5p)	regulation	NA	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000169692	NA	729082	10555	cyrano|linc-OIP5	1-AGPAT2|BSCL|BSCL1|LPAAB|LPAAT-beta	Long noncoding RNA OIP5-AS1 causes cisplatin resistance in osteosarcoma through inducing the LPAATbeta/PI3K/AKT/mTOR signaling pathway by sponging the miR-340-5p.	30548308	RID00154	ceRNA or sponge
Hepatocellular carcinoma	NORAD	miR-202-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);TGF-beta signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	NA	LINC00657	NA	The long noncoding RNA NORAD enhances the TGF-beta pathway to promote hepatocellular carcinoma progression by targeting miR-202-5p.NORAD overexpression was demonstrated to promote HCC cell migration and invasion.	30537113	RID00155	ceRNA or sponge
Malignant glioma	GACAT3	NAMPT	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-135a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000105835	NA	104797537	10135	LINC01458|lncRNA-AC130710	1110035O14Rik|PBEF|PBEF1|VF|VISFATIN	Long noncoding RNA GACAT3 promotes glioma progression by sponging miR-135a.the present study was the first to show that GACAT3 regulates the expression of NAMPT to promote glioma progression by sponging miR-135a.	30536379	RID00156	ceRNA or sponge
Osteosarcoma	GClnc1	CDKN1A	negatively-E	qRT-PCR	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);p53 signaling pathway(-)	NA	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_6:159679116-159681261	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA GClnc1 promotes tumorigenesis in osteosarcoma by inhibiting p53 signaling. Mechanistically, GClnc1 directly binds to p53 and blocks the binding of p53 to acetyltransferase p300, and thereby suppresses acetylation of p53, leading to the reduced expression of p21 and BAX.	30454890	RID00157	expression association
Retinoblastoma	GClnc1	TP53	interact	RNA pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);p54 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Retinoblastoma	lncRNA	TF	NA	GRCh38_6:159679116-159681261	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA GClnc1 promotes tumorigenesis in osteosarcoma by inhibiting p53 signaling. Mechanistically, GClnc1 directly binds to p53 and blocks the binding of p53 to acetyltransferase p300, and thereby suppresses acetylation of p53, leading to the reduced expression of p21 and BAX.	30454890	RID00158	interact with protein
Non-small cell lung cancer	ZEB1-AS1	ZEB1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell growth(+);apoptosis process(-)	ceRNA(miR-409-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA ZEB1-AS1/miR-409-3p/ZEB1 feedback loop is involved in the progression of non-small cell lung cancer. Our study found that ZEB1-AS1 was upregulation in NSCLC cells and knockdown of ZEB1-AS1 significantly inhibited cell growth and induced cell apoptosis. Mechanically, miR-409-3p was confirmed as a direct target of ZEB1-AS1 and negatively regulated by ZEB1-AS1 via competing endogenous RNA (ceRNA) mechanism; miR-409-3p inhibited ZEB1 expression by directly binding to the 3'UTR.	30448056	RID00159	ceRNA or sponge
Cholangiocarcinoma	PVT1	ANGPTL4	negatively-E	RIP	upregulation	sequencing;qRT-PCR	GSE61850	GSE61850.zip	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000167772	NA	5820	51129	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ARP4|FIAF|HARP|HFARP|NL2|PGAR|TGQTL|UNQ171|pp1158	Long Non-coding RNA PVT1 Promotes Cell proliferation and Migration by Silencing ANGPTL4 Expression in Cholangiocarcinoma. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth,migration, and apoptosis progression.	30388624	RID00160	epigenetic regulation
Asthma	WSPAR	TIMMDC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Respiratory system disease	Asthma	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000113845	NA	105664404	51300	LncTCF7|TCONS_00009511	C3orf1|MC1DN31	lncTCF7 regulated TIMMDC1 expression indeed and PDGF-BB treated ASMCs exhibited elevated levels of lncTCF7 and TIMMDC1.Our study uncovered that lncTCF7 facilitated human ASMCs growth and migration via targeting TIMMDC1 thus activating AKT signaling, providing a novel possible target for asthma therapy.	30528236	RID00161	expression association
Cervical cancer	AL589986.2	MDM2	interact	RNA pull-down assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell invasion(-);angiogenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000236427	GRCh38_1:152205858-152207057	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer. DHX9 bound to E3 ubiquitin ligase MDM2, and this interaction is enhanced by lnc-CCDST. Thus, lnc-CCDST promotes DHX9 degradation by serving as a scaffold to facilitate the formation of MDM2 and DHX9 complexes. A long noncoding RNA, named lnc-CCDST, is significantly downregulated in CC tissues, and binds to pro-oncogenic DHX9. DHX9 is upregulation in CC tissue, and promotes CC cell motility and angiogenesis.	30518908	RID00162	interact with protein
Cervical cancer	AL589986.2	DHX9	interact	RNA pull-down assay;RIP	downregulation	microarray;qRT-PCR	NA	NA	cell invasion(-);angiogenesis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000236427	GRCh38_1:152205858-152207057	ENSG00000135829	NA	NA	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer. DHX9 bound to E3 ubiquitin ligase MDM2, and this interaction is enhanced by lnc-CCDST. Thus, lnc-CCDST promotes DHX9 degradation by serving as a scaffold to facilitate the formation of MDM2 and DHX9 complexes. A long noncoding RNA, named lnc-CCDST, is significantly downregulated in CC tissues, and binds to pro-oncogenic DHX9. DHX9 is upregulation in CC tissue, and promotes CC cell motility and angiogenesis.	30518908	RID00163	interact with protein
Cervical cancer	C5orf66-AS1	RING1	positively-E	RIP;luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	CESC.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249082	GRCh38_5:135038831-135040047	ENSG00000204227	NA	101927953	6015	Epist	RING1A|RNF1	Long non-coding RNA C5orf66-AS1 promotes cell proliferation in cervical cancer by targeting miR-637/RING1 axis. LncRNA C5orf66-AS1, as a competitive endogenous RNA (ceRNA), regulated the effect of RING1 on the proliferation, apoptosis and cell cycle of cervical cancer cells through adsorbing miR-637.	30518760	RID00164	ceRNA or sponge
Pancreatic cancer	SNHG1	NOTCH1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148400	NA	23642	4851	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AOS5|AOVD1|TAN1|hN1	Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch-1 signaling pathway in pancreatic cancer.SNHG1 was significantly upregulation in PC cells. Knockdown of SNHG1 could obviously suppress cell proliferation, invasion, and migration. Furthermore, SNHG1 knockdown inhibited the activation of the Notch-1 signaling pathway and inhibited the expression of N-cadherin, Hes1, Vimentin, Notch-1.The inhabitation was reversed when Notch-1 was overexpressed in si-SNHG1 cells.	30520072	RID00165	expression association
Salivary gland adenoid cystic carcinoma	ADAMTS9-AS2	ITGA6	positively-E	luciferase reporter assay;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);PI3K/AKT signaling pathway(+);MEK/ERK signaling pathway(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Salivary gland carcinoma	lncRNA	PCG	ENSG00000241684	GRCh38_3:64684909-65053439	ENSG00000091409	NA	100507098	3655	NA	CD49f|ITGA6B|VLA-6	Upregulation of lncRNA ADAMTS9-AS2 Promotes Salivary Adenoid Cystic Carcinoma Metastasis via PI3K/Akt and MEK/Erk Signaling.Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, and thus it activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis.	30217729	RID00166	ceRNA or sponge
Breast cancer	SNHG6	MAPK6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000069956	NA	641638	5597	HBII-276HG|NCRNA00058|U87HG	ERK3|HsT17250|PRKM6|p97MAPK	Long non-coding RNA SNHG6 enhances cell proliferation, migration and invasion by regulating miR-26a-5p/MAPK6 in breast cancer.In the present study, we found that SNHG6 was highly expressed in BC tissues and cell lines, which was associated with poorer clinicopathologic features.SNHG6 serves as an endogenous sponge by directly binding to miR-26a-5p and down-regulating miR-26a-5p expression. Knockdown of SNHG6 inhibited BC cell proliferation, migration and invasion in vitro and in vivo. Furthermore, bioinformatics analysis and luciferase reporter indicated that MAPK6 was validated as a target of miR-26a-5p. Therefore, our study may reveal a novel SNHG6/miR-26a-5p/MAPK6 pathway regulatory axis in BC pathogenesis.	30522015	RID00167	ceRNA or sponge
Hepatocellular carcinoma	LINC00472	PDCD4	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell migration(-)	ceRNA(miR-93-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000150593	NA	79940	27250	C6orf155|P53RRA	H731	Long non-coding RNA LINC00472 suppresses hepatocellular carcinoma cell proliferation, migration and invasion through miR-93-5p/PDCD4 pathway.In the present study, we have demonstrated that long non-coding RNA (lncRNA) LINC00472 was low expressed in human HCC tissues and cell lines compared with adjacent non-tumor liver tissues and normal liver cell lines respectively. LINC00472 was also low expressed in HCC tissues from patients with metastasis compared with tissues from patients without metastasis. Forced expression of LINC00472 suppressed cell proliferation, migration, invasion and promoted cell apoptosis in HCC cells Huh-7 and SMMC-7721. MiR-93-5p was a direct target of LINC00472, and miR-93-5p directly targeted PDCD4. The miR-93-5p/PDCD4 pathway mediated the suppressing role of LINC00472 in HCC cells.	30522853	RID00168	ceRNA or sponge
Laryngeal squamous cell carcinoma	snaR	TGFB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	NA	association	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	NA	GRCh38_19:47918429-47918550	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Overexpression of lncRNA snaR is correlated with progression and predicts poor survival of laryngeal squamous cell carcinoma.In the present study, we found that plasma levels of snaR were upregulated in patients with laryngeal squamous cell carcinoma (LSCC) than in healthy controls. Overexpression of snaR resulted in upregulation of TGF-beta1 in cells of human LSCC cell lines, while exogenous TGF-beta1 treatment showed no significant effect on snaR expression. snaR overexpression and exogenous TGF-beta1 treatment promoted LSCC cell proliferation, migration, and invasion.Therefore, overexpression of lncRNA snaR is correlated with progression and predicts poor survival of LSCC and the mechanism of its actions is likely related to TGF-beta1.	30506952	RID00169	expression association
Non-small cell lung cancer	AFAP1-AS1	AFAP1	positively-E	western blot;luciferase reporter assay	upregulation	sequencing;qRT-PCR	NA	NA	cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	Long non-coding RNA AFAP1-AS1 plays an oncogenic role in promoting cell migration in non-small cell lung cancer.In this study, we conducted global lncRNA profiling and identified that AFAP1-AS1 is significantly upregulated in NSCLC, suggesting that AFAP1-AS1 may be important for lung cancer development. AFAP1-AS1 functions through positively regulating the expression of AFAP1 protein.this study demonstrates that AFAP1-AS1 acts as an oncogene in NSCLC to promote cell migration partly by upregulating AFAP1 expression	30293090	RID00170	expression association
Osteosarcoma	SNHG4	miR-224-3p	negatively-F	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	NA	NA	prognosis;cell growth(+);cancer recurrence(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000281398	GRCh38_5:139274102-139284899	NA	NA	724102	NA	NCRNA00059|U19H	NA	LncRNA SNHG4 promotes tumour growth by sponging miR-224-3p and predicts poor survival and recurrence in human osteosarcoma.The expression level of lncRNA SNHG4 was significantly elevated in osteosarcoma samples and cell lines as compared with the adjacent normal tissues. Our findings demonstrated that LncRNA SNHG4 promoted tumour growth by sponging miR-224-3p and represented a poor prognostic factor in patients with osteosarcoma.we found that lncRNA SNHG4 acted as a sponge of miR-224-3p, and miR-224-3p mimic reversed SNHG4 induced tumour-promoting effects in osteosarcoma cells.	30152090	RID00171	ceRNA or sponge
Renal cell carcinoma	HOTAIR	ST8SIA4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113532	NA	100124700	7903	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PST|PST1|SIAT8D|ST8SIA-IV	Long noncoding RNA HOTAIR promotes renal cell carcinoma malignancy through alpha-2, 8-sialyltransferase 4 by sponging microRNA-124.In this study, HOTAIR level was confirmed to be significantly upregulated in RCC samples and RCC cell lines compared with those in the paired adjacent tissues and normal renal cell line. HOTAIR directly bound to miR-124, while miR-124 mediated the expression of ST8SIA4 in RCC cell lines. ST8SIA4 was upregulated in RCC tissues and RCC cell lines.Further results indicated that HOTAIR promoted the proliferation and metastasis as a competing endogenous RNA to regulate ST8SIA4 expression by sponging miR-124 in RCC.	30105850	RID00172	ceRNA or sponge
Lung cancer	UCA1	MAPK1	positively-E	immunoblot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000100030	NA	652995	5594	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.Suppression of long non-coding RNA UCA1 inhibits proliferation and invasion and induces apoptosis in human lung cancer cells.the lncRNA UCA1 suppression (p < 0.05) significantly inhibited the migration and invasion of the NCI-H23 lung cancer at least in part via inhibition of mitogen-activated protein kinase 1 (MAPK1).	30556875;30468471	RID00173	expression association
Lung cancer	UCA1	miR-143	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.It was found that the lncRNA UCA was significantly upregulated in the lung cancer cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.	30556875	RID00174	expression association
Non-small cell lung cancer	FENDRR	miR-761	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell growth(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000268388	GRCh38_16:86474529-86509099	NA	NA	400550	NA	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	NA	Long non-coding RNA FENDRR inhibits NSCLC cell growth and aggressiveness by sponging miR-761.We found a marked down-regulation of FENDRR in NSCLC tissues compared to tumor-adjacent tissues. Moreover, the over-expression of FENDRR restrained the growth of NSCLC cell in vivo. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. We found that there were potential binding sites between FENDRR and miR-761 and the level of miR-761 was inversely associated with the expression of ENDRR in NSCLC tissues. Finally, the rescue experiments suggested that the anti-oncogenic role of FENDRR was at least partially mediated by miR-761 in NSCLC.	30556873	RID00175	ceRNA or sponge
Colorectal cancer	LINC01503	FOXK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-4492)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000164916	NA	100506119	221937	NA	FOXK1L	Long non-coding RNA LINC01503 promotes colorectal cancer cell proliferation and invasion by regulating miR-4492/FOXK1 signaling.The present study indicated that LINC01503 was significantly upregulated in CRC tissues compared with that in adjacent normal tissues. it was revealed that LINC01503 serves as a sponge for microRNA (miR)-4492, which targets forkhead box K1 (FOXK1) in CRC cells. it was demonstrated that restoration of FOXK1 abolished the inhibitory effect of LINC01503 knockdown on CRC cell proliferation and invasion.	30542444	RID00176	ceRNA or sponge
Lung cancer	LINC00662	LIN28A	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell stemness(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	CSC	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Lung cancer	lncRNA	TF	ENSG00000261824	GRCh38_19:27681072-27794005	ENSG00000131914	NA	148189	79727	NA	NA	Long non-coding RNA Linc00662 promotes cell invasion and contributes to cancer stem cell-like phenotypes in lung cancer cells. Linc00662 had direct interaction with Lin28, and the Linc00662 function was dependent on Lin28. We demonstrate that overexpression of Linc00662 enhances lung cancer cell metastasis and CSC stemness by interacting with Lin28 in human lung cancer, which could be utilized as a potential diagnostic and therapeutic target for lung cancer patients.The interaction between Linc00662 and Lin28 was confirmed by RNA immunoprecipitation and RNA pulldown assay.	30256974	RID00177	interact with mRNA
Renal cell carcinoma	TUG1	YAP1	positively-E	western blot;immunofluorescence	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-9)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000137693	NA	55000	10413	LINC00080|NCRNA00080|TI-227H	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA TUG1 promotes cell proliferation and migration of renal cell carcinoma via regulation of YAP. In the current study, we observed a positive correlation between TUG1 expression and YAP expression in RCC. In addition, we found that TUG1 could bind to miR-9; therefore, TUG1 could positively control YAP expression via downregulation of miR-9 level. Furthermore, we observed that inhibition of cell proliferation and cell migration induced by TUG1 silencing could be reversed by overexpression of YAP in RCC cell lines.Using microRNA database (miRDB), the sequencealignment of TUG1, YAP 3'UTR, and miR-9 showed complementary binding sites of TUG1 and YAP 3'UTR for miR-9.	30132963	RID00178	ceRNA or sponge
Colon cancer	PVT1	miR-26b	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA Plasmacytoma Variant Translocation 1 (PVT1) Promotes Colon Cancer Progression via Endogenous Sponging miR-26b. We demonstrate that the expression of PVT1 was significantly higher in tumor tissue compared with the adjacent normal tissue with a lower expression of miR-26b. Our results suggest that PVT1 could promote metastasis and proliferation of colon cancer via endogenous sponging and inhibiting the expression of miR-26b, which may highlight the significance of lncRNA PVT1 in colon cancer tumorigenesis.	30504754	RID00179	ceRNA or sponge
Prostate cancer	LINC00844	NDRG1	positively-E	ChIP;western blot	downregulation	sequencing;qRT-PCR	ERP000550	ERP000550	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000237949	GRCh38_10:58999482-59066396	ENSG00000104419	NA	100507008	10397	NA	CAP43|CMT4D|DRG-1|DRG1|GC4|HMSNL|NDR1|NMSL|PROXY1|RIT42|RTP|TARG1|TDD5	Novel lncRNA LINC00844 Regulates Prostate Cancer Cell Migration and Invasion through AR Signaling. The expression of LINC00844 is higher in normal prostate compared with malignant and metastatic prostate cancer clinical specimens. Mechanistic evidence reveals that LINC00844 is important in facilitating AR binding to the chromatin. Finally, LINC00844 mediates its phenotypic effects in part by activating the expression of NDRG1, a crucial cancer metastasis suppressor. This study highlights the function of the lncRNA, LINC00844, in regulating global AR-regulated genes in prostate cancer by modulating AR binding to chromatin.	30115758	RID00180	transcriptional regulation
Multiple myeloma	CYTOR	miR-497	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	NA	Long intergenic non-protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA-497.It was identified that the expression of LINC00152 was significantly upregulated in plasma cells from patients with MM vs. healthy subjects. A luciferase reporter assay indicated that microRNA (miR)-497 is a direct target of LINC00152, and its expression levels were inversely correlated with those of LINC00152 in MM tissues.knockdown of LINC00152 promoted caspase-3/9 activity and apoptosis in MM cells.knockdown of LINC00152 by transfecting MM cells with LINC00152-specific short hairpin RNA expression plasmids significantly inhibited cell proliferation.	30272368	RID00181	ceRNA or sponge
Pituitary adenoma	IFNG-AS1	ESRP2	interact	RNA pull-down assay	upregulation	qRT-PCR;FISH	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	PCG	ENSG00000255733	GRCh38_12:67989445-68234686	ENSG00000103067	NA	100885789	80004	GS1-410F4.2|NEST|Tmevpg1	RBM35B	Long-noncoding RNA IFNG-AS1 exerts oncogenic properties by interacting with epithelial splicing regulatory protein 2 (ESRP2) in pituitary adenomas. shRNA-mediated IFNG-AS1 knockdown in HP75 cells significantly inhibited tumor progression. Epithelial splicing regulatory protein 2 (ESRP2) was demonstrated to be a target protein of IFNG-AS1 in PA; knocking down ESRP2 reversed the tumor-inhibitory effects of IFNG-AS1 knockdown, and overexpressing ESRP2 abolished the tumor-promoting effects of IFNG-AS1 overexpression in HP75 cells.	30322807	RID00182	interact with protein
Gastric cancer	TP73-AS1	SDAD1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000198301	NA	57212	55153	KIAA0495|PDAM	NA	LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis.TP73-AS1 was upregulated in GC tissues and cell lines. Furthermore, TP73-AS1 exerted oncogenic role in GC through promoting cell growth and metastasis. In addition, TP73-AS1 was certified as a ceRNA by regulating miR-194-5p/SDAD1 axis.	30279010	RID00183	ceRNA or sponge
Prostate cancer	AR	TMPO-AS1	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	prognosis;cancer progression(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000257167	GRCh38_12:98512973-98516422	367	100128191	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	Overexpression of AR-regulated lncRNA TMPO-AS1 correlates with tumor progression and poor prognosis in prostate cancer. we found that TMPO-AS1 could be a useful diagnostic and prognostic marker for PCa, whose expression was upregulated in PCa samples and associated with poorer prognosis. In PCa cells, TMPO-AS1 was predominantly localized in the cytoplasm and directly down-regulated by AR. Based on primary screening, we found that TMPO-AS1 could be a useful diagnostic and prognostic marker for PCa, whose expression was upregulated in PCa samples and associated with poorer prognosis.	30105831	RID00184	transcriptional regulation
Pre-eclampsia	MEG3	SMAD7	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000101665	NA	55384	4092	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CRCS3|MADH7|MADH8	The Role and Molecular Mechanism of Long Nocoding RNA-MEG3 in the Pathogenesis of Preeclampsia.The expression of MEG3 was lower in tissues from patients with preeclampsia having an EMT decline, as well as a messenger RNA expression of smad7. In HTR-8/SVneo cells with overexpressed MEG3, the invasion and migration functions were enhanced and accompanied by higher EMT and a significantly increased expression of smad7.	29361889	RID00185	expression association
Urinary bladder cancer	CEBPB	UCA1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell viability(+);cell growth(+);colony formation(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	TF	lncRNA	ENSG00000172216	NA	ENSG00000214049	GRCh38_19:15828206-15836328	1051	652995	C/EBP-beta|IL6DBP|NF-IL6|TCF5	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	C/EBPbeta promotes the viability of human bladder cancer cell by contributing to the transcription of bladder cancer specific lncRNA UCA1.Here we report that the expression of UCA1 was dramatically inhibited in 5637 cells with C/EBPbeta down-regulation. Additionally, the function tests indicated that C/EBPbeta could promote 5637 cells growth and colony formation by inducing the expression level of UCA1.	30376994	RID00186	transcriptional regulation
Hepatocellular carcinoma	CDKN2B-AS1	ARHGAP18	positively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+);cell migration(+)	ceRNA(miR-153-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000146376	NA	100048912	93663	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	MacGAP|SENEX|bA307O14.2	LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis. CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. CDKN2BAS upregulated the expression of Rho GTPase activating protein 18 (ARHGAP18) by sponging microRNA-153-5p (miR-153-5p), and thus promoted HCC cell migration.Luciferase reporter assay showed that miR-153-5p inhibited the luciferase activity of ARHGAP18 wt-3'UTR but had no effect on the ARHGAP18 mut-3'UTR. Besides, CDKN2BAS downregulated the expression of Kruppel-like factor 13 (KLF13) and activated MEK-ERK1/2 signaling, thus reducing apoptosis in HCC cells.	30510148	RID00187	ceRNA or sponge
Hepatocellular carcinoma	CDKN2B-AS1	KLF13	negatively-E	luciferase reporter assay	upregulation	microarray;qRT-PCR	NA	NA	MEK/ERK signaling pathway(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000169926	NA	100048912	51621	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	BTEB3|FKLF2|NSLP1|RFLAT-1|RFLAT1	LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis. CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. CDKN2BAS upregulated the expression of Rho GTPase activating protein 18 (ARHGAP18) by sponging microRNA-153-5p (miR-153-5p), and thus promoted HCC cell migration.Luciferase reporter assay showed that miR-153-5p inhibited the luciferase activity of ARHGAP18 wt-3'UTR but had no effect on the ARHGAP18 mut-3'UTR. Besides, CDKN2BAS downregulated the expression of Kruppel-like factor 13 (KLF13) and activated MEK-ERK1/2 signaling, thus reducing apoptosis in HCC cells. knockdown of CDKN2BAS up-regulated KLF13 protein level	30510148	RID00188	expression association
Gastric cancer	LINC00707	ELAVL1	interact	RNA pull-down assay;RIP	upregulation	microarray;qRT-PCR	GSE58828	GSE58828.zip	cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000066044	NA	100507127	1994	NA	ELAV1|HUR|Hua|MelG	The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR.In this study, we identified that LINC00707 was excessively expressed in GC tissues and correlated with advanced stage, larger tumor size, lymph node metastasis and poorer prognosis in GC patients.	30502359	RID00189	interact with protein
Triple-receptor negative breast cancer	PDCD4-AS1	PDCD4	positively-F	RIP;RNA stability assay;RNA pull-down assay	downregulation	sequencing;qRT-PCR	NA	NA	cancer progression(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000203497	GRCh38_10:110869868-110872233	ENSG00000150593	NA	282997	27250	NA	H731	A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability.Both PDCD4-AS1 and PDCD4 show reduced expression in TNBC cell lines and in patients, and depletion of PDCD4-AS1 compromised the cellular levels and activity of PDCD4. Mechanistically, PDCD4-AS1 stabilizes PDCD4 RNA by forming RNA duplex and controls the interaction between PDCD4 RNA and RNA decay promoting factors such as HuR. Our studies demonstrate crucial roles played by NAT lncRNAs in regulating post-transcriptional gene expression of key oncogenic or tumor suppressor genes, thereby contributing to TNBC progression.	30496290	RID00190	interact with mRNA
Endometriosis	CCDC144NL-AS1	MMP9	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000233098	GRCh38_17:20868433-21002276	ENSG00000100985	NA	440416	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Knockdown of long non-coding RNA CCDC144NL-AS1 attenuates migration and invasion phenotypes in endometrial stromal cells from endometriosis. CCDC144NL-AS1 expression was up-regulated in EC tissues compared to EU and normal endometrial (NE) tissues.Western blot analysis revealed that knockdown of CCDC144NL-AS1 attenuated the protein levels of vimentin filaments and MMP-9, but not N-cadherin or beta-catenin. CCDC144NL-AS1 depletion suppressed the migration and invasion of hEM15A cells, but exerted no effects on cell adhesion, proliferation, apoptosis or cell cycle.	30496345	RID00191	expression association
Endometriosis	CCDC144NL-AS1	VIM	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000233098	GRCh38_17:20868433-21002276	ENSG00000026025	NA	440416	7431	NA	NA	Knockdown of long non-coding RNA CCDC144NL-AS1 attenuates migration and invasion phenotypes in endometrial stromal cells from endometriosis.Western blot analysis revealed that knockdown of CCDC144NL-AS1 attenuated the protein levels of vimentin filaments and MMP-9, but not N-cadherin or beta-catenin. CCDC144NL-AS1 depletion suppressed the migration and invasion of hEM15A cells, but exerted no effects on cell adhesion, proliferation, apoptosis or cell cycle.	30496345	RID00192	expression association
Triple-receptor negative breast cancer	MIR4435-2HG	FZD7	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111036776-111523376	ENSG00000155760	NA	541471	8324	NA	FzE3	LncRNA AWPPH promotes the growth of triple-negative breast cancer by up-regulating frizzled homolog 7 (FZD7).We observed that AWPPH was significantly up-regulated in tumor tissues than in paired adjacent healthy tissues of patients. AWPPH overexpression promoted cancer cell proliferation and up-regulated FZD7 expression. We conclude that LncRNA AWPPH may promote the growth of triple-negative breast cancer by up-regulating FZD7.	30333256	RID00193	expression association
Hepatocellular carcinoma	CDKN2B-AS1	NAP1L1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	microarray;qRT-PCR	GSE65485;TCGA	GSE65485.zip;LIHC.zip	cell growth(+);cell metastasis(+);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(let-7c-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000187109	NA	100048912	4673	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NAP1|NAP1L|NRP	LncRNA CDKN2B-AS1 promotes tumor growth and metastasis of human hepatocellular carcinoma by targeting let-7c-5p/NAP1L1 axis. Here, we identified a novel oncogenic lncRNA CDKN2B-AS1, which was highly expressed in HCC and positively associated with large tumor size, microvascular invasion, high tumor grade, advanced tumor stage and reduced survival of HCC patients. Mechanistically, CDKN2B-AS1 promoted nucleosome assembly protein 1 like 1 (NAP1L1) expression by sponging let-7c-5p, thereby activated PI3K/AKT/mTOR signaling in HCC cells.	30165194	RID00194	ceRNA or sponge
Urinary bladder cancer	OIP5-AS1	OIP5	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000104147	NA	729082	11339	cyrano|linc-OIP5	5730547N13Rik|CT86|LINT-25|MIS18B|MIS18beta|hMIS18beta	LncRNA OIP5-AS1 predicts poor prognosis and regulates cell proliferation and apoptosis in bladder cancer.There was a positive association between OIP5-AS1 expression and OIP5 expression in bladder cancer tissues.OIP5-AS1 is a useful biomarker for predicting clinical progression and poor prognosis and promotes cell proliferation through modulating OIP5 expression.	30485498	RID00195	expression association
Colorectal cancer	MAP3K20-AS1	CDKN1A	negatively-E	RT-qPCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000238133	GRCh38_2:173166446-173282036	ENSG00000124762	NA	339751	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA MLK7-AS1 promotes proliferation in human colorectal cancer via downregulation of p21 expression.this is the first study to report that MLK7-AS1 has potential as a biomarker and may promote proliferation in CRC partially through downregulating p21 expression.Furthermore, RT-qPCR and western blot assays revealed that p21 may be a potential downstream target of MLK7-AS1.	30535460	RID00196	transcriptional regulation
Hepatocellular carcinoma	ZEB1	HCCL5	positively-E	ChIP-qPCR	upregulation	qRT-PCR	NA	NA	cell migration(+);cell viability(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000148516	NA	ENSG00000263080	GRCh38_16:11341809-11345299	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	NA	Super-enhancer-associated long non-coding RNA HCCL5 is activated by ZEB1 and promotes the malignancy of hepatocellular carcinoma.HCCL5 was transcriptionally driven by ZEB1 via a super-enhancer and was significantly and frequently overexpressed in human HCC tissues, correlating with worse overall survival of HCC patients. this study characterizes HCCL5 as a super-enhancer-driven lncRNA promoting HCC cell viability, migration, and EMT.	30482773	RID00197	transcriptional regulation
Hepatoblastoma	STAT3	LUCAT1	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	LIHC.zip	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000248323	GRCh38_5:91054834-91314547	6774	100505994	ADMIO|ADMIO1|APRF|HIES	SCAL1|SCAT5	STAT3-activated lncRNA LUCAT1 drives cell proliferation, migration and invasion in hepatoblastoma through regulating miR-301b/STAT3 axis. Further mechanism investigation revealed that LUCAT1 increased STAT3 expression through competitively binding to miR-301b.In conclusion, LUCAT1 was activated by STAT3 and promoted cell proliferation, migration and invasion in hepatoblastoma through modulating miR-301b/STAT3 axis.	30479162	RID00198	transcriptional regulation
Hepatoblastoma	LUCAT1	STAT3	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	LIHC.zip	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-301b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000168610	NA	100505994	6774	SCAL1|SCAT5	ADMIO|ADMIO1|APRF|HIES	STAT3-activated lncRNA LUCAT1 drives cell proliferation, migration and invasion in hepatoblastoma through regulating miR-301b/STAT3 axis. Further mechanism investigation revealed that LUCAT1 increased STAT3 expression through competitively binding to miR-301b.In conclusion, LUCAT1 was activated by STAT3 and promoted cell proliferation, migration and invasion in hepatoblastoma through modulating miR-301b/STAT3 axis.	30479162	RID00199	ceRNA or sponge
Malignant glioma	NEAT1	CDK14	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-107)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000058091	NA	283131	5218	LINC00084|NCRNA00084|TncRNA|VINC	PFTAIRE1|PFTK1	Knockdown of NEAT1 repressed the malignant progression of glioma through sponging miR-107 and inhibiting CDK14.it was revealed that NEAT1 could modulate miR-107 via serving as an endogenous sponge of miR-107. The direct binding correlation between NEAT1 and miR-107 was validated in our study. In addition, cyclin dependent kinase 14 (CDK14) was predicted as an messenger RNA target of miR-107 and the association between them was confirmed in our research.	30480816	RID00200	ceRNA or sponge
Retinoblastoma	NEAT1	CXCR4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000121966	NA	283131	7852	LINC00084|NCRNA00084|TncRNA|VINC	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR-204/CXCR4 axis.We found NEAT1 and CXCR4 expression levels were elevated, whereas miR-204 expression was decreased in RB tissues and cells. NEAT1 functioned as a competing endogenous RNA for miR-204 to regulate CXCR4 expression.	30479013	RID00201	ceRNA or sponge
Papillary thyroid carcinoma	LINC00460	SPHK2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-613)	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000063176	NA	728192	56848	NA	SK 2|SK-2|SPK 2|SPK-2	Long noncoding RNA LINC00460 promotes carcinogenesis via sponging miR-613 in papillary thyroid carcinoma.knockdown of LINC00460 suppressed cell proliferation, migration, and invasion, and inhibited expression of sphingosine kinase 2 (SphK2, a target of miR-613) in PTC cells, at least in part, by regulating miR-613. These findings suggested that LINC00460 could function as a competing endogenous RNA to regulate SphK2 expression by sponging miR-613 in PTC.	30478856	RID00202	ceRNA or sponge
T-cell leukemia	CDKN2B-AS1	CDKN1A	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);NF-kB signaling pathway(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000124762	NA	100048912	1026	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA ANRIL Supports Proliferation of Adult T-Cell Leukemia Cells through Cooperation with EZH2. In the present study, we show that the expression level of the lncRNA ANRIL was elevated in HTLV-1-infected cell lines and clinical ATL samples. In addition, we observed that the ANRIL/EZH2 complex repressed p21/CDKN1A transcription through H3K27 trimethylation of the p21/CDKN1A promoter. Taken together, our results implicate that the lncRNA ANRIL, by cooperating with EZH2, supports the proliferation of HTLV-1-infected cells, which is thought to be critical for oncogenesis. In this study, we demonstrated that the lncRNA ANRIL was important for maintaining the proliferation of ATL cells in vitro and in vivo ANRIL was shown to activate NF-kB signaling through forming a ternary complex with EZH2 and p65. Furthermore, epigenetic inactivation of p21/CDKN1A was involved in the oncogenic function of ANRIL.	30258009	RID00203	epigenetic regulation
Triple-receptor negative breast cancer	CERNA2	CDK6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(let-7b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000105810	NA	642934	1021	HOST2|lncRNA-HOST2	MCPH12|PLSTIRE	Knockdown of long non-coding RNA HOST2 inhibits the proliferation of triple negative breast cancer via regulation of the let-7b/CDK6 axis.A positive correlation was identified between the expression of HOST2 and cyclin-dependent kinase 6 (CDK6) in tumor tissues.It was hypothesized and confirmed that let-7b, a previously reported target miRNA of HOST2, was able to directly bind to the 3'UTR of CDK6 and repress its expression.	30483747	RID00204	ceRNA or sponge
Prostate cancer	PANTR1	ROCK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000067900	NA	100506421	6093	LINC01158|linc-Brn1a|linc-POU3F3	P160ROCK|ROCK-I	Long noncoding RNA POU3F3 promotes cancer cell proliferation in prostate carcinoma by upregulating rho-associated protein kinase 1. In this study we found that POU3F3 and rho-associated protein kinase 1 (ROCK1) were both increased in tumor tissues than in adjacent healthy tissues of patients with prostate carcinoma. lncRNA POU3F3 may promote cancer cell proliferation in prostate carcinoma by upregulating ROCK1.	30474879	RID00205	expression association
Hepatocellular carcinoma	LSINCT5	HMGA2	interact	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000149948	NA	101234261	8091	NA	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516.RIP in combination with mass spectrometry identified HMGA2 as the LSINCT5 binding partner. LSINCT5 could bind to HMGA2 and decrease proteasome-mediated HMGA2 degradation leading to EMT activation.	30472720	RID00206	interact with protein
Hepatocellular carcinoma	LSINCT5	STAT3	positively-E	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-)	ceRNA(miR-4516)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000168610	NA	101234261	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516. LSINCT5 also served as a competing endogenous RNA (ceRNA) for miR-4516, resulting in increased STAT3/BclxL expression and attenuated apoptosis.Previous results showed that miR-4516 targets STAT3 transcript and downregulates STAT3, pSTAT3, and BclxL expression.	30472720	RID00207	ceRNA or sponge
Hepatocellular carcinoma	LSINCT5	BCL2L1	positively-E	RIP;mass spectrometry	upregulation	microarray;qRT-PCR	NA	NA	cancer progression(+);apoptosis process(-)	ceRNA(miR-4516)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000171552	NA	101234261	598	NA	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with High-Mobility Group AT-hook 2 and MiR-4516. LSINCT5 also served as a competing endogenous RNA (ceRNA) for miR-4516, resulting in increased STAT3/BclxL expression and attenuated apoptosis.Previous results showed that miR-4516 targets STAT3 transcript and downregulates STAT3, pSTAT3, and BclxL expression.	30472720	RID00208	ceRNA or sponge
Ulcerative colitis	CDKN2B-AS1	miR-323b-5p	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00209	expression association
Ulcerative colitis	CDKN2B-AS1	TLR4	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000136869	NA	100048912	7099	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARMD10|CD284|TLR-4|TOLL	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00210	expression association
Ulcerative colitis	CDKN2B-AS1	MYD88	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000172936	NA	100048912	4615	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	MYD88D	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00211	expression association
Ulcerative colitis	CDKN2B-AS1	RELA	negatively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	NA	association	NA	NA	NA	NA	Gastrointestinal system disease	Colitis	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000173039	NA	100048912	5970	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CMCU|NFKB3|p65	Long noncoding RNA ANRIL contributes to the development of ulcerative colitis by miR-323b-5p/TLR4/MyD88/NF-kB pathway.LncRNA ANRIL was highly expressed in patients with UC.Suppression of ANRIL alleviated LPS-induced cell injury by negatively regulating the expression of miR-323b-5p. Suppression of ANRIL alleviated LPS-induced injury in FHC cells, which was achieved by negatively regulating miR-323b-5p. Moreover, miR-323b-5p negatively regulated TLR4 expression and TLR4 was a target of miR-323b-5p.The results showed that suppression of ANRIL decreased LPS-induced up-regulation of TLR4, MyD88, and NF-kB p65, which was further reversed after inhibition of miR-323b-5p at the same time. Furthermore, the effects of ANRIL on LPS-induced cell injury were achieved by TLR4/MyD88/NF-kB pathway. Our data indicate that suppression of ANRIL may inhibit the development of UC by regulating miR-323b-5p/TLR4/MyD88/NF-kB pathway.	30477744	RID00212	expression association
Colon cancer	AC123023.1	JAG2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000236452	GRCh38_3:34203244-34268811	ENSG00000184916	NA	NA	3714	NA	HJ2|SER2	Long noncoding RNA ENST00000455974 plays an oncogenic role through up-regulating JAG2 in human DNA mismatch repair-proficient colon cancer.Here, firstly, we observed that ENST00000455974 was gradual increased across colon normal-adenoma-carcinoma-metastasis sequence by quantitative real-time PCR. ENST00000455974 was mainly located in the nucleus of colon cancer cells and it promoted the growth and metastasis of pMMR CC cells through up-regulating JAG2.	30473216	RID00213	expression association
Urinary bladder cancer	CARMN	AXIN2	positively-E	luciferase reporter assay	downregulation	sequencing;qRT-PCR	TCGA	BLCA.zip	WNT/beta-catenin signaling pathway(-);cancer progression(-)	ceRNA(miR-1275)	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000249669	GRCh38_5:149406689-149432835	ENSG00000168646	NA	728264	8313	NA	AXIL|ODCRCS	LncRNA miR143HG suppresses bladder cancer development through inactivating Wnt/beta-catenin pathway by modulating miR-1275/AXIN2 axis.miR143HG was identified to inhibit the level of miR-1275, whereas miR-1275 directly targeted AXIN2, a negative regulator of the Wnt/beta-catenin pathway. Restoration of miR-1275 or knockdown of AXIN2 significantly rescued the proliferation, migration, and invasion abilities of BCa cells. We found that miR143HG might be acompeting endogenous RNA (ceRNA) for miR-1275. There were two potential binding sites for miR-1275 in miR143HG. miR143HG directly interacted with miR-1275.	30471109	RID00214	ceRNA or sponge
Oral squamous cell carcinoma	CASC2	miR-21	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cancer recurrence(-)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Downregulation of lncRNA CASC2 promotes the postoperative local recurrence of early oral squamous cell carcinoma.Transfection of CASC2 expression vectors led to significantly inhibited tumor cell proliferation and reduced miRNA-21 expression levels.	30467776	RID00215	expression association
Retinoblastoma	XIST	ZEB1	positively-E	RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA XIST promotes the epithelial to mesenchymal transition of retinoblastoma via sponging miR-101. Moreover,we found that XIST functioned as a competing endogenous RNA (ceRNA) for miR-101 to regulate the de-repression of its endogenous targets ZEB1 and ZEB2.	30472203	RID00216	ceRNA or sponge
Retinoblastoma	XIST	ZEB2	positively-E	RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169554	NA	7503	9839	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA XIST promotes the epithelial to mesenchymal transition of retinoblastoma via sponging miR-101. Moreover,we found that XIST functioned as a competing endogenous RNA (ceRNA) for miR-101 to regulate the de-repression of its endogenous targets ZEB1 and ZEB2.	30472203	RID00217	ceRNA or sponge
Bladder urothelial carcinoma	MEG3	miR-96	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.MEG3 overexpression resulted in miR-96 downregulation along with TPM1 upregulation, which inhibited cell proliferation and cell cycle but promoted cell apoptosis of bladder urothelial carcinoma cells in vitro, and at the same time inhibited tumor growth in vivo.	30461333	RID00218	expression association
Bladder urothelial carcinoma	MEG3	TPM1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000140416	NA	55384	7168	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	C15orf13|CMD1Y|CMH3|HEL-S-265|HTM-alpha|LVNC9|TMSA	Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.MEG3 overexpression resulted in miR-96 downregulation along with TPM1 upregulation, which inhibited cell proliferation and cell cycle but promoted cell apoptosis of bladder urothelial carcinoma cells in vitro, and at the same time inhibited tumor growth in vivo.	30461333	RID00219	expression association
Gastric cancer	UCA1	ZEB2	positively-E	luciferase reporter assay;RIP	upregulation	microarray;sequencing	GSE53137;GSE93512;TCGA	GSE53137.zip;GSE93512.zip;STAD.zip	cell metastasis(+)	ceRNA(miR-203)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000169554	NA	652995	9839	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer.Our findings indicated that UCA1 plays a critical role in metastatic GC by mediating sponge regulatory axis miR-203/ZEB2.we detected that expression level of ZEB2, a transcription factor related to tumor metastasis, was regulated by UCA1 in GC cells. we found that UCA1 could directly interact with miR-203 and lead to the release of miR-203-targeted transcripts ZEB2.	30464170	RID00220	ceRNA or sponge
Atherosclerosis	GAS5	miR-26a	negatively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	apoptosis process(+);cell autophagy(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Knockdown of growth-arrest specific transcript 5 restores oxidized low-density lipoprotein-induced impaired autophagy flux via upregulating miR-26a in human endothelial cells.We further demonstrated that GAS5 directly bound to miR-26a in HAECs. GAS5 knockdown inhibited cell apoptosis and activated autophagy flux, whereas inhibition of miR-26a reversed the effect of GAS5 in HAECs.	30468731	RID00221	ceRNA or sponge
Head and neck squamous cell carcinoma	MIR31HG	HIF1A	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);tumorigenesis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000100644	NA	554202	3091	LncHIFCAR|hsa-lnc-31	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA MIR31HG targets HIF1A and P21 to facilitate head and neck cancer cell proliferation and tumorigenesis by promoting cell-cycle progression.MIR31HG overexpression or co-expression of HIF1A-positive and p21-negative could serve as a poor prognostic factor for LSCC patients.MIR31HG KD decreased the expression of HIF1A and CCND1 but increased expression of p21. The ingenuity pathway analysis and Western blot indicated that MIR31HG regulated cell cycle progression via HIF1A and p21 in HNSCC.	30458787	RID00222	expression association
Head and neck squamous cell carcinoma	MIR31HG	CDKN1A	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);apoptosis process(-);tumorigenesis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000124762	NA	554202	1026	LncHIFCAR|hsa-lnc-31	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MIR31HG targets HIF1A and P21 to facilitate head and neck cancer cell proliferation and tumorigenesis by promoting cell-cycle progression.MIR31HG overexpression or co-expression of HIF1A-positive and p21-negative could serve as a poor prognostic factor for LSCC patients.MIR31HG KD decreased the expression of HIF1A and CCND1 but increased expression of p21. The ingenuity pathway analysis and Western blot indicated that MIR31HG regulated cell cycle progression via HIF1A and p21 in HNSCC.	30458787	RID00223	expression association
Endometrial cancer	NEAT1	LEF1	positively-E	western blot;luciferase reporter assay	downregulation	microarray	GSE29435	GSE29435.zip	cell cycle(+);cell viability(+)	ceRNA(miR-146b-5p)	regulation	NA	progesterone	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000138795	NA	283131	51176	LINC00084|NCRNA00084|TncRNA|VINC	LEF-1|TCF10|TCF1ALPHA|TCF7L3	Investigations on the mechanism of progesterone in inhibiting endometrial cancer cell cycle and viability via regulation of long noncoding RNA NEAT1/microRNA-146b-5p mediated Wnt/beta-catenin signaling.Lymphoid enhancing factor 1 (LEF1) was positively associated with NEAT1, and eventually hsa_miR-146b-5p was validated to target both LEF1 and NEAT1.Downstream gene c-myc or MMP9 regulated by upstream gene LEF1 in Wnt/beta-catenin signaling pathway was remarkably increased in Ishikawa cells and positively related with NEAT1. Progesterone inhibited cell cycle and viability through regulating NEAT1/miR-146b-5p axis via Wnt/beta-catenin signaling pathway.	30452118	RID00224	ceRNA or sponge
Gastric cancer	NORAD	FOXO6	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-608)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	NA	NA	647979	100132074	LINC00657	NA	The long noncoding RNA NORAD promotes the growth of gastric cancer cells by sponging miR-608.NORAD acted as a competitive endogenous RNA (ceRNA), which sponged miR-608 and suppressed the expression of miR-608 in gastric cancer cells. Further experiments demonstrated that miR-608 targeted the forkhead box O6 (FOXO6) and negatively regulated the expression of FOXO6.Overexpression of FOXO6 attenuated the inhibitory effect of miR-608 on the gastric cancer cell growth.	30453063	RID00225	ceRNA or sponge
Osteosarcoma	BDNF-AS	CASP3	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000164305	NA	497258	836	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CPP32|CPP32B|SCA-1	LncRNA BDNF-AS is associated with the malignant status and regulates cell proliferation and apoptosis in osteosarcoma.The in vitro studies indicated that BDNF-AS overexpression inhibits OS cell proliferation and promotes cell apoptosis through regulating cleaved caspase-3.	30352834	RID00226	expression association
Gastric cancer	NBAT1	SOX9	negatively-F	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000125398	NA	729177	6662	CASC14|NBAT-1	CMD1|CMPD1|SRA1|SRXX2|SRXY10	A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.NBAT1 interacted with Sox9, and reduced its protein stability by promoting it from polyubiquitination and proteasome-dependent degradation. Moreover, we revealed that Sox9 could occupy the NBAT1 promoter to inactivate its transcription.	30287498	RID00227	interact with protein
Gastric cancer	SOX9	NBAT1	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Gastric cancer	TF	lncRNA	ENSG00000125398	NA	ENSG00000260455	GRCh38_6:22133205-22147193	6662	729177	CMD1|CMPD1|SRA1|SRXX2|SRXY10	CASC14|NBAT-1	A negative feedback loop between long noncoding RNA NBAT1 and Sox9 inhibits the malignant progression of gastric cancer cells.NBAT1 interacted with Sox9, and reduced its protein stability by promoting it from polyubiquitination and proteasome-dependent degradation. Moreover, we revealed that Sox9 could occupy the NBAT1 promoter to inactivate its transcription.	30287498	RID00228	transcriptional regulation
Melanoma	UCA1	miR-185-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell motility(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/beta-catenin signaling pathway.We found that miR-185-5p could directly bind to UCA1 at the miRNA recognition site, and there existed a negative relationship between UCA1 and miR-185-5p. Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/beta-catenin signaling pathway.	30144501	RID00229	ceRNA or sponge
Malignant glioma	SNHG12	FOXP1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000114861	NA	85028	27086	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	12CC4|HSPC215|MFH|QRF1|hFKH1B	Long noncoding RNA SNHG12 facilitates the tumorigenesis of glioma through miR-101-3p/FOXP1 axis.it was found that SNHG12 harbored the complementary binding sites with miR-101-3p at 3'-UTR, acting as a miRNA 'sponge'. Furthermore, miR-101-3p also targeted the 3'-UTR of FOXP1 mRNA.	30098431	RID00230	ceRNA or sponge
Melanoma	FOXD2-AS1	AKT1	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	TCGA	SKCM.zip	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000142208	NA	84793	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	FOXD2-AS1 correlates with the malignant status and regulates cell proliferation, migration, and invasion in cutaneous melanoma.The results of loss-of-function study showed that inhibition of FOXD2-AS1 suppresses cutaneous melanoma cell proliferation, migration and invasion through regulating phospho-Akt expression.	30426532	RID00231	expression association
Prostate cancer	IGF2-AS	IGF2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000167244	NA	51214	3481	IGF2-AS1|IGF2AS|PEG8	C11orf43|GRDF|IGF-II|PP9974	Long Noncoding RNA IGF2AS is Acting as an Epigenetic Tumor Suppressor in Human Prostate Cancer.IGF2AS was downregulated in both PCa cell lines and human PCa tumors. IGF2 was downregulated by IGF2AS overexpression. Conversely, IGF2 upregulation revered the suppressing function of IGF2AS on PCa proliferation and invasion.	30423304	RID00232	expression association
Systemic lupus erythematosus	THRIL	CCL2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell injury(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Immune system disease	Lupus erythematosus	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000108691	NA	102659353	6347	BRI3BP-AS1|BRI3BPAS1|Linc1992|TCONS_00020260	NA	Long noncoding RNA THRIL contributes in lipopolysaccharide-induced HK-2 cells injury by sponging miR-34a.THRIL worked as a sponge of microRNA-34a (miR-34a) and it could directly target MCP-1.LncRNA THRIL was highly expressed in the LPS stimulated cells, and THRIL overexpression aggravated LPS-induced cell damage as cell viability was decreased, and apoptosis and the release of proinflammatory cytokines were increased.THRIL overexpression aggravated LPS-induced injury possibly via sponging miR-34a, and thus preventing MCP-1 from degradation by miR-34a. The THRIL/miR-34a/MCP-1 axis might play critical roles in SLE.	30414207	RID00233	ceRNA or sponge
Oral squamous cell carcinoma	STAT3	HNF1A-AS1	positively-E	ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000241388	GRCh38_12:120941728-120980965	6774	283460	ADMIO|ADMIO1|APRF|HIES	C12orf27|HAS1|NCRNA00262	STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.HNF1A-AS1 was positively regulated by the transcription factor STAT3. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00234	transcriptional regulation
Oral squamous cell carcinoma	HNF1A-AS1	NOTCH1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000148400	NA	283460	4851	C12orf27|HAS1|NCRNA00262	AOS5|AOVD1|TAN1|hN1	It was uncovered that the expression of Notch1 and Hes1 (the core factors of Notch signaling pathway) was negatively regulated by HNF1A-AS1 knockdown. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00235	expression association
Oral squamous cell carcinoma	HNF1A-AS1	HES1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000114315	NA	283460	3280	C12orf27|HAS1|NCRNA00262	HES-1|HHL|HRY|bHLHb39	It was uncovered that the expression of Notch1 and Hes1 (the core factors of Notch signaling pathway) was negatively regulated by HNF1A-AS1 knockdown. STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.	30404566	RID00236	expression association
Ovarian cancer	HOTTIP	CTNNB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HOTTIP is a significant indicator of ovarian cancer prognosis and enhances cell proliferation and invasion.we demonstrated that inhibition of lncRNA HOTTIP suppressed Wnt/beta-catenin signaling by downregulating beta-catenin expression.	30452402	RID00237	expression association
Hepatocellular carcinoma	FER1L4	PTEN	positively-E	immunohistochemical staining;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA Fer-1-like family member 4 suppresses hepatocellular carcinoma cell proliferation by regulating PTEN in vitro and in vivo. PTEN was highly expressed in HCC tissues compared with normal adjacent tissues and was positively associated with FER1L4.	30431133	RID00238	expression association
Non-small cell lung cancer	FLVCR1-DT	E2F3	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-573)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000198468	GRCh38_1:212852105-212858126	ENSG00000112242	NA	642946	1871	NA	E2F-3	Long non-coding RNA FLVCR1-AS1 contributes to the proliferation and invasion of lung cancer by sponging miR-573 to upregulate the expression of E2F transcription factor 3.Results revealed that FLVCR1-AS1 was markedly upregulated in NSCLC tissues and cell lines. FLVCR1-AS1 functioned as a competing endogenous RNA (ceRNA) by directly binding to miRNA-573, and E2F transcription factor 3 (E2F3) was identified as a down-stream target of miR-573.	30309647	RID00239	ceRNA or sponge
Lung adenocarcinoma	SNHG6	E2F7	positively-E	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	TCGA	LUAD.zip	cell motility(+);epithelial to mesenchymal transition(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000165891	NA	641638	144455	HBII-276HG|NCRNA00058|U87HG	NA	SNHG6 functions as a competing endogenous RNA to regulate E2F7 expression by sponging miR-26a-5p in lung adenocarcinoma.mechanistic experiments identified that SNHG6 functions as a competing endogenous RNA (ceRNA) through competitively sponging miR-26a-5p to regulate E2F7 expression, cell motility and EMT in LUAD cells.	30257360	RID00240	ceRNA or sponge
Hepatocellular carcinoma	DBH-AS1	miR-138	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000225756	GRCh38_9:133654586-133657313	NA	NA	138948	NA	NCRNA00118	NA	LncRNA DBH-AS1 facilitates the tumorigenesis of hepatocellular carcinoma by targeting miR-138 via FAK/Src/ERK pathway.DBH-AS1 acted as a molecular sponge of miR-138 to downregulate miR-138 expression. DBH-AS1 silencing and miR-138 overexpression reduced cell viability, inhibited colony formation, and induced apoptosis. Also, DBH-AS1 overexpression attenuated miR-138-mediated anti-proliferation and pro-apoptosis effects. Additionally, miR-138 overexpression gave rise to a blockage on FAK/Src/ERK pathway, while this effect was undermined by increased DBH-AS1.	30142544	RID00241	ceRNA or sponge
Colorectal cancer	kcna3	YAP1	negatively-E	Immunofluorescence assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177272	GRCh38_1:110653560-110674940	ENSG00000137693	NA	NA	10413	NA	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA kcna3 inhibits the progression of colorectal carcinoma through down-regulating YAP1 expression.up-regulation of lncRNA kcna3 decreased YAP1 protein expression and accelerated its degradation. The effects of lncRNA kcna3 overexpression on cell growth and tumorigenesis inhibition and apoptosis promotion were weakened when the expression of YAP1 was up-regulated.	30099342	RID00242	expression association
Gastric cancer	LINC00473	MMP2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000087245	NA	90632	4313	C6orf176|LNC473|bA142J11.1	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LINC00473 predicts poor prognosis and regulates cell migration and invasion in gastric cancer.The study in vitro indicated that silencing of LINC00473 had no effect on GC cell viability, but inhibited GC cell migration and invasion through modulating MMP2 and MMP9 expression.	30071345	RID00243	expression association
Gastric cancer	LINC00473	MMP9	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	prognosis;cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000100985	NA	90632	4318	C6orf176|LNC473|bA142J11.1	CLG4B|GELB|MANDP2|MMP-9	LINC00473 predicts poor prognosis and regulates cell migration and invasion in gastric cancer.The study in vitro indicated that silencing of LINC00473 had no effect on GC cell viability, but inhibited GC cell migration and invasion through modulating MMP2 and MMP9 expression.	30071345	RID00244	expression association
Ovarian cancer	GAS5	HOXA5	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cancer progression(-)	ceRNA(miR-196a-5p)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106004	NA	60674	3202	NCRNA00030|SNHG2	HOX1|HOX1.3|HOX1C	Lowly-expressed lncRNA GAS5 facilitates progression of ovarian cancer through targeting miR-196-5p and thereby regulating HOXA5.LncRNA GAS5 depressed OA development by targeting miR-196a-5p and thereby down-regulating HOXA5 expression, providing substance for developing lncRNA-based strategies to treat OA.The HOXA5 was found to reverse the effects imposed by miR-196a-5p on viability, proliferation and apoptosis of OA cells	30201235	RID00245	ceRNA or sponge
Endometrial cancer	NIFK-AS1	miR-146a	negatively-F	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000236859	GRCh38_2:121649320-121728563	NA	NA	254128	NA	NA	NA	Long non-coding RNA NIFK-AS1 inhibits M2 polarization of macrophages in endometrial cancer through targeting miR-146a. The expression of NIFK-AS1 and miR-146a were decreased and increased in tumor-associated macrophages of endometrial cancer patients, respectively. NIFK-AS1 could interact with miR-146a and increased the expression of Notch1 through downregulating miR-146a. Further experiments revealed that miR-146a overexpression attenuated the effect of NIFK-AS1 on suppressing the M2 polarization of macrophages and the estrogen-induced proliferation, migration and invasion of endometrial cancer cells.	30176290	RID00246	ceRNA or sponge
Colon cancer	FALEC	STAT3	interact	RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	phosphorylation	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colon cancer	lncRNA	TF	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000168610	NA	100874054	6774	FAL1|LINC00568|ncRNA-a1	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA FAL1 promotes proliferation and inhibits apoptosis of human colon cancer cells.FAL1 was found to interact with STAT3 at 200 to 400 bp and promote phosphorylation of STAT3. In addition, we found that knockdown of STAT3 in HT29 cells abolished the effects of FAL1 on cell proliferation as well as the expression of TGF-beta1 and Bcl-2.our results indicate that FAL1 expression was remarkably up-regulated in colon tumor tissues as compared to corresponding tumor-adjacent normal tissues.	30290064	RID00247	interact with protein
Glioblastoma	LINC00599	KLF16	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);apoptosis process(+)	ceRNA(miR-185-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	TF	ENSG00000253230	GRCh38_8:9899871-9906678	ENSG00000129911	NA	157627	83855	NA	BTEB4|DRRF|NSLP2	Long noncoding RNA-RNCR3 overexpression deleteriously affects the growth of glioblastoma cells through miR-185-5p/Kruppel-like factor 16 axis.we found that RNCR3 overexpression promotes Kruppel-like factor 16 (KLF16) expression through inhibiting the level of miR-185-5p. We demonstrated that KLF16 is a direct target of miR-185-5p. An increased miR-185-5p level by a miR-185-5p mimic or decreased KLF16 by KLF16 small interfering RNA both reversed the function of RNCR3 overexpression on GBM cell growth and apoptosis.	29953649	RID00248	ceRNA or sponge
Epithelial ovarian cancer	XIST	miR-214-3p	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Upregulation of lncRNA XIST may suppress EOC development, possibly through sponging effect to induce hsa-miR-214-3p downregulation. Lentivirus-mediated XIST upregulation had significant anticancer effects in CAOV3 and OVCAR3 cells by suppressing cancer cell proliferation, invasion, increasing cisplatin chemosensitivity and inhibiting in vivo tumor growth.	30207107	RID00249	ceRNA or sponge
Oral squamous cell carcinoma	HOTAIR	MAP1LC3B	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000140941	NA	100124700	81631	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ATG8F|LC3B|MAP1A/1BLC3|MAP1LC3B-a	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00250	expression association
Oral squamous cell carcinoma	HOTAIR	ATG3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000144848	NA	100124700	64422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APG3|APG3-LIKE|APG3L|PC3-96	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00251	expression association
Oral squamous cell carcinoma	HOTAIR	ATG7	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000197548	NA	100124700	10533	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APG7-LIKE|APG7L|GSA7	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00252	expression association
Oral squamous cell carcinoma	HOTAIR	MTOR	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(-);cell autophagy(+);apoptosis process(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000198793	NA	100124700	2475	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	RNA interference of long noncoding RNA HOTAIR suppresses autophagy and promotes apoptosis and sensitivity to cisplatin in oral squamous cell carcinoma.After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. proliferation, migration, and invasion of OSCC cells were suppressed.	30053324	RID00253	expression association
Clear cell renal cell carcinoma	miR-182-5p	MALAT1	negatively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);colony formation(-);apoptosis process(+)	NA	association	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Elevated miR-182-5p Associates with Renal Cancer Cell Mitotic Arrest through Diminished MALAT-1 Expression.Overexpression of miR-182-5p-inhibited cell proliferation, colony formation, apoptosis, and led to G2-M-phase cell-cycle arrest by directly targeting MALAT-1 .Transient knockdown of MALAT-1 mimicked the effects of miR-182-5p overexpression.	30037856	RID00254	expression association
Non-small cell lung cancer	MIR4435-2HG	miR-6754-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000172965	GRCh38_2:111036776-111523376	NA	NA	541471	NA	NA	NA	Long noncoding RNA LINC00978 promotes cell proliferation and invasion in non-small cell lung cancer by inhibiting miR-6754-5p.it was demonstrated that LINC00978 served as a competing endogenous RNA sponge for microRNA (miR)-6754-5p, which was downregulated in NSCLC tissues.it was demonstrated that inhibition of miR-6754-5p reversed the effects of LINC00978 knockdown on NSCLC cell proliferation, migration, invasion and apoptosis.	30221669	RID00255	ceRNA or sponge
Atherosclerosis	MALAT1	SOCS1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+);apoptosis process(-)	ceRNA(miR-155)	regulation	NA	NA	NA	Tumor Promoting Inflammation;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185338	NA	378938	8651	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CIS1|CISH1|JAB|SOCS-1|SSI-1|SSI1|TIP-3|TIP3	The suppression of ox-LDL-induced inflammatory cytokine release and apoptosis of HCAECs by long non-coding RNA-MALAT1 via regulating microRNA-155/SOCS1 pathway.we found that MALAT1 could suppress the inflammatory cytokine release and cell apoptosis via sponging miR-155 to increase SOCS1 level, which in turn restrained JAK-STAT pathway. miR-155 regulatedthe production of pro-inflammatory cytokines and theapoptosis of HCAECs via directly targeting SOCS1.	30314869	RID00256	ceRNA or sponge
Gastric cancer	SOX2-OT	miR-194-5p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell motility(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000242808	GRCh38_3:180989762-181836880	NA	NA	347689	NA	NCRNA00043|SOX2OT	NA	The SOX2OT/miR-194-5p axis regulates cell proliferation and mobility of gastric cancer through suppressing epithelial-mesenchymal transition.the in vitro experiments revealed that knockdown of SOX2OT inhibited cell proliferation and mobility through suppressing EMT via targeting miR-194-5p in GC.miR-194-5p expression was negatively regulated by SOX2OT expression in GC cells	30405772	RID00257	ceRNA or sponge
Breast cancer	MALAT1	miR-145	negatively-E	RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 promotes angiogenesis of breast cancer.knockdown of endogenous MALAT1 significantly increased miR-145 levels in MCF-7 cells.This outcome revealed that MALAT1 promoted angiogenesis in BC, which may be related to the expression of miR-145.	30226550	RID00258	expression association
Prostate cancer	VPS9D1-AS1	MYC	positively-E	luciferase reporter assay	upregulation	sequencing;qRT-PCR	TCGA	PRAD.zip	cell proliferation(+)	ceRNA(miR-184)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000261373	GRCh38_16:89711856-89718165	ENSG00000136997	NA	100128881	4609	MYU	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA MYU promotes prostate cancer proliferation by mediating the miR-184/c-Myc axis.lncRNA MYU upregulated c-Myc by competitively binding miR-184 and then induced the proliferation of prostate cancer. RNAhybrid (34) was used to predict the binding sites of miR-184 /MYU and miR-184/3'UTR of c-Myc.	30132573	RID00259	ceRNA or sponge
Malignant glioma	HOXA10-AS	HOXA10	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);cell survival(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	TF	ENSG00000253187	GRCh38_7:27168619-27171915	ENSG00000253293	NA	100874323	3206	HOXA-AS4	HOX1|HOX1.8|HOX1H|PL	HOXA10-AS: A novel oncogenic long non-coding RNA in glioma.HOXA10-AS markedly regulated the expression of the homeobox A10 (HOXA10) gene.The results of the present study demonstrated that HOXA10-AS promoted cell growth and survival through activation of HOXA10 gene expression in glioma.Further statistical analysis demonstrated a significant and positive correlation between HOXA10 and HOXA10-AS gene expression	30132568	RID00260	expression association
Renal ischemia-reperfusion injury	MALAT1	HIF1A	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100644	NA	378938	3091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The long non-coding RNA MALAT1 is increased in renal ischemia-reperfusion injury and inhibits hypoxia-induced inflammation.Knockdown of MALAT1 by siRNA significantly up-regulated the expression of HIF-1a and NF-kB proteins in CoCl2-treated HK2 cells. The expression of MALAT1 is increased in renal ischemia-reperfusion injury. It is likely that MALAT1 inhibits the hypoxia-induced inflammatory response through the NF-kB pathway.	30277425	RID00261	expression association
Renal ischemia-reperfusion injury	MALAT1	NFKB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	The long non-coding RNA MALAT1 is increased in renal ischemia-reperfusion injury and inhibits hypoxia-induced inflammation.Knockdown of MALAT1 by siRNA significantly up-regulated the expression of HIF-1a and NF-kB proteins in CoCl2-treated HK3 cells. The expression of MALAT1 is increased in renal ischemia-reperfusion injury. It is likely that MALAT1 inhibits the hypoxia-induced inflammatory response through the NF-kB pathway	30277425	RID00262	expression association
Hepatocellular carcinoma	IATPR	ROCK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000067900	NA	101929447	6093	NA	P160ROCK|ROCK-I	Long non-coding RNA linc-ITGB1 promotes cell proliferation, migration, and invasion in human hepatoma carcinoma by up-regulating ROCK1.We conclude that lncRNA LINC-ITGB1 can promote the proliferation, migration, and invasion of HCC cells by up-regulating ROCK1.	30279202	RID00263	expression association
Multiple myeloma	RMRP	MYC	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	TF	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000136997	NA	6023	4609	CHH|NME1|RMRPR|RRP2	MRTL|MYCC|bHLHe39|c-Myc	c-Myc, RMRP, and miR-34a-5p form a positive-feedback loop to regulate cell proliferation and apoptosis in multiple myeloma.RMRP functions as a miR-34a-5p sponge to promote cell proliferation and repress cell apoptosis through upregulation of c-Myc in MM.c-Myc isa direct target of miR-34a-5p.	30389523	RID00264	ceRNA or sponge
Colorectal cancer	TMEM75	SIM2	positively-E	RNAi	upregulation	qRT-PCR	GSE70880	GSE70880.zip	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280055	GRCh38_8:127946559-127948723	ENSG00000159263	NA	641384	6493	NA	HMC13F06|HMC29C01|SIM|bHLHe15	Long noncoding RNA TMEM75 promotes colorectal cancer progression by activation of SIM2.We also found that the expression of SIM2 was upregulated and positively correlated that of TMEM75 in colorectal cancer tissues. Furthermore, ectopic expression of SIM2 rescued TMEM75 depletion-induced inhibition on cell proliferation, migration and invasion in colorectal cancer.	29964097	RID00265	expression association
Papillary thyroid carcinoma	HOXA-AS2	HOXA3	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-15a-5p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000105997	NA	285943	3200	HOXA3as	HOX1|HOX1E	LncRNA HOXA-AS2 facilitates tumorigenesis and progression of papillary thyroid cancer through modulating miR-15a-5p/HOXA3 axis.Further mechanism investigation revealed that HOXA-AS2 upregulated the expression of HOXA3 by sponging miR-15a-5p.Additionally, FOXD2-AS1 was found to upregulate HOXA3 expression by binding to miR-15a-5p. the putative binding sequence between miR-15a-5p and HOXA3 was obtained from TargetScan.	30375256	RID00266	ceRNA or sponge
Pre-eclampsia	PSG10P	IL1RAP	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000248257	GRCh38_19:42839368-42855718	ENSG00000196083	NA	653492	3556	PSG10|PSG12	C3orf13|IL-1RAcP|IL1R3	Potential regulatory network in the PSG10P/miR-19a-3p/IL1RAP pathway is possibly involved in preeclampsia pathogenesis.Lower levels of miR-19a-3p, but higher levels of PSG10P and IL1RAP were observed in PE placentas and the trophoblast cells in hypoxia. Luciferase reporter assays confirmed that PSG10P and IL1RAP were both direct targets of miR-19a-3p. Exposure to hypoxia inhibited cell viability, migration, and invasion of HET8/SVneo and TEV-1 cells.	30370628	RID00267	ceRNA or sponge
Endometriosis	MALAT1	CDKN1A	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	ERK/MAPK signaling pathway(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Down-regulation of long non-coding RNA MALAT1 inhibits granulosa cell proliferation in endometriosis by up-regulating P21 via activation of the ERK/MAPK pathway.We first found that MALAT1 lncRNA was significantly down-regulated in endometriosis GCs.	30371869	RID00268	expression association
Pancreatic cancer	DUXAP8	CDKN1A	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000124762	NA	503637	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID00269	epigenetic regulation
Pancreatic cancer	DUXAP8	KLF2	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000127528	NA	503637	10365	NA	LKLF	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID00270	epigenetic regulation
Renal cell carcinoma	LINC00961	SNAI2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cancer progression(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000235387	GRCh38_9:35909483-35937153	ENSG00000019549	NA	NA	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.the messenger RNA and protein expression levels of epithelial-mesenchymal transition (EMT)-associated markers Slug and N-cadherin in RCC cell lines were dramatically inhibited by overexpressing LINC00961.LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.	30367453	RID00271	expression association
Renal cell carcinoma	LINC00961	CDH2	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-);cancer progression(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000235387	GRCh38_9:35909483-35937153	ENSG00000170558	NA	NA	1000	NA	CD325|CDHN|CDw325|NCAD	LINC00962 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.the messenger RNA and protein expression levels of epithelial-mesenchymal transition (EMT)-associated markers Slug and N-cadherin in RCC cell lines were dramatically inhibited by overexpressing LINC00961.LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma	30367453	RID00272	expression association
Cervical cancer	DANCR	ROCK1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-335-5p)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000067900	NA	57291	6093	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	P160ROCK|ROCK-I	LncRNA DANCR promotes cervical cancer progression by upregulating ROCK1 via sponging miR-335-5p.Further cellular behavioral this study demonstrated that DANCR promoted cervical cancer progression by functioning as a competing endogenous RNA (ceRNA) to regulate ROCK1 expression via sponging miR-335-5p.experiments revealed that miR-335-5p mimics and ROCK1 knockdown reversed the effects of upregulated DANCR on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of cervical cancer cells by rescue assays. DANCR andROCK1 share the similar binding sites for miR-335-5p.	30362591	RID00273	ceRNA or sponge
Hepatocellular carcinoma	H19	TWIST1	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Involvement of H19/miR-326 axis in hepatocellular carcinoma development through modulating TWIST1.The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR-326 and modulate TWIST1 levels in HCC pathogenesis. we observed that inhibition of H19 can repress HCC cell growth, migration, and invasion in vitro. miR-326 mimics can also inhibit HCC progression.the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression.TWIST1 was a direct target of miR-326.	303625122270:275	RID00274	ceRNA or sponge
Cervical cancer	HOTAIR	HIF1A	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100644	NA	100124700	3091	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Overexpression of HOTAIR leads to radioresistance of human cervical cancer via promoting HIF-1alpha expression. HOTAIR also upregulated the expression of HIF-1alpha in HeLa and C33A cell exposed to radiation. HIF-1alpha knockdown reversed increasing cell viability and reducing apoptosis of HeLa and C33A cell induced by HOTAIR overexpression.	30355300	RID00275	expression association
Malignant glioma	DLX6-AS1	E2F1	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-197-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000101412	NA	285987	1869	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	E2F-1|RBAP1|RBBP3|RBP3	Long noncoding RNA DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.our finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.In the cellular functional assays, silenced DLX6-AS1 expression by siRNAs inhibited the proliferation, invasion and tumor growth in vitro and in vivo.we found that E2F1acted as the target protein of miR-197-5p with the 3'UTR combination.	30366080	RID00276	ceRNA or sponge
Cervical cancer	GAS5	STAT3	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000168610	NA	60674	6774	NCRNA00030|SNHG2	ADMIO|ADMIO1|APRF|HIES	Growth arrest-specific 5 attenuates cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21. the decrease of miR-21 associated proteins phosphorylated STAT3 and E2F3 was seen in GAS5 overexpressed cells.The GAS5 deficiency also reduced miR-21 target proteins TIMP3 and PDCD4 expressions.We proved GAS5 could suppress miR-21 expression. The overexpressions of GAS5 expression reduced the basal levels of E2F3 and phosphorylated STAT3, which could be elevated byintroducing siGAS5 (Figure 4c). Levels of two miR-21 target proteins,TIMP3, and PDCD4, were reduced by siGAS5.	30352127	RID00277	expression association
Cervical cancer	GAS5	miR-21	negatively-F	RNAi;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemosensitivity(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt.Growth arrest-specific 5 attenuates cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21. the decrease of miR-21 associated proteins phosphorylated STAT3 and E2F3 was seen in GAS5 overexpressed cells.The GAS5 deficiency also reduced miR-21 target proteins TIMP3 and PDCD4 expressions.We proved GAS5 could suppress miR-21 expression. The overexpressions of GAS5 expression reduced the basal levels of E2F3 and phosphorylated STAT3, which could be elevated byintroducing siGAS5 (Figure 4c). Levels of two miR-21 target proteins,TIMP3, and PDCD4, were reduced by siGAS5.	28472815;30352127	RID00278	ceRNA or sponge
Cervical cancer	GAS5	PTEN	positively-E	western blot;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt.In this study, we found a negative correlation between GAS5 and miR-21 in CC tissue and cell lines and identified a repression feedback between GAS5 and miR-21. GAS5 can function as a tumor suppressor by regulating growth, apoptosis, invasion, and migration in CC cells by regulating PTEN and PDCD4 that are also miR-21 targets.	28472815	RID00279	expression association
Cervical cancer	GAS5	AKT1	negatively-E	western blot;qRT-PCR;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000142208	NA	60674	207	NCRNA00030|SNHG2	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Our results indicate that GAS5 is a direct target of miR-21 and can predict the clinical staging of cervical cancer. high expression of GAS5 and low expression of miR-21 can enhance the sensitivity of SiHa/cDDP cancer cells to cisplatin. A further experiment for identifying the mechanism of cisplatin resistance by GAS5 showed that GAS5 can not only regulate phosphatase and tensin homolog through miR-21 but also influence the phosphorylation of Akt. GAS5 overexpression and SiHa/cDDP cells with miR-21 knockdown  had a down-regulated level of pAkt.	28472815	RID00280	expression association
Colon cancer	HOTAIR	IGF2BP2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell proliferation(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000073792	NA	100124700	10644	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IMP-2|IMP2|VICKZ2	Long noncoding RNA HOTAIR silencing inhibits invasion and proliferation of human colon cancer LoVo cells via regulating IGF2BP2.the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial-mesenchymal transition.The dual luciferase reporter gene assay was initially used for testify the regulating relationship between lncRNA HOTAIR and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)	30335892	RID00281	transcriptional regulation
Clear cell renal cell carcinoma	MALAT1	ACVR2B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-194-5p)	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000114739	NA	378938	93	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ACTRIIB|ActR-IIB|HTX4	LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR-194-5p/ACVR2B signaling.MALAT1 could directly target miR-194-5p to suppress its expression, and ACVR2B was the targeted molecule of miR-194-5p. Finally, ACVR2B could reverse the effects exerted by miR-194-5p on viability, proliferation, and apoptosis of KIRC cells.	30334578	RID00282	ceRNA or sponge
Cervical cancer	ZEB1-AS1	ZEB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA ZEB1-AS1 promotes cell invasion and epithelial to mesenchymal transition through inducing ZEB1 expression in cervical cancer.we found that knockdown of ZEB1-AS1 significantly inhibited ZEB1 expression.	30425516	RID00283	expression association
Gastric cancer	HNF1A-AS1	CDC34	positively-E	RIP	upregulation	qRT-PCR	NA	NA	cell cycle(+)	ceRNA(miR-661)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000099804	NA	283460	997	C12orf27|HAS1|NCRNA00262	E2-CDC34|UBC3|UBCH3|UBE2R1	EGR1-Mediated Transcription of lncRNA-HNF1A-AS1 Promotes Cell-Cycle Progression in Gastric Cancer.HNF1A-AS1 functioned as competing endogenous RNA (ceRNA) by binding to miR-661, upregulating the expression of cell division cycle 34 (CDC34), which is a direct target of miR-661.Overexpression of HNF1A-AS1 enhanced cell proliferation and promoted cell-cycle progression, whereas knockdown of HNF1A-AS1 elicited the opposite effects.	30185552	RID00284	ceRNA or sponge
Gastric cancer	EGR1	HNF1A-AS1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000120738	NA	ENSG00000241388	GRCh38_12:120941728-120980965	1958	283460	AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268|ZNF225	C12orf27|HAS1|NCRNA00262	Early growth response protein 1 (EGR1) directly bound the HNF1A-AS1 promoter region and activated its transcription. Overexpression of EGR1 enhanced cell proliferation and promoted cell-cycle promotion, similar to the function of HNF1A-AS1.	30185552	RID00285	transcriptional regulation
Osteosarcoma	APTR	YAP1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000137693	NA	100505854	10413	RSBN1L-AS1	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA APTR contributes to osteosarcoma progression through repression of miR-132-3p and upregulation of yes-associated protein 1.We confirmed miR-132-3p to be a target for APTR, and its expression was demonstrated to be inhibited by APTR.knockdown of APTR and overexpression of miR-132-3p both,remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis.Yes-associated protein 1 (YAP1) was determined as an inhibitory target of miR-132-3p. knockdown of APTR and overexpression of miR-132-3p both,remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis.our findings demonstrated that the repression of YAP1 protein expression and the suppression of Ki-67, MMP9, and Bcl2 expression induced by APTR knockdown required increased miR-132-3p. Thus, APTR contributed to OS progression through repression of miR-132-3p and upregulation of YAP1 expression	30317613	RID00286	ceRNA or sponge
Cholangiocarcinoma	Lnc-EPIC1	MYC	interact	RIP;CRISPR/Cas9	upregulation	qRT-PCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA EPIC1 promotes cholangiocarcinoma cell growth.our results show that Lnc-EPIC1 promotes CCA cancer progression by targeting Myc.Loss-and-gain of Lnc-EPIC1 contributes to the CCA cell growth, colony formation, cell apoptosis and also cell cycle. Myc has been reported to directly interact with Lnc-EPIC1 in several cancer cells.	30205958	RID00287	interact with protein
Laryngeal squamous cell carcinoma	PVT1	miR-519d-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR-519d-3p.LncRNA PVT1 is consistently overexpressed in human LSCC, and overexpression of lncRNA PVT1 contributes to the proliferation and migration of LSCC through inhibiting miR-519d-3p expression.Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR-519d-3p.	30304557	RID00288	ceRNA or sponge
Parkinson's disease	SNHG1	GSK3B	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cytotoxicity(+)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Tumor Promoting Inflammation	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000082701	NA	23642	2932	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Upregulated lncRNA small nucleolar RNA host gene 1 promotes 1-methyl-4-phenylpyridinium ion-induced cytotoxicity and reactive oxygen species production through miR-15b-5p/GSK3beta axis in human dopaminergic SH-SY5Y cells.SNHG1 was demonstrated to interact with miR-15b-5p. Moreover, SNHG1 could attenuate the inhibitory effects of miR-15b-5p on MPP+ -induced cytotoxicity and production of ROS.The inhibitory effects of SNHG1 knockdown or miR-15b-5p overexpression on MPP+ -induced cytotoxicity and reactive oxygen species (ROS) production were abrogated by upregulation of GSK3beta.GSK3betais a target gene of miR-15b-5p.	30302821	RID00289	ceRNA or sponge
Cervical cancer	MNX1-AS1	MAPK3	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000102882	NA	645249	5595	CCAT5	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00290	interact with protein
Cervical cancer	MNX1-AS1	MAPK1	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000100030	NA	645249	5594	CCAT5	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00291	interact with protein
Cervical cancer	MNX1-AS1	MAPK8	positively-F	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);MAPK signaling pathway(+)	phosphorylation	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000243479	GRCh38_7:157010805-157016426	ENSG00000107643	NA	645249	5599	CCAT5	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	LncRNA MNX1-AS1 promotes the progression of cervical cancer through activating MAPK pathway.it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK.	30302806	RID00292	interact with protein
Atherosclerosis	UCA1	miR-26a	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA UCA1 sponges miR-26a to regulate the migration and proliferation of vascular smooth muscle cells.This study reveals that lncRNA UCA1 act as an endogenous sponge of miR-26a and downregulates miR-26a expression levels, and thereby relieving the inhibition of its target gene PTEN and alleviates VSMCs proliferation against atherosclerosis.LncRNA UCA1 sponges miR-26a to regulate the migration and proliferation of vascular smooth muscle cells.	29908280	RID00293	ceRNA or sponge
Gastric cancer	HOXC-AS3	YBX1	interact	RNA pull-down assay;mass spectrometry	upregulation	sequencing	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251151	GRCh38_12:53981509-53985519	ENSG00000065978	NA	100874365	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	A novel long noncoding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1.our data demonstrate that abnormal histone modification-activated HOXC-AS3 may play important roles in gastric cancer oncogenesis.A novel long noncoding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1.	30286788	RID00294	interact with protein
Liver fibrosis	miR-212	MEG3	negatively-F	RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Gastrointestinal system disease	Fibrosis	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	LncRNA-MEG3 inhibits activation of hepatic stellate cells through SMO protein and miR-212.MEG3 was confirmed as a target of microRNA-212 (miR-212). miR-212 was partly responsible for the effects of MEG3 on EMT process.we demonstrate that MEG3 inhibits Hh-mediated EMT process in liver fibrosis via SMO protein and miR-212.LncRNA-maternally expressed gene 3 (MEG3) functions as a tumor suppressor in cancers and has been shown to play a vital role in EMT process.Accordingly,MEG3-inhibited EMT process could be partly suppressed by miR-212.	30282972	RID00295	ceRNA or sponge
Liver fibrosis	MEG3	SMO	interact	RIP;deletion-mapping analysis	downregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000128602	NA	55384	6608	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CRJS|FZD11|Gx|SMOH	LncRNA-MEG3 inhibits activation of hepatic stellate cells through SMO protein and miR-212.an interaction between MEG3 and SMO protein was predicted.we demonstrate that MEG3 inhibits Hh-mediated EMT process in liver fibrosis via SMO protein and miR-212.LncRNA-maternally expressed gene 3 (MEG3) functions as a tumor suppressor in cancers and has been shown to play a vital role in EMT process.	30282972	RID00296	interact with protein
Gastric cancer	LINC00460	KDM2A	positively-E	luciferase reporter assay;RIP	upregulation	sequencing;qRT-PCR	TCGA 	STAD.zip	cell proliferation(+);cell migration(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000173120	NA	728192	22992	NA	CXXC8|FBL11|FBL7|FBXL11|JHDM1A|LILINA	LINC00460 modulates KDM2A to promote cell proliferation and migration by targeting miR-342-3p in gastric cancer.we confirmed that LINC00460 could up-regulate KDM2A expression by competitively binding to miR-342-3p in GC cells. Furthermore, the suppressive effects of LINC00460 down-regulation on GC cell proliferation, migration and invasion were partially reversed by a miR-342-3p inhibitor.	30323616	RID00297	ceRNA or sponge
Malignant glioma	UBE2CP3-001	MMP9	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_4:57072549-57073311	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas. The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U87 glioma cells.Downregulation of UBE2CP3-001 could inhibit cell migration (p< 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01).	30393485	RID00298	expression association
Malignant glioma	UBE2CP3-001	TRAF3IP2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_4:57072549-57073311	ENSG00000056972	NA	NA	10758	NA	ACT1|C6orf2|C6orf4|C6orf5|C6orf6|CANDF8|CIKS|PSORS13	The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas. The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U88 glioma cells.Downregulation of UBE2CP3-001 could inhibit cell migration (p< 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01).	30393485	RID00299	expression association
Epithelial ovarian cancer	MIAT	miR-330-5p	negatively-F	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	LncRNA myocardial infarction-associated transcript promotes cell proliferation and inhibits cell apoptosis by targeting miR-330-5p in epithelial ovarian cancer cells.LncRNA MIAT promoted cell proliferation and inhibited cell apoptosis by negative regulation of miR-330-5p in epithelial ovarian cancer cells.we revealed that MIAT might function as an endogenous miR-330-5p sponge to regulate the target gene of miR-330-5p in epithelial ovarian cancer progression.	30393480	RID00300	ceRNA or sponge
Osteosarcoma	HAGLR	CDKN1C	negatively-E	RIP;western blot;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000129757	NA	401022	1028	HOXD-AS1|MIR7704HG|Mdgt	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2.our study confirmed that HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis.	30119259	RID00301	epigenetic regulation
Osteosarcoma	SNHG12	MCL1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-320a)	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000143384	NA	85028	4170	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Long noncoding RNA SNHG12 mediates doxorubicin resistance of osteosarcoma via miR-320a/MCL1 axis.knockdown of SNHG12 contributed to the upregulation of miR-320a and improved the sensitivity of doxorubicin. Additionally, miR-320a inhibited the expression of Myeloid cell leukemia 1 (MCL1).miR-320a targeted to MCL1.	30119255	RID00302	ceRNA or sponge
Colorectal cancer	MEG3	PDCD4	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	chemoresistance(-)	ceRNA(miR-141)	regulation	NA	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150593	NA	55384	27250	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	H731	Overexpression of MEG3 sensitizes colorectal cancer cells to oxaliplatin through regulation of miR-141/PDCD4 axis.MEG3 suppressed miR-141 expression in HCT116/OXA cells. Moreover, MEG3 elevated PDCD4 expression through targeting miR-141, acting as a competing endogenous RNA (ceRNA). Low MEG3 expression was correlated with poor prognosis of CRC patients. Overexpression of MEG3 improved oxaliplatin sensitivity of HT29/OXA and HCT116/OXA cells.	30119236	RID00303	ceRNA or sponge
Esophagus squamous cell carcinoma	FTH1P3	SP1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000185591	NA	2498	6667	FTHL3|FTHL3P	NA	Long non-coding RNA FTH1P3 regulated metastasis and invasion of esophageal squamous cell carcinoma through SP1/NF-kB pathway.Knockdown of FTH1P3 notably decreased the proliferation, migration, and invasion capacity of ESCC cells. Silencing of FTH1P3 decreased the expression of specificity protein 1 (Sp1) and NF-kB (p65) in EC9706 and EC1.	30119232	RID00304	expression association
Esophagus squamous cell carcinoma	FTH1P3	RELA	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000213453	GRCh38_2:27392784-27393367	ENSG00000173039	NA	2498	5970	FTHL3|FTHL3P	CMCU|NFKB3|p65	Long non-coding RNA FTH1P3 regulated metastasis and invasion of esophageal squamous cell carcinoma through SP1/NF-kB pathway.Knockdown of FTH1P3 notably decreased the proliferation, migration, and invasion capacity of ESCC cells. Silencing of FTH1P3 decreased the expression of specificity protein 1 (Sp1) and NF-kB (p65) in EC9706 and EC1.	30119232	RID00305	expression association
Cervical cancer	NORAD	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000169554	NA	647979	9839	LINC00657	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA NORAD upregulate SIP1 expression to promote cell proliferation and invasion in cervical cancer.the underlying mechanism studies showed that lncRNA NORAD could sponge miR-590-3p to promote the proliferation and invasion of CC cells via upregulating SIP1 expression.Previous study showed that SIP1 could act as a target of miR-590-3pin intrahepatic cholangiocarcinoma.	30119219	RID00306	ceRNA or sponge
Osteosarcoma	OIP5-AS1	CDK14	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-223)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000058091	NA	729082	5218	cyrano|linc-OIP5	PFTAIRE1|PFTK1	Long noncoding RNA OIP5-AS1 accelerates CDK14 expression to promote osteosarcoma tumorigenesis via targeting miR-223.miR-223 was predicted to target the 3'-UTR of OIP5-AS1 and constituted RNA induced silencing complex, which was confirmed by RNA immunoprecipitation and luciferase reporter assay. Besides, miR-223 targeted the CDK14 mRNA 3'-UTR.	30119217	RID00307	ceRNA or sponge
Retinoblastoma	THORLNC	MYC	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	TF	ENSG00000226856	GRCh38_2:118132128-118222250	ENSG00000136997	NA	100506797	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	LncRNA THOR acts as a retinoblastoma promoter through enhancing the combination of c-myc mRNA and IGF2BP1 protein. Down-regulation of lncRNA THOR with siRNA significantly repressed cell growth, migration and S phase accumulation, while induced cell apoptosis and G1 phase reduction and reduced the expression of c-myc.this study makes clear that lncRNA THOR is up-regulated in retinoblastoma, and its over-expression significantly enhances the malignant phenotype transformation of retinoblastoma cells through up-regulating c-myc expression via enhancing its combination with TGF2BP1 protein.	30119193	RID00308	expression association
Osteoarthritis	FOXD2-AS1	CCND1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000110092	NA	84793	595	NA	BCL1|D11S287E|PRAD1|U21B31	LncRNA FOXD2-AS1 regulates chondrocyte proliferation in osteoarthritis by acting as a sponge of miR-206 to modulate CCND1 expression.qRT-PCR showed that expression of FOXD2-AS1 and Cyclin D1 (CCND1) was upregulated in OA cartilage tissues, while miR-206 expression was significantly decreased.TargetScan showed a potential miR-206 binding sequence in the 3'UTR of CCND1 (Fig. 4A). Luciferase reporter assay revealed that miR-206 mi-mics reduced the luciferase activity of CCND1-Wt group but not CCND1-Mut group in HEK293 T cells.	30119190	RID00309	ceRNA or sponge
Non-small cell lung cancer	HAGLR	MMP9	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000100985	NA	401022	4318	HOXD-AS1|MIR7704HG|Mdgt	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA HOXD-AS1 promotes non-small cell lung cancer migration and invasion through regulating miR-133b/MMP9 axis.we found that miR-133b was a direct downstream target of HOXD-AS1 in NSCLC. miR-133b inhibition reverse the inhibitory effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of MMP-9 (a target of miR-133b) in NSCLC cells.Increased HAGLR expression promotes non-small cell lung cancer proliferation and invasion via enhanced de novo lipogenesis.Furthermore, the expression levels of p21 and matrix metallopeptidase-9 (MMP-9) were dysregulated when HAGLR expression was suppressed.	29958139;28443464	RID00311	ceRNA or sponge
Oral squamous cell carcinoma	LOC441178	ROCK1	negatively-E	RNAi;immunohistochemistry	downregulation	microarray	GSE30784;GSE9844	GSE30784.zip;GSE9844.zip	cell migration(-);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENST00000400831	GRCh38_6:167679626-167683787	ENSG00000067900	NA	NA	6093	NA	P160ROCK|ROCK-I	Long Noncoding RNA LOC441178 Reduces the Invasion and Migration of Squamous Carcinoma Cells by Targeting ROCK1.we found that rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) is one of the functionally relevant targets of LOC441178 in squamous cells, which is negatively correlated with LOC441178 in tumor tissues from OSCC patients.	30364063	RID00312	transcriptional regulation
Osteosarcoma	TUG1	miR-219a-5p	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Targeting the FOXM1-regulated long noncoding RNA TUG1 in osteosarcoma. we found that TUG1 was upregulated by FOXM1 (Forkhead Box M1) in osteosarcoma cells. TUG1 accelerated osteosarcoma proliferation, migration, and invasion by competitively sponging miR-219a-5p, leading to upregulation of Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase Catalytic Subunit Alpha and activation of the protein kinase B (AKT) signaling pathway. In addition, the AKT pathway activation promoted TUG1 expression by upregulating the expression of FOXM1, forming a positive feedback loop in osteosarcoma.	30099814	RID00313	ceRNA or sponge
Osteosarcoma	FOXM1	TUG1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000111206	NA	ENSG00000253352	GRCh38_22:30969245-30979395	2305	55000	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LINC00080|NCRNA00080|TI-227H	Targeting the FOXM1-regulated long noncoding RNA TUG1 in osteosarcoma. we found that TUG1 was upregulated by FOXM1 (Forkhead Box M1) in osteosarcoma cells. TUG1 accelerated osteosarcoma proliferation, migration, and invasion by competitively sponging miR-219a-5p, leading to upregulation of Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase Catalytic Subunit Alpha and activation of the protein kinase B (AKT) signaling pathway. In addition, the AKT pathway activation promoted TUG1 expression by upregulating the expression of FOXM1, forming a positive feedback loop in osteosarcoma.	30099814	RID00314	transcriptional regulation
Hirschsprung's disease	FALEC	AKT1	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-637)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000142208	NA	100874054	207	FAL1|LINC00568|ncRNA-a1	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA FAL1 functions as a ceRNA to antagonize the effect of miR-637 on the down-regulation of AKT1 in Hirschsprung's disease. FAL1 could positively regulate AKT1 expression by competitively binding to miR-637. FAL1 regulates the miR-637 target gene, AKT1. Cell functional analyses indicated that FAL1 overexpressing notably promoted cell proliferation and migration.	30062828	RID00315	ceRNA or sponge
Gastric cancer	LINC01606	miR-423-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell metastasis(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000253301	GRCh38_8:57142659-57244793	NA	NA	100507651	NA	NA	NA	The long non-coding RNA LINC01606 contributes to the metastasis and invasion of human gastric cancer and is associated with Wnt/beta-catenin signaling.We also revealed that LINC01606 might be associated with miR-423-5p to regulate the level to which the Wnt/beta-catenin signaling pathway is activated.	30142387	RID00316	expression association
Breast cancer	SNHG14	PABPC1	positively-E	ChIP;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+);tumorigenesis(+)	histone modification	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000224078	GRCh38_15:24978583-25420336	ENSG00000070756	NA	104472715	26986	115HG|IC-SNURF-SNRPN|LNCAT|NCRNA00214|U-UBE3A-ATS|UBE3A-AS|UBE3A-AS1|UBE3A-ATS|UBE3AATS	PAB1|PABP|PABP1|PABPC2|PABPL1	Long non-coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation.ChIP assays demonstrated that lncRNA SNHG14 may induce PABPC1 expression through modulating H3K27 acetylation in the promoter of PABPC1 gene, thus resulting in the activation of Nrf2 signalling pathway. These data suggest that lncRNA SNHG14 promotes breast cancer tumorigenesis and trastuzumab resistance through regulating PABPC1 expression through H3K27 acetylation.	30063126	RID00317	epigenetic regulation
Retinoblastoma	HOTAIR	MET	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105976	NA	100124700	4233	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AUTS9|DFNB97|HGFR|RCCP2|c-Met	LncRNA HOTAIR/miR-613/c-met axis modulated epithelial-mesenchymal transition of retinoblastoma cells.HOTAIR was verified to directly target miR-613, and c-met was the direct target gene of miR-613 (P < 0.05).up-regulated HOTAIR and down-regulated miR-613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). c-met prohibited the functioning of miR-613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05).	30030888	RID00318	ceRNA or sponge
Malignant glioma	PVT1	GREM1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);cancer progression(+);BMP signaling pathway(+)	ceRNA(miR-128-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000166923	NA	5820	26585	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	C15DUPq|CKTSF1B1|CRAC1|CRCS4|DAND2|DRM|DUP15q|GREMLIN|HMPS|HMPS1|IHG-2|MPSH|PIG2	LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway.lncRNA PVT1 acted as a sponge of miR-128-3p and, thus, influenced the BMP signaling pathway downstream proteins BMP2 and BMP4 through regulating GREM1. MiR-128-3p Targeted and Regulated GREM1.	30120709	RID00319	ceRNA or sponge
Colorectal cancer	GAS5	FOXO3	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000118689	NA	60674	2309	NCRNA00030|SNHG2	AF6q21|FKHRL1|FKHRL1P2|FOXO2|FOXO3A	lncRNA GAS5 inhibits colorectal cancer cell proliferation via the miR-182-5p/FOXO3a axis.A dual-luciferase reporter assay showed that GAS5 could negatively regulate the expression of microRNA (miR)-182-5p. Upregulated miR-182-5p abrogated the effect of GAS5 overexpression on CRC cell proliferation and apoptosis.Furthermore, GAS5 positively regulated the expression of FOXO3a in CRC cells. It has been reported that FOXO3a, a pro-apoptotic transcription factor and direct target of the PI3K-AKT signaling pathway, may be the direct target of miR-182-5p. Binding sites between GAS5 and miR-182-5p were predicted using DIANA tools.	30066886	RID00320	ceRNA or sponge
Pre-eclampsia	uc003fir	CCL5	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	NA	ENSG00000271503	NA	NA	6352	NA	D17S136E|RANTES|SCYA5|SIS-delta|SISd|TCP228|eoCP	LncRNA uc003fir promotes CCL5 expression and negatively affects proliferation and migration of trophoblast cells in preeclampsia.The chemokine CCL5 was directly regulated by lncRNA uc003fir. LncRNA uc003fir regulated CCL5 directly, which may mediate the recruitment of pro-inflammatory cytokines released from monocytes and other leukocytes.	30527126	RID00321	transcriptional regulation
Non-small cell lung cancer	TBILA	GCSAM	positively-E	RIP;RNA pull-down assay	upregulation	sequencing;qRT-PCR	TCGA	LUSC_LUAD.zip	S100A7/JAB1 signaling pathway(+);cancer progression(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000261488	GRCh38_3:112133423-112135359	ENSG00000174500	NA	112806053	257144	NA	NA	The TGFbeta-induced lncRNA TBILA promotes non-small cell lung cancer progression in vitro and in vivo via cis-regulating HGAL and activating S100A7/JAB1 signaling.Upregulated TBILA promotes human germinal center-associated lymphoma (HGAL) expression by binding to the Smad transcription factor complex, thereby enhancing RhoA activation.The TGFbeta-induced lncRNA TBILA promotes non-small cell lung cancer progression in vitro and in vivo via cis-regulating HGAL and activating S100A7/JAB1 signaling.	29908210	RID00322	interact with protein
Colorectal cancer	SNHG1	CDKN2B	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000147883	NA	23642	1030	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00323	epigenetic regulation
Colorectal cancer	SNHG1	KLF2	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000127528	NA	23642	10365	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	LKLF	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00324	epigenetic regulation
Colorectal cancer	SNHG1	CCND2	negatively-E	luciferase reporter assay;western blot	upregulation	sequencing;microarray;qRT-PCR	TCGA;GSE9348;GSE8671	COAD.zip;GSE9348.zip;GSE8671.zip	cell growth(+)	ceRNA(miR-154-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000118971	NA	23642	894	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	KIAK0002|MPPH3	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.SNHG1 acted as a sponge for miR-154-5p, reducing its ability to repress Cyclin D2 (CCND2) expression.SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID00325	ceRNA or sponge
Atherosclerosis	NEAT1	miR-342-3p	negatively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	inflammatory response(+)	transcriptional regulation	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Blockade of NEAT1 represses inflammation response and lipid uptake via modulating miR-342-3p in human macrophages THP-1 cells.miR-342-3p was predicted as a downstream target of NEAT1 and the correlation between them was confirmed in our study. Moreover, overexpression of miR-342-3p could also greatly suppress inflammation response and lipid uptake in THP-1 cells. we observed that NEAT1 was significantly increased in THP-1 cells	30259979	RID00326	transcriptional regulation
Atherosclerosis	GSC-DT	BMI1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell migration(+);PI3K/AKT signaling pathway(+)	ceRNA(miR-134)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_14:94770642-94773607	ENSG00000168283	NA	108868751	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134.DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways.	30158376	RID00327	ceRNA or sponge
Lung cancer	NKX2-1-AS1	CD274	negatively-E	RNAi;RIP;ChIP	downregulation	qRT-PCR	NA	NA	cell migration(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253563	GRCh38_14:36519278-36523016	ENSG00000120217	NA	100506237	29126	NA	B7-H|B7H1|PD-L1|PDCD1L1|PDCD1LG1|PDL1|hPD-L1	NKX2-1-AS1 negatively regulates CD274/PD-L1, cell-cell interaction genes, and limits human lung carcinoma cell migration.Furthermore, NKX2-1-AS1 interferes with NKX2-1 protein binding to the CD274-promoter, likely by NKX2-1 protein-NKX2-1-AS1 interactions.	30258080	RID00328	transcriptional regulation
Cervical cancer	ZEB1-AS1	VIM	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000026025	NA	220930	7431	NA	NA	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00329	expression association
Cervical cancer	ZEB1-AS1	CDH2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000170558	NA	220930	1000	NA	CD325|CDHN|CDw325|NCAD	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00330	expression association
Cervical cancer	ZEB1-AS1	CDH1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000039068	NA	220930	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00331	expression association
Cervical cancer	ZEB1-AS1	MAPK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000100030	NA	220930	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Non-Coding RNA ZEB1-Antisense 1 Affects Cell Migration and Invasion of Cervical Cancer by Regulating Epithelial-Mesenchymal Transition via the p38MAPK Signaling Pathway.Inhibition of ZEB1-AS1 can block the p38MAPK signaling pathway, ultimately restricting the EMT and suppressing cell migration and invasion of cervical cancer cells. Both ZEB1-AS1 siRNA and SB203580 effectively reduced p-p38 expression and the migration and invasion of Hela cells, with elevation of E-cadherin and reduction of Vimentin and N-cadherin.	30253398	RID00332	expression association
Hepatocellular carcinoma	CDKN2B-AS1	miR-191	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Knockdown long non-coding RNA ANRIL inhibits proliferation, migration and invasion of HepG2 cells by down-regulation of miR-191.These data demonstrated that ANRIL knockdown suppressed proliferation, migration, invasion, and promoted apoptosis in HepG2 cells by down-regulating miR-191 and inactivating NF-kB and Wnt/beta-catenin signaling pathways.	30249208	RID00333	expression association
Ovarian cancer	MAP3K20-AS1	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000238133	GRCh38_2:173166446-173282036	ENSG00000137693	NA	339751	10413	NA	COB1|YAP|YAP2|YAP65|YKI	Long noncoding RNA MLK7-AS1 promotes ovarian cancer cells progression by modulating miR-375/YAP1 axis.Taken together, our study showed for the first time that MLK7-AS1 interacted with miR-375 to promote proliferation, metastasis, and EMT process in ovarian cancer cells through upregulating YAP1.	30249278	RID00334	ceRNA or sponge
Non-small cell lung cancer	TWIST1	DUXAP9	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000122691	NA	ENSG00000225210	GRCh38_14:19062316-19131167	7291	503638	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	NA	Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.Mechanical studies showed that INC01296 harbored miR-598, acting as a microRNA sponge. Besides, miR-598 targeted the 3'-UTR of Twist1. Interestingly, transcription factor Twist1 could bind with the promoter of INC01296 and activate its transcriptional level.Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.	30240003	RID00335	transcriptional regulation
Non-small cell lung cancer	DUXAP9	TWIST1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-598)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000122691	NA	503638	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.Mechanical studies showed that INC01296 harbored miR-598, acting as a microRNA sponge. Besides, miR-598 targeted the 3'-UTR of Twist1. Interestingly, transcription factor Twist1 could bind with the promoter of INC01296 and activate its transcriptional level.Positive feedback loop of lncRNA LINC01296/miR-598/Twist1 promotes non-small cell lung cancer tumorigenesis.	30240003	RID00336	ceRNA or sponge
Urinary bladder cancer	DGCR5	CDKN1A	positively-E	RIP;RNA pull-down assay;ChIP	downregulation	qRT-PCR	NA	NA	prognosis;cancer progression(-)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000124762	NA	26220	1026	LINC00037|NCRNA00037	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulation of lncRNA DGCR5 correlates with better prognosis and inhibits bladder cancer progression via transcriptionally facilitating P21 expression.Knockdown of P21 could significantly rescue the suppressed proliferation, migration, and invasion of BCa cells by DGCR5 overexpression. we found that DGCR5 interacted with AT-rich interaction domain 1A (ARID1A), a chromatin remodeling protein, to promote P21 transcription.	30238982	RID00337	epigenetic regulation
Papillary thyroid carcinoma	SNHG15	YAP1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	Hippo signaling pathway(+)	ceRNA(miR-200a-3p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000137693	NA	285958	10413	C7orf40|Linc-Myo1g|MYO1GUT	COB1|YAP|YAP2|YAP65|YKI	LncRNA SNHG15 acts as a ceRNA to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma.The mechanical investigation indicated that SNHG15 upregulated YAP1 by sponging miR-200a-3p. LncRNA SNHG15 acts as a ceRNA to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma.The binding sites between 3¡äUTR of YAP1and miR-200a-3p were predicted (Fig.6c). Similarly,luciferase reporter vectors were constructed to demon-strate the combination between miR-200a-3p and YAP1.	30237435	RID00338	ceRNA or sponge
Non-small cell lung cancer	SNHG8	CCND1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell cycle(+)	ceRNA(miR-542-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000110092	NA	100093630	595	LINC00060|NCRNA00060	BCL1|D11S287E|PRAD1|U21B31	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00339	ceRNA or sponge
Non-small cell lung cancer	SNHG8	CASP3	negatively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000164305	NA	100093630	836	LINC00060|NCRNA00060	CPP32|CPP32B|SCA-1	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00340	expression association
Non-small cell lung cancer	SNHG8	CDK6	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell cycle(+)	ceRNA(miR-542-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269893	GRCh38_4:118278709-118285316	ENSG00000105810	NA	100093630	1021	LINC00060|NCRNA00060	MCPH12|PLSTIRE	SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6.SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.	30275712	RID00341	ceRNA or sponge
Cardiac hypertrophy	CASC15	TLR4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cardiac hypertrophy(+)	ceRNA(miR-432-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000136869	NA	401237	7099	CANT|LINC00340|lnc-SOX4-1	ARMD10|CD284|TLR-4|TOLL	Upregulation of lncRNA VDR/CASC15 induced by facilitates cardiac hypertrophy through modulating miR-432-5p/TLR4 axis.CASC15 can upregulate TLR4 by competitively binding miR-432-5p. CASC15 was highly expressed in cardiac hypertrophic model. Results of immunofluorence staining revealed that cell surface area enlarged by Ang-II was decreased when CASC15 was silenced.	29966657	RID00342	ceRNA or sponge
Colorectal cancer	WSPAR	TCF7	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000081059	NA	105664404	6932	LncTCF7|TCONS_00009511	TCF-1	Down-regulation of lncTCF7 inhibits cell migration and invasion in colorectal cancer via inhibiting TCF7 expression. RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays showed that LncTCF7 recruits BAF170 to activate the TCF7 promoter and regulate TCF7 expression.	30225781	RID00343	transcriptional regulation
Pre-eclampsia	DLX6-AS1	GADD45A	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-376c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000116717	NA	285987	1647	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	DDIT1|GADD45	Long non-coding RNA DLX6-AS1 is upregulated in preeclampsia and modulates migration and invasion of trophoblasts through the miR-376c/GADD45A axis.DLX6-AS1 interacted with miR-376c, and that overexpression of DLX6-AS1 significantly reduced expression of miR-376c in HTR-8/SVneo cells. Also, miR-376c targeted and downregulated GADD45A in HTR-8/SVneo cells. Overexpression of GADD45A effectively attenuated a miR-376c-induced increase in the proliferation, migration and invasion of HTR-8/SVneo cells. lncRNA DLX6-AS1 was confirmed to be significantly upregulated in the placentas of patients with preeclampsia, compared with normal controls.	30055134	RID00344	ceRNA or sponge
Colon cancer	LINC-ROR	miR-145	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Non-Coding RNA lincRNA-ROR Promotes the Progression of Colon Cancer and Holds Prognostic Value by Associating with miR-145.Knockdown of lincRNA-ROR restored the expression of miR-145, and had a significant influence on colon cancer cell proliferation, migration and invasion.	27071407	RID00345	expression association
Lung cancer	CCAT1	miR-218	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Epigenetic silencing of miR-218 by the lncRNA CCAT1, acting via BMI1, promotes an altered cell cycle transition in the malignant transformation of HBE cells induced by cigarette smoke extract.Depletion of CCAT1 attenuated the CSE-induced decreases of miR-218 levels, suggesting that miR-218 is negatively regulated by CCAT1 in HBE cells exposed to CSE.This epigenetic silencing of miR-218 by CCAT1 induces an altered cell cycle transition through BMI1 and provides a new mechanism for CSE-induced lung carcinogenesis.	27212446	RID00346	epigenetic regulation
Neuroblastoma	LncND	miR-143-3p	negatively-F	Ago2-IP;luciferase reporter assay	downregulation	RT-qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Neuroblastoma	lncRNA	miRNA	NA	GRCh38_2:663814-666523	NA	NA	NA	NA	NA	NA	A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.Binding and release of miR-143-3p by LncND control the expression of Notch receptors.	27263970	RID00347	ceRNA or sponge
Immune thrombocytopenia	MEG3	miR-125a-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	immune response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Immune Detection	Immune system disease	Thrombocytopenia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 inhibits microRNA-125a-5p expression and induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura.MEG3 interacted with miR-125a-5p and inhibited its expression, and MEG3/miR-125a-5p contributed to induce immune imbalance of Treg/Th17 in ITP.	27522004	RID00348	ceRNA or sponge
Osteoarthritis	linc-UFC1	miR-34a	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	NA	GRCh38_1:161152776-161158856	NA	NA	NA	NA	NA	NA	Long Noncoding RNA UFC1 Promotes proliferation of Chondrocyte in Osteoarthritis by Acting as a Sponge for miR-34a.	27529373	RID00349	ceRNA or sponge
Liver fibrosis	TP53COR1	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	fibrotic(-)	ceRNA(miR-181b)	association	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000171862	NA	102800311	5728	TRP53COR1|linc-p21|lincRNA-p21	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Identification of a Novel lincRNA-p21-miR-181b-PTEN Signaling Cascade in Liver Fibrosis.We demonstrated that lincRNA-p21 enhanced PTEN expression by competitively binding miR-181b.	27610008	RID00350	ceRNA or sponge
Cardiac hypertrophy	MIAT	miR-150	negatively-F	RNAi;bioinformatics	upregulation	qPCR	NA	NA	cell growth(+);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Cardiac hypertrophy	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression. MIAT inhibition also partly restored the miR-150 levels under Ang II treatment. MIAT can suppress miR-150 expression in cardiomyocytes and miR-150 is a downstream effector of MIAT in the development of cardiac hypertrophy.	27649667	RID00351	ceRNA or sponge
Leukemia	HOTAIRM1	miR-20a	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00352	ceRNA or sponge
Leukemia	HOTAIRM1	miR-125b	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00353	ceRNA or sponge
Leukemia	HOTAIRM1	miR-106b	negatively-F	ChIP;western blot;luciferase reporter assay;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000233429	GRCh38_7:27095647-27100265	NA	NA	100506311	NA	HOXA-AS1|HOXA1-AS1|NCRNA00179	NA	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2.	27740626	RID00354	ceRNA or sponge
Pancreatic carcinoma	LINC-ROR	miR-124	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	gemcitabine	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Linc-ROR confers gemcitabine resistance to pancreatic cancer cells via inducing autophagy and modulating the miR-124/PTBP1/PKM2 axis.Linc-ROR siRNA significantly sensitized PANC-1 and MIAPaCa-2 cells to gemcitabine, while linc-ROR overexpression significantly reduced the sensitivity. In both pancreatic cell lines and PADC tissues, linc-ROR is negatively correlated with miR-124 expression. In addition, dual luciferase assay verified two 8mer binding sites between miR-124 and linc-ROR.	27785603	RID00355	ceRNA or sponge
Pancreatic carcinoma	LINC-ROR	PKM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	NA	association	NA	gemcitabine	NA	Sustained Angiogenesis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000067225	NA	100885779	5315	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	Linc-ROR confers gemcitabine resistance to pancreatic cancer cells via inducing autophagy and modulating the miR-124/PTBP1/PKM2 axis.Linc-ROR siRNA showed similar effect as 3-MA on enhancing gemcitabine-induced cell apoptosis and also reduced PKM2 expression. In addition, miR-124 mimics also alleviated autophagy in pancreatic cancer cells. Both miR-124 mimics and PKM2 siRNA enhanced gemcitabine-induced cell apoptosis.	27785603	RID00356	expression association
Osteosarcoma	PVT1	BCL2	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00357	ceRNA or sponge
Osteosarcoma	PVT1	CCND1	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000110092	NA	5820	595	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00358	ceRNA or sponge
Osteosarcoma	PVT1	FASN	positively-E	RNAi;ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-);cancer progression(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000169710	NA	5820	2194	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FAS|OA-519|SDR27X1	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.To study the role of miR-195 in the mechanisms and functions of PVT1, we analyzed direct targets of miR-195 using oncomiRDB and found that BCL2, CCND1, and FASN may be related to miR-195. Silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1-induced apoptosis of U2OS cells.we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells.	27813492	RID00359	ceRNA or sponge
Kidney disease	MALAT1	ELAVL1	negatively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-23c)	regulation	NA	NA	NA	Evading Apoptosis	Urinary system disease	Kidney disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy. luciferase assays showed that miR-23c, as a target of MALAT1, directly repressed ELAVL1 expression and then decreased the expression of its downstream protein NLRP3. The expression of MALAT1 antagonized the effect of miR-23c on the downregulation of its target ELAVL1 and inhibited hyperglycemia-induced cell pyroptosis.	27964927	RID00360	ceRNA or sponge
Breast cancer	TUG1	miR-9	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA Taurine-Upregulated Gene 1 Promotes Cell proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells.The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. Using the starBase v2.0 database, miR-9 was found to potentially bind to TUG1.To verify the relationship between TUG1 and miR-9, a dual luciferase reporter assay was performed by constructing a reporter containing the binding site in TUG1-WT or the mutant. The luciferase activity of the reporter containing TUG1-WT was reduced in cells transfected with the miR-9 mimic.	28053623	RID00361	ceRNA or sponge
Liver fibrosis	HOTAIR	PTEN	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	fibrotic(+)	DNA methylation;ceRNA(miR-29b)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis.HOTAIR was confirmed a target of miR-29b and lack of the miR-29b binding site in HOTAIR prevented the suppression of miR-29b, suggesting HOTAIR contributes to PTEN expression downregulation via sponging miR-29b. Collectively, we demonstrate that HOTAIR downregulates miR-29b expression and attenuates its control on epigenetic regulation, leading to enhanced PTEN methylation, which contributes to the progression of liver fibrosis.	28129115	RID00362	epigenetic regulation;ceRNA or sponge
Diabetic retinopathy	MIAT	miR-29b	negatively-F	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Nervous system disease	Diabetic retinopathy	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	Long non-coding RNA MIAT acts as a biomarker in diabetic retinopathy by absorbing miR-29b and regulating cell apoptosis.miR-29b controled MIAT to regulate its expression and MIAT overexpression suppressed miR-29b.luciferase activity assay was used to detect the target-specific selectivity between miR-29b and MIAT.	28246353	RID00363	ceRNA or sponge
Myocardial infarction	ZFAS1	CRP	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000132693	NA	441951	1401	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	PTX1	Knockdown of Long Non-Coding RNA-ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti-Apoptosis by Regulating miR-150/CRP.The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150.C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150.The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP.	28295592	RID00364	ceRNA or sponge
Lung adenocarcinoma	LINC-ROR	FSCN1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-145)	regulation	NA	docetaxel	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000075618	NA	100885779	6624	ROR|lincRNA-RoR|lincRNA-ST8SIA3	FAN1|HSN|SNL|p55	Long noncoding RNA ROR regulates chemoresistance in docetaxel-resistant lung adenocarcinoma cells via epithelial mesenchymal transition pathway.The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145.The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145, therefore, releasing the miR-145 target FSCN1, and thus contributing to the acquisition of chemoresistance and EMT phenotypes of docetaxel-resistant LAD cells.	28388536	RID00365	ceRNA or sponge
Cardiac fibrosis	GAS5	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell growth(-);fibrotic(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cardiovascular system disease	Fibrosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA GAS5 controls cardiac fibroblast activation and fibrosis by targeting miR-21 via PTEN/MMP-2 signaling pathway. In this study, we confirmed that GAS5 was lowly expressed in cardiac fibrosis tissues as well as activated cardiac fibroblast. We found that up-regulated GAS5 decreased the expression of miR-21 significantly. GAS5 has a complementary region with miR-21, and it can repress the expression of miR-21 in RISC complex. Furthermore, GAS5 that upregulated or downregulated the expression of PTEN through miR-21 in cardiac fibroblasts.	28526319;23933812	RID00366	ceRNA or sponge
Pancreatic ductal adenocarcinoma	LINC-ROR	let-7family	negatively-F	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.We observed that linc-ROR expression was increased in CSLCs. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.We conclude that, as a crucial oncogene, linc-ROR promotes cell proliferation, invasiveness and contributes to stem cell properties of CSLCs in PDAC via acting as a ceRNA to regulate function of microRNAs.	28580169	RID00367	ceRNA or sponge
Colon cancer	PART1	DNMT3A	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	DNA methylation;ceRNA(miR-143)	regulation	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000119772	NA	25859	1788	NCRNA00206	DNMT3A2|M.HsaIIIA|TBRS	PART-1 functions as a competitive endogenous RNA for promoting tumor progression by sponging miR-143 in colorectal cancer.PART-1 functioned as a ceRNA of DNMT3A,by sponging miR-143. Finally, PART-1 induced tumor progression by regulating DNMT3A.	28619512	RID00368	epigenetic regulation;ceRNA or sponge
Lung injury	FOXD3-AS1	miR-150	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Respiratory system disease	Injury	lncRNA	miRNA	ENSG00000230798	GRCh38_1:63320884-63324441	NA	NA	100996301	NA	pasFOXD3	NA	Long noncoding RNA FOXD3-AS1 regulates oxidative stress-induced apoptosis via sponging microRNA-150.	28655711	RID00369	ceRNA or sponge
Osteosarcoma	cir-GLI2	miR-125b-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	circRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	Circular RNA GLI2 promotes osteosarcoma cell proliferation, migration, and invasion by targeting miR-125b-5p. functional experiments validated that cir-GLI2 exerted the tumor-promoting effects on osteosarcoma cells via negatively targeting miR-125b-5p	28695772	RID00370	ceRNA or sponge
Breast cancer	PTENP1	PTEN	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell growth(-);tumorigenesis(-)	ceRNA(miR-19b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	PTENP1 acts as a ceRNA to regulate PTEN by sponging miR-19b and explores the biological role of PTENP1 in breast cancer.Moreover, PTENP1 could upregulate PTEN via its ceRNA interaction on miR-19b, as well as induced the upregulation of p53 and downregulation of p-AKT. Enhanced PTENP1 could inhibit BC cell growth, metastasis and tumourigenicity by inhibiting miR-19b and facilitating PTEN in BC, thereby may represent a novel target for diagnosis and treatment of BC.	28731027	RID00371	ceRNA or sponge
Epithelial ovarian carcinoma	PCA3	miR-106b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000225937	GRCh38_9:76691980-76863307	NA	NA	50652	NA	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	NA	Research results show that lncRNA PCA3 may coordinate EOC tumorigenesis through disrupting miR-106b regulated gene expression.Bioinformatic predictions and dual-luciferase reporter assays indicate that the 3'UTR of PCA3 has potential binding sites for miR-106b-5p	28864116	RID00372	ceRNA or sponge
Non-small cell lung cancer	SNHG12	miR-138	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long Noncoding RNA Small Nucleolar RNA Host Gene 12 Inhibits Cell Growth and Induces Apoptosis by Upregulating miR-138 in Nonsmall Cell Lung Cancer.	28872894	RID00373	ceRNA or sponge
Triple-receptor negative breast cancer	circGFRA1	GFRA1	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	ceRNA(miR-34a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	circRNA	PCG	NA	NA	ENSG00000151892	NA	NA	2674	NA	GDNFR|GDNFRA|GFR-ALPHA-1|RET1L|RETL1|TRNR1	circGFRA1 and GFRA1 act as ceRNAs in triple negative breast cancer by regulating miR-34a.Knockdown of circGFRA1 inhibited proliferation and promoted apoptosis in TNBC. we conclude that circGFRA1 may function as a competing endogenous RNA (ceRNA) to regulate GFRA1 expression through sponging miR-34a to exert regulatory functions in TNBC.	29037220	RID00374	ceRNA or sponge
Pulmonary fibrosis	LNCRNA-ATB	ZEB1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Respiratory system disease	Fibrosis	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000148516	NA	114004396	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA-ATB promotes EMT during silica-induced pulmonary fibrosis by competitively binding miR-200c.Collectively, silica-stimulated macrophages secreted TGF-beta1 to induce lncRNA-ATB in epithelia cells, promoting EMT by binding with miR-200c and releasing ZEB1.	29113749	RID00375	ceRNA or sponge
Ischemic stroke	MEG3	PDCD4	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell death(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150593	NA	55384	27250	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	H731	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate ischemic neuronal death by targeting miR-21/PDCD4 signaling pathway.MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with programmed cell death 4 (PDCD4) mRNA for directly binding to miR-21, which mediates ischemic neuronal death	29238035	RID00376	ceRNA or sponge
Kidney disease	LINC01619	FOXO1	positively-E	luciferase reporter assay;RIP;western blot	downregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-27a)	binding/interaction	RNA-RNA	NA	NA	NA	Urinary system disease	Kidney disease	lncRNA	TF	ENSG00000257242	GRCh38_12:91984976-92142914	ENSG00000150907	NA	256021	2308	C12orf79	FKH1|FKHR|FOXO1A	Long Noncoding RNA LINC01619 Regulates MicroRNA-27a/Forkhead Box Protein O1 and Endoplasmic Reticulum Stress-Mediated Podocyte Injury in Diabetic Nephropathy.LINC01619 exerted biological function by serving as a sponge for miR-27a, which negatively targeted forkhead box protein O1 (FOXO1) and activated ER stress	29334763	RID00377	ceRNA or sponge
Glioblastoma	TUSC7	miR-10a	negatively-F	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Long non-coding RNA TUSC7 inhibits temozolomide resistance by targeting miR-10a in glioblastoma.TUSC7 acted by directly targeting and silencing expression of miR-10a gene, and miR-10a mediated TUSC7-induced inhibition on TMZ resistance in U87TR cells.	29397407	RID00378	ceRNA or sponge
Brain injury	GAS5	miR-23a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell injury(+);hippocampal neuron function(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Other	Injury	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury. Mechanistically, GAS5 regulated hippocampal neuron function by sponging miR-23a.	29428721	RID00379	ceRNA or sponge
Glioblastoma	MALAT1	miR-101	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA-101 in glioblastoma. Importantly, we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR-101 signaling pathway via directly binding it in GBM cells.	29479863	RID00380	ceRNA or sponge
Hepatocellular carcinoma	LINC-ROR	RAD18	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	radioresistance(+);DNA repair(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Genome Instability and Mutation	Cancer	Liver cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000070950	NA	100885779	56852	ROR|lincRNA-RoR|lincRNA-ST8SIA3	RNF73	Long non-coding RNA ROR promotes radioresistance in hepatocelluar carcinoma cells by acting as a ceRNA for microRNA-145 to regulate RAD18 expression.Further mechanistic investigations revealed that lincRNA-ROR exerted its biological effects by acting as a competing endogenous RNA (ceRNA) for miR-145 to regulate RAD18 expression, thereby promoting DNA repair	29559320	RID00381	ceRNA or sponge
Hepatocellular carcinoma	FLVCR1-DT	MET	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-513c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000198468	GRCh38_1:212852105-212858126	ENSG00000105976	NA	642946	4233	NA	AUTS9|DFNB97|HGFR|RCCP2|c-Met	LncRNA FLVCR1-AS1 acts as miR-513c sponge to modulate cancer cell proliferation, migration, and invasion in hepatocellular carcinoma.In mechanism, FLVCR1-AS1 acted as a competitive endogenous RNAs to sponge miR-513c which targeted the mRNA of MET for degradation. By directly sponging miR-513c, FLVCR1-AS1 increased MET expression in HCC, and then promoted HCC progression.	29574975	RID00382	ceRNA or sponge
Osteosarcoma	NEAT1	BCL2	positively-E	RNAi;starBase	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34c)	regulation	NA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000171791	NA	283131	596	LINC00084|NCRNA00084|TncRNA|VINC	Bcl-2|PPP1R50	Knockdown of the oncogene lncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma.overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c The results in vivo also confirmed that knockdown of NEAT1 sensitized the OS cells to DPP-induced tumor regression, delayed the tumor growth with reduced levels of Ki-67, BCL-2, and cyclin D1 signals, suggesting that NEAT1 is an oncogene and chemotherapy resistant factor in OS.	29654165	RID00383	ceRNA or sponge
Osteosarcoma	NEAT1	CCND1	positively-E	RNAi;starBase	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34c)	regulation	NA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000110092	NA	283131	595	LINC00084|NCRNA00084|TncRNA|VINC	BCL1|D11S287E|PRAD1|U21B31	Knockdown of the oncogene lncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma.overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c The results in vivo also confirmed that knockdown of NEAT1 sensitized the OS cells to DPP-induced tumor regression, delayed the tumor growth with reduced levels of Ki-67, BCL-2, and cyclin D1 signals, suggesting that NEAT1 is an oncogene and chemotherapy resistant factor in OS.	29654165	RID00384	ceRNA or sponge
Acute myeloid leukemia	UCA1	HK2	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glucose metabolic process(+)	ceRNA(miR-125a)	regulation	NA	adriamycin	NA	Reprogramming Energy Metabolism	Cancer	Leukemia	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000159399	NA	652995	3099	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HKII|HXK2	Knockdown of LncRNA-UCA1 suppresses chemoresistance of pediatric AML by inhibiting glycolysis through the microRNA-125a/hexokinase 2 pathway.Additionally, UCA1 functioned as a ceRNA of miR-125a by directly binding to miR-125a. HK2, a target of miR-125a, was positively regulated by UCA1 in HL60 and HL60/ADR cells	29663500	RID00385	ceRNA or sponge
Kidney injury	NEAT1	miR-204	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis	Other	Injury	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 plays an important role in sepsis-induced acute kidney injury by targeting miR-204 and modulating the NF-kB pathway.	29669307	RID00386	ceRNA or sponge
Invasive bladder transitional cell carcinoma	MALAT1	FOXQ1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164379	NA	378938	94234	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HFH1	LncRNA MALAT1 promotes tumor growth and metastasis by targeting miR-124/foxq1 in bladder transitional cell carcinoma (BTCC).MALAT1 may function as a ceRNA to sponge miR-124, thus modulating the derepression of foxq1, miR-124 target gene, in post-transcriptional levels	29736319	RID00387	ceRNA or sponge
Gastric cancer	LINC00483	SPAG9	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);MAPK signaling pathway(+)	ceRNA(miR-30a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000167117	GRCh38_17:50761029-50767557	ENSG00000008294	NA	NA	9043	NA	CT89|HLC-6|HLC4|HLC6|JIP-4|JIP4|JLP|PHET|PIG6	Linc00483 as ceRNA regulates proliferation and apoptosis through activating MAPKs in gastric cancer. Linc00483 regulates SPAG9 by acting as a ceRNA and interacting with miR-30a-3p	29761936	RID00388	ceRNA or sponge
Temporal lobe epilepsy	H19	let-7b	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Nervous system disease	Epilepsy	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 contributes to apoptosis of hippocampal neurons by inhibiting let-7b in a rat model of temporal lobe epilepsy.Finally, we show that H19 might function as a competing endogenous RNA to sponge microRNA let-7b in the regulation of cellular apoptosis	29795132	RID00389	ceRNA or sponge
Esophagus squamous cell carcinoma	DUXAP10	CDKN1A	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000244306	GRCh38_14:19268853-19337730	ENSG00000124762	NA	503639	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA DUXAP10 modulates cell proliferation in esophageal squamous cell carcinoma through epigenetically silencing p21. Results of mechanism experiments suggested that DUXAP10 motivated ESCC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21.	30215547	RID00390	epigenetic regulation
Ovarian cancer	LINC01139	TGFB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000105329	NA	339535	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LINK-A lncRNA promotes migration and invasion of ovarian carcinoma cells by activating TGF-beta pathway.LINK-A overexpression led to up-regulated TGF-beta1 in ovarian carcinoma cells and promoted cell migration and invasion.	30061183	RID00391	expression association
Ovarian cancer	snaR	GAB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_19:47918429-47918550	ENSG00000033327	NA	NA	9846	NA	NA	LncRNA snaR upregulates GRB2-associated binding protein 2 and promotes proliferation of ovarian carcinoma cells.	30093110	RID00392	expression association
Osteosarcoma	SNHG20	RUNX2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);apoptosis process(-)	ceRNA(miR-139)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124813	NA	654434	860	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	LncRNA SNHG20 knockdown suppresses the osteosarcoma tumorigenesis through the mitochondrial apoptosis pathway by miR-139/RUNX2 axis.Bioinformatics analysis revealed that miR-139 both targeted with the 3'-UTR of runt-related transcription factor 2 (RUNX2) and SNHG20, which was verified by luciferase reporter assay and RNA immunoprecipitation (RIP).	30072099	RID00393	ceRNA or sponge
Hepatocellular carcinoma	WDFY3-AS2	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180769	GRCh38_4:84965534-85011277	ENSG00000170558	NA	NA	1000	NA	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00394	expression association
Hepatocellular carcinoma	MIAT	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000170558	NA	440823	1000	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00395	expression association
Hepatocellular carcinoma	MEG3	CDH2	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000170558	NA	55384	1000	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CD325|CDHN|CDw325|NCAD	EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database.loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion	30037433	RID00396	expression association
Glioblastoma	LINC01446	TPT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-489-3p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000205628	GRCh38_7:53655508-53811952	ENSG00000133112	NA	401337	7178	GS1-179L18.1	HRF|TCTP|p02|p23	LncRNA LINC01446 promotes glioblastoma progression by modulating miR-489-3p/TPT1 axis.Mechanistically, bioinformatics analysis showed that LINC01446 acted as a sponge for miR-489-3p which targeted TPT1	30029885	RID00397	ceRNA or sponge
Lung cancer	Lnc-EPIC1	MYC	interact	RIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000224271	GRCh38_22:47630827-48023004	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA EPIC1 promotes human lung cancer cell growth. Together, our results show that Lnc-EPIC1 promotes human lung cancer cell growth possibly by targeting MYC. Long non-coding RNA (LncRNA) EPIC1 (Lnc-EPIC1) is a MYC-interacting LncRNA. Lnc-EPIC1 directly associated with MYC protein in the nuclei of A549 cells.	30029875	RID00398	interact with protein
Hepatocellular carcinoma	RAD51-AS1	RAD51	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	chemosensitivity(+);radiosensitivity(+);DNA repair(-)	interact with mRNA	binding/interaction	RNA-RNA	melatonin;corylin;chemotherapeutic agent etoposide (VP16)	NA	Genome Instability and Mutation	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245849	GRCh38_15:40686183-40695107	ENSG00000051180	NA	100505648	5888	TODRA	BRCC5|FANCR|HRAD51|HsRad51|HsT16930|MRMV2|RAD51A|RECA	Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair.Whole-transcriptome and gain- and loss-of-function analyses revealed that melatonin induces expression of the long noncoding RNA RAD51-AS1, which binds to RAD51 mRNA to inhibit its translation, effectively decreasing the DNA repair capacity of HCC cells and increasing their sensitivity to chemotherapy and radiotherapy.Animal models further demonstrated that a combination of melatonin and the chemotherapeutic agent etoposide (VP16) can significantly enhance tumor growth inhibition compared with monotherapy. Our results show that melatonin is a potential adjuvant treatment for chemotherapy and radiotherapy in HCC.RAD51-AS1, which bound to RAD51 mRNA, thereby inhibiting RAD51 protein expression, thus inhibiting the DNA damage repair ability of HCC cells.	30201872;29749376	RID00399	interact with mRNA
Colorectal cancer	SLCO4A1-AS1	CTNNB1	positively-F	RNA pull-down assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell growth(+);cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000232803	GRCh38_20:62663019-62666724	ENSG00000168036	NA	100127888	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA SLCO4A1-AS1 facilitates growth and metastasis of colorectal cancer through beta-catenin-dependent Wnt pathway.SLCO4A1-AS1 interacts with beta-catenin. Mechanistically, SLCO4A1-AS1 activates Wnt/beta-catenin signaling. SLCO4A1-AS1 enhanced the stability of beta-catenin by impairing the interaction of beta-catenin with GSKbeta and inhibiting its phosphorylation.	30201010	RID00400	interact with protein
Lung cancer	SMAD4	LINP1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000223784	GRCh38_10:6709530-6740532	7040	108570035	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	TGF-beta/SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer.Here, we demonstrated that the transcription of lncRNA in nonhomologous end joining (NHEJ) pathway 1 (LINP1) was inhibited by TGF-beta1 in a SMAD4-dependent manner	30416386	RID00401	transcriptional regulation
Gastric cancer	lncR-D63785	MEF2D	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-422a)	regulation	NA	doxorubicin	NA	NA	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_17:34610748-34611354	ENSG00000116604	NA	NA	4209	NA	NA	The Long Noncoding RNA D63785 Regulates Chemotherapy Sensitivity in Human Gastric Cancer by Targeting miR-422a.This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.These results indicate that lnRNA-D63785 could be related to doxorubicin (DOX) resistance in human gastric cancer.	30195778	RID00402	ceRNA or sponge
Pre-eclampsia	HOXA11-AS	RND3	negatively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000115963	NA	221883	390	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ARHE|Rho8|RhoE|memB	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID00403	epigenetic regulation
Pre-eclampsia	HOXA11-AS	HOXA7	positively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000122592	NA	221883	3204	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ANTP|HOX1|HOX1.1|HOX1A	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.In the cytoplasm, HOXA11-AS modulates HOXA7 expression by sponged miR-15b-5p,affecting trophoblast cell proliferation.	30195759	RID00404	ceRNA or sponge
Atherosclerosis	HOTAIR	miR-330-5p	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Silence of long intergenic noncoding RNA HOTAIR ameliorates oxidative stress and inflammation response in ox-LDL-treated human macrophages by upregulating miR-330-5p.By carrying out bioinformatics analysis, miR-330-5p was predicted as a target of HOTAIR and the correlation between them was validated in our current study	30187491	RID00405	ceRNA or sponge
Atherosclerosis	XIST	NOD2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-320)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000167207	NA	7503	64127	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ACUG|BLAU|BLAUS|CARD15|CD|CLR16.3|IBD1|NLRC2|NOD2B|PSORAS1|YAOS	Further experiments identified XIST regulated the expression of Nucleotide-Binding Oligomerization Domain 2 (NOD2) by sponging miR-320.	29902461	RID00406	ceRNA or sponge
Urinary bladder cancer	LINC01605	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000253161	GRCh38_8:37421341-37554183	ENSG00000100985	NA	100507420	4318	LincDUSP	CLG4B|GELB|MANDP2|MMP-9	High LINC01605 expression predicts poor prognosis and promotes tumor progression via up-regulation of MMP9 in bladder cancer. our results shed light on that LINC01605, as a new prognostic biomarker, could promote the proliferation, migration, and invasion of BC cells via activating EMT signaling pathway and up-regulating MMP9 expression	30054424	RID00407	expression association
Colorectal cancer	NEAT1	DDX5	interact	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000108654	NA	283131	1655	LINC00084|NCRNA00084|TncRNA|VINC	G17P1|HLR1|HUMP68|p68	The lncRNA NEAT1 activates Wnt/beta-catenin signaling and promotes colorectal cancer progression via interacting with DDX5. Mechanistically, we found that NEAT1 directly bound to the DDX5 protein, regulated its stability, and sequentially activated Wnt signaling.	30185232	RID00408	interact with protein
Hepatocellular carcinoma	MIR31HG	ST7L	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	ceRNA(miR-575)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000007341	NA	554202	54879	LncHIFCAR|hsa-lnc-31	FAM4B|ST7R|STLR	Long noncoding RNA MIR31HG inhibits hepatocellular carcinoma proliferation and metastasis by sponging microRNA-575 to modulate ST7L expression.	30176933	RID00409	ceRNA or sponge
Laryngeal squamous cell carcinoma	SNHG1	YAP1	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-375)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000137693	NA	23642	10413	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	COB1|YAP|YAP2|YAP65|YKI	A positive feedback regulation between long noncoding RNA SNHG1 and YAP1 modulates growth and metastasis in laryngeal squamous cell carcinoma.Mechanistically, SNHG1 promotes YAP1 expression and Hippo signaling activity by competitively sponging miR-375	30323965	RID00410	ceRNA or sponge
Thyroid carcinoma	MEG3	miR-182	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	131I	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 enhances 131I sensitivity in thyroid carcinoma via sponging miR-182	30021359	RID00411	ceRNA or sponge
Renal cell carcinoma	HOTTIP	LATS2	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000150457	NA	100316868	26524	HOXA-AS6|HOXA13-AS1|NCRNA00213	KPM	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID00412	epigenetic regulation
Meningioma	LINC00460	MMP9	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-539)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Meningioma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000100985	NA	728192	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA LINC00460 targets miR-539/MMP-9 to promote meningioma progression and metastasis.Bioinformatics tools predicted that miR-539 both targeted with the 3'-UTR of LINC00460 and MMP-9 mRNA,which was confirmed by luciferase reporter assay and western blot analysis. In summary, our study reveals that LINC00460 promotes MMP-9 expression through targeting miR-539	29906745	RID00413	ceRNA or sponge
Malignant glioma	HOXB13-AS1	HOXB13	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000229637	GRCh38_17:48720802-48724758	ENSG00000159184	NA	NA	10481	NA	HPC9|PSGD	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma. Mechanistically, we showed that HOXB13-AS1 overexpression increased DNMT3B-mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP),epigenetically suppressing HOXB13 expression.	30105866	RID00414	epigenetic regulation
Alzheimer's disease	RP11-543N12.1	miR-324-3p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	miRNA	ENSG00000261410	GRCh38_16:83383016-83398170	NA	NA	NA	NA	NA	NA	Regulatory effects of the long non-coding RNA RP11-543N12.1 and microRNA-324-3p axis on the neuronal apoptosis induced by the inflammatory reactions of microglia. RP11-543N12.1 targeted miR-324-3p to suppress proliferation and promote apoptosis in the AD cell model.The interaction between RP11-543N12.1 and miR-324-3p was confirmed with a dual-luciferase reporter gene assay	29956723	RID00415	ceRNA or sponge
Myocardial infarction	CRRL	HOPX	positively-E	luciferase reporter assay;RT-qPCR	upregulation	qPCR;sequencing	ERR315356;ERR315430;SRR643778;SRR643779	ERR315356;ERR315430;SRR643778;SRR643779	cardiomyocyte regeneration(-);cardiac repair(-)	ceRNA(miR-199a-3p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000050165	GRCh38_11:11965873-11979916	ENSG00000171476	NA	NA	84525	NA	NA	Loss of long non-coding RNA CRRL promotes cardiomyocyte regeneration and improves cardiac repair by functioning as a competing endogenous RNA.Furthermore, we demonstrated that CRRL acts as a competing endogenous RNA (ceRNA) by directly binding to miR-199a-3p and thereby increasing the expression of Hopx,a target gene of miR-199a-3p and a critical negative regulatory factor of CM proliferation	30125571	RID00416	ceRNA or sponge
Multiple myeloma	MALAT1	NFE2L1	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000082641	NA	378938	4779	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.	29487387	RID00417	expression association
Multiple myeloma	MALAT1	KEAP1	positively-E	RIP;ChIP;IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116044	NA	378938	9817	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.	29487387	RID00418	epigenetic regulation
Gastric cancer	SNHG6	CDKN1A	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells.Knockdown of SNHG6 stimulated p21 expression and the tumor-suppressive effect of SNHG6 in GC cells was dependent on p21.Our findings show that SNHG6 knockdown inhibits GC development by upregulating p21; this effect is dependent on the activation of the JNK pathway and suppression of EZH2 expression.	30031062	RID00419	epigenetic regulation
Ischemic stroke	TUG1	AURKA	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000087586	NA	55000	6790	LINC00080|NCRNA00080|TI-227H	AIK|ARK1|AURA|BTAK|PPP1R47|STK15|STK6|STK7	LncRNA TUG1 promotes cells proliferation and inhibits cells apoptosis through regulating AURKA in epithelial ovarian cancer cells.	30200102	RID00420	expression association
Papillary thyroid carcinoma	UCA1	BRD4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000141867	NA	652995	23476	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP|HUNK1|HUNKI|MCAP	Furthermore, UCA1 competed with BRD4 for miR-204 binding. miR-204 knockdown enhanced BRD4 expression	30015945	RID00421	ceRNA or sponge
Anaplastic thyroid carcinoma	UCA1	MYC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-135a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000136997	NA	652995	4609	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA UCA1 promotes anaplastic thyroid cancer cell proliferation via miR-135a-mediated c-myc activation.In addition, using luciferase assays, it was confirmed that miR-135a directly bound to UCA1 and the 3' untranslated region of c-myc, and UCA1 competed with c-myc for miR-135a binding. miR-135a inhibition may upregulate c-myc expression	30015867	RID00422	ceRNA or sponge
Parkinson's disease	SNHG1	SIAH1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cytotoxicity(+)	ceRNA(miR-15b-5p)	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000196470	NA	23642	6477	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	SIAH1A	LncRNA SNHG1 promotes alpha-synuclein aggregation and toxicity by targeting miR-15b-5p to activate SIAH1 in human neuroblastoma SH-SY5Y cells	29217406	RID00423	ceRNA or sponge
Esophagus squamous cell carcinoma	lncRNA-ECM	ICAM1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENST00000589379	GRCh38_19:10285801-10289019	ENSG00000090339	NA	NA	3383	NA	BB2|CD54|P3.58	LncRNA-ECM is overexpressed in esophageal squamous cell carcinoma and promotes tumor metastasis.The expression level of ICAMI was directly correlated with the expression of lncRNA-ECM, suggesting that ICAM1 may be the downstream target gene of lncRNA-ECM.	30128011	RID00424	expression association
Malignant glioma	UCA1	ZEB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000148516	NA	652995	6935	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA UCA1 sponges miR-204-5p to promote migration, invasion and epithelial-mesenchymal transition of glioma cells via upregulation of ZEB1.	30107990	RID00425	ceRNA or sponge
Hepatocellular carcinoma	XIST	miR-155-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p	30091314	RID00426	ceRNA or sponge
Hepatocellular carcinoma	JPX	XIST	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);tumorigenesis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	lncRNA	ENSG00000225470	GRCh38_X:73944182-74070408	ENSG00000229807	GRCh38_X:73820649-73852723	554203	7503	DCBALD06|ENOX|LINC00183|NCRNA00183	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p. JPX knock-in significantly increased XIST expression and inhibited HepG2 cell growth in vitro or tumor formation in vivo in a XIST dependent manner.	30091314	RID00427	expression association
Hepatocellular carcinoma	SNHG5	GSK3B	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-26a-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000082701	NA	387066	2932	C6orf160|LINC00044|NCRNA00044|U50HG	NA	Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-26a-5p/GSK3beta signal pathway.Taken together, SNHG5 promotes HCC progression by competitively binding miR-26a-5p and regulating GSK3beta and Wnt/beta-catenin signal pathway.	30166525	RID00428	ceRNA or sponge
Breast cancer	AGAP2-AS1	MYD88	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000172936	NA	100130776	4615	PUNISHER	MYD88D	SP1-induced lncRNA AGAP2-AS1 expression promotes chemoresistance of breast cancer by epigenetic regulation of MyD88.ChIP assays showed that AGAP2-AS1-bound CBP increased the enrichment of H3K27ac at the promoter region of MyD88, thus resulting in the upregulation of MyD88.	30157918	RID00429	epigenetic regulation
Non-small cell lung cancer	ANCR	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000105329	NA	282	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	lncRA ANCR Inhibits Non-Small Cell Lung Cancer Cell Migration and Invasion by Inactivating TGF-beta Pathway.ANCR can inhibit NSCLC cell migration and invasion by downregulating TGF-beta1 expression.	30154397	RID00430	expression association
Ovarian cancer	NEAT1	miR-506	negatively-F	RIP;western blot;RNA pull-down assay	upregulation	qPCR;microarray	GSE45158	GSE45158.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long noncoding RNA NEAT1, regulated by LIN28B, promotes cell proliferation and migration through sponging miR-506 in high-grade serous ovarian cancer	30154460	RID00431	ceRNA or sponge
Urinary bladder cancer	RP11-79H23.3	PTEN	positively-E	RIP;western blot	downregulation	qPCR;microarray	GSE89006	GSE89006.zip	angiogenesis(-);tumorigenesis(-);cell metastasis(-)	ceRNA(miR-107)	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_8:78837529-78840522	ENSG00000171862	NA	NA	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer.upregulation of RP11-79H23.3 inhibited the angiogenesis, tumorigenesis, and lung metastasis in vivo, whereas RP11-79H23.3 knockdown exerted a contrary role.	30149689	RID00432	ceRNA or sponge
Malignant glioma	CDKN2B-AS1	miR-203a	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell cycle(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Effect of lncRNA ANRIL silencing on anoikis and cell cycle in human glioma via microRNA-203a	30197521	RID00433	expression association
Prostate cancer	TINCR	TRIP13	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000071539	NA	257000	9319	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	16E1BP|MVA3	LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer.TINCR plays a tumor suppressive role in regulating prostate cancer cell proliferation, migration and invasion through modulating TRIP13 expression	30154672	RID00434	expression association
Gastric cancer	CDKN2B-AS1	BMI1	positively-E	RNAi;Targetscan	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-99a)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000168283	NA	100048912	648	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Knockdown of long non-coding RNA ANRIL inhibits tumorigenesis in human gastric cancer cells via microRNA-99a-mediated down-regulation of BMI1.	30156609	RID00435	ceRNA or sponge
Osteosarcoma	CDKN2B-AS1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164305	NA	100048912	836	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CPP32|CPP32B|SCA-1	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Moreover, our mechanistic research findings verified that ANRIL-influenced growth and apoptosis may be partly through regulation of caspase-3 and Bcl-2.	30147340	RID00436	expression association
Osteosarcoma	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Moreover, our mechanistic research findings verified that ANRIL-influenced growth and apoptosis may be partly through regulation of caspase-3 and Bcl-2.	30147340	RID00437	expression association
Osteosarcoma	CDKN2B-AS1	MTA1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000182979	NA	100048912	9112	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin	30147340	RID00438	expression association
Osteosarcoma	CDKN2B-AS1	TIMP2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000035862	NA	100048912	7077	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CSC-21K|DDC8	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin.	30147340	RID00439	expression association
Osteosarcoma	CDKN2B-AS1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000039068	NA	100048912	999	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of lncRNA ANRIL suppresses growth and metastasis in human osteosarcoma cells.Migration and invasion were influenced via ANRIL-mediated regulation of MTA1, TIMP-2, and E-cadherin	30147340	RID00440	expression association
Colorectal cancer	DLEU1	KPNA3	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000102753	NA	10301	3839	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	IPOA4|SRP1|SRP1gamma|SRP4|hSRP1	LncRNA DLEU1 contributes to colorectal cancer progression via activation of KPNA3.Here we revealed that DLEU1 was crucial for activation of KPNA3 by recruiting SMARCA1, an essential subunit of the NURF chromatin remodeling complex, in CRC. DLEU1 was indispensible for the deposition of SMARCA1 at the promoter of KPNA3 gene.	30098595	RID00441	epigenetic regulation
Gastric cancer	E2F1	LSINCT5	positively-E	ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000281560	GRCh38_5:2712591-2715237	1869	101234261	E2F-1|RBAP1|RBBP3|RBP3	NA	E2F1 induces LSINCT5 transcriptional activity and promotes gastric cancer progression by affecting the epithelial-mesenchymal transition.Mechanistic investigations showed that LSINCT5 is a direct transcriptional target of E2F1.	30127643	RID00442	transcriptional regulation
Renal fibrosis	DNMT1	MEG3	negatively-E	RNAi;5-ethynyl-2'- deoxyuridine assay;bisulfite DNA sequencing assay	downregulation	qPCR	NA	NA	cell viability(-);cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Urinary system disease	Fibrosis	PCG	lncRNA	ENSG00000130816	NA	ENSG00000214548	GRCh38_14:100779410-100861031	1786	55384	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	miR-185 affected the EMT, cell viability and proliferation via DNMT1/MEG3 pathway in TGF-beta1-induced renal fibrosis.Furthermore, we demonstrated that DNMT1 regulated the MEG3 expression via altering the CpGs methylation level of MEG3 promoter in TGF-beta1-induced renal fibrosis	30095214	RID00443	epigenetic regulation
Hepatocellular carcinoma	NEAT1	IL6	positively-E	RNAi	upregulation	sequencing	TCGA	LIHC.zip	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000136244	NA	283131	3569	LINC00084|NCRNA00084|TncRNA|VINC	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	NEAT1 paraspeckle promotes human hepatocellular carcinoma progression by strengthening IL-6/STAT3 signaling.Destruction of paraspeckle formation by silencing the paraspeckle essential components NEAT1_2 or NONO could suppress IL-6-induced STAT3 phosphorylation in HCC cells.Our results demonstrate that paraspeckle can nuclear entrap the inhibitors of IL-6/STAT3 signaling as well as DNA damage, and then strengthen the promoting effect on HCC progression by IL-6. Mechanistically, paraspeckle promotes IL-6-induced STAT3 phosphorylation by binding and trapping peroxiredoxin-5 (PRDX5) mRNA in nucleus, decreasing protein level of PRDX5 which can directly interact with STAT3 and inhibit STAT3 phosphorylation.	30377567	RID00444	expression association
Colorectal cancer	PVT1-214	LIN28A	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR;microarray	GSE109454	GSE109454.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-128)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENST00000522875	GRCh38_8:129001506-129108902	ENSG00000131914	NA	NA	79727	NA	NA	Long noncoding RNA PVT1-214 promotes proliferation and invasion of colorectal cancer by stabilizing Lin28 and interacting with miR-128.we found that PVT1-214 not only upregulation Lin28 protein expression in CRC cells by stabilizing Lin28, but also participated in crosstalk with Lin28 mRNA through competition for miR-128 binding, imposing an additional level of post-transcriptional regulation	30076414	RID00445	ceRNA or sponge
Papillary thyroid carcinoma	PVT1	IGF1R	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	ceRNA(miR-30a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000140443	NA	5820	3480	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CD221|IGFIR|IGFR|JTK13	Long noncoding RNA PVT1 enhances the viability and invasion of papillary thyroid carcinoma cells by functioning as ceRNA of microRNA-30a through mediating expression of insulin like growth factor 1 receptor.	29803929	RID00446	ceRNA or sponge
Lung cancer	TINCR	FBXW7	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-544a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000109670	NA	257000	55294	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer;TINCR acted as a competing endogenous RNA (ceRNA) to sequester miR-544a from its target gene FBXW7	29324317	RID00447	ceRNA or sponge
Neuroblastoma	ETS1-AS1	HNRNPK	interact	RIP;EMSA;RNA pull-down assay	upregulation	qPCR;microarray;sequencing	GSE16476	GSE16476.zip	cancer progression(+);beta-catenin signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000254588	GRCh38_11:128526142-128530389	ENSG00000165119	NA	101929517	3190	pancEts-1	AUKS|CSBP|HNRPK|TUNP	Long Noncoding RNA pancEts-1 Promotes Neuroblastoma Progression through hnRNPK-Mediated beta-Catenin Stabilization;pancEts-1(ETS1-AS1) bound to hnRNPK to facilitate its physical interaction with beta-catenin	29311158	RID00448	interact with protein
Papillary thyroid carcinoma	GAS8-AS1	ATG5	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell autophagy(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000221819	GRCh38_16:90028908-90029901	ENSG00000057663	NA	750	9474	C16orf3	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	LncRNA GAS8-AS1 inhibits cell proliferation through ATG5-mediated autophagy in papillary thyroid cancer;GAS8-AS1 inhibited proliferation, activated autophagy, and increased ATG5 expression. Downregulation of ATG5 reversed GAS8-AS1-mediated activation of autophagy leading to cell death.	29327301	RID00449	expression association
Nasopharynx carcinoma	FOXD2-AS1	S100A1	positively-E	luciferase reporter assay	upregulation	sequencing	TCGA	HNSC.zip	tumorigenesis(+);cell growth(+)	ceRNA(miR-363-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000160678	NA	84793	6271	NA	S100|S100-alpha|S100A	Long non-coding RNA FOXD2-AS1 aggravates nasopharyngeal carcinoma carcinogenesis by modulating miR-363-5p/S100A1 pathway;FOXD2-AS1 contributed to NPC progression by regulating miR-363-5p/S100A1 signal pathway. Partially through sponging miR-363-5p,and then up-regulating S100A1, FOXD2-AS1 facilitates NPC cell growth.	29248577	RID00450	ceRNA or sponge
Melanoma	PVT1	miR-200c	negatively-E	RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma. the lncRNA PVT1 may contribute to the tumorigenesis and metastasis of melanoma through binding to EZH2 and regulating the expression of miR-200c	29286144	RID00451	epigenetic regulation
Oral squamous cell carcinoma	H19	EZH2	positively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE3524	GSE3524.zip	cell proliferation(+);cell invasion(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA H19 promotes cell proliferation and invasion by acting as a ceRNA of miR-138 and releasing EZH2 in oral squamous cell carcinoma;H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138.our findings suggest that H19 functions as an oncogene by inhibiting miR-138 and facilitating EZH2 expression in OSCC. Thus, lncRNA H1 may represent a potential therapeutic target for OSCC.	29344674	RID00452	ceRNA or sponge
Melanoma	H19	E2F3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+);cell growth(+)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000112242	NA	283120	1871	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-3	Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis;H19 may function as the sponge of miR-106a-5p to up-regulate E2F3 expression, and consequently promote the glucose metabolism and growth of melanoma	29350287	RID00453	ceRNA or sponge
Malignant glioma	CDKN2B-AS1	SIRT1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	ceRNA(miR-34a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000096717	NA	100048912	23411	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	SIR2|SIR2L1|SIR2alpha	Knockdown of long non-coding RNA ANRIL inhibits proliferation, migration, and invasion but promotes apoptosis of human glioma cells by upregulation of miR-34a;ANRIL was upregulation in glioma, and its inhibition could repress cell proliferation, migration and invasion but inhibit cell apoptosis through miR-34a-mediated downregulation of Sirt1, involving the inactivation of the PI3K/AKT and mTOR pathways	29057547	RID00454	ceRNA or sponge
Gastric cancer	XIST	TGFB1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-185)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000105329	NA	7503	7040	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	XIST promotes gastric cancer (GC) progression through TGF-beta1 via targeting miR-185;XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-beta1 by sponging miR-185 in GC	29053187	RID00455	ceRNA or sponge
Osteosarcoma	HIF1A	UCA1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+);PTEN/AKT signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000100644	NA	ENSG00000214049	GRCh38_19:15828206-15836328	3091	652995	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HIF-1alpha-induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway;lncRNA UCA1 was induced by HIF-1alpha and HIF-1alpha interacts with the HIF-1alpha response element in the promoter region of UCA1. Finally, we observed that HIF-1alpha induced cell growth through the UCA1/PTEN/AKT signaling pathway	29328452	RID00456	transcriptional regulation
Osteosarcoma	TUG1	SOX4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124766	NA	55000	6659	LINC00080|NCRNA00080|TI-227H	EVI16	Long Non-Coding RNA TUG1 Promotes Proliferation and Inhibits Apoptosis of Osteosarcoma Cells by Sponging miR-132-3p and Upregulating SOX4 Expression;TUG1 knockdown suppressed proliferation and promoted apoptosis by upregulating miR-132-3p and downregulating SOX4 in primary OS cells	29436190	RID00457	ceRNA or sponge
Malignant glioma	HOXA9	HOTAIR	positively-E	ChIP	upregulation	microarray	TCGA	GBM.zip	prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Brain glioma	TF	lncRNA	ENSG00000078399	NA	ENSG00000228630	GRCh38_12:53962308-53974956	3205	100124700	ABD-B|HOX1|HOX1.7|HOX1G	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The long non-coding RNA HOTAIR is transcriptionally activated by HOXA9 and is an independent prognostic marker in patients with malignant glioma;HOXA9 binds directly to the promoter of HOTAIR;GBM patients with high HOTAIR expression had a significantly reduced overall survival, independently of other prognostic variables	29644006	RID00458	transcriptional regulation
Pancreatic cancer	SPRY4-IT1	CDC20	positively-E	western blot;RNAi	NA	NA	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000117399	NA	100642175	991	SPRIGHTLY	CDC20A|bA276H19.3|p55CDC	Long non-coding RNA SPRY4-IT1 promotes cell proliferation and invasion by regulation of Cdc20 in pancreatic cancer cells;suppression of SPRY4-IT1 inhibited the expression of Cdc20 in pancreatic cancer cells	29489909	RID00459	expression association
Hepatocellular carcinoma	LNC00312	CCNB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	ENSG00000134057	NA	NA	891	NA	CCNB	Long non-coding RNA 00312 downregulates cyclin B1 and inhibits hepatocellular carcinoma cell proliferation in vitro and in vivo; Lnc00312 downregulated cyclin B1 and induced G2-M cell cycle arrest in HCC cells	29432732	RID00460	expression association
Rhabdomyosarcoma	MYCNOS-01	MYCN	negatively-E	RNAi;western blot;immunofluorescence	upregulation	qPCR;microarray	NA	NA	cell growth(-)	post-transcriptional level	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skeletal muscle cancer	lncRNA	TF	ENST00000641263	GRCh38_2:15936265-15941582	ENSG00000134323	NA	NA	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	The long non-coding RNA MYCNOS-02 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells;MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels;MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein level;Reduction of MYCNOS-01 or MYCN expression decreased cell growth. An alternative transcript of MYCNOS, MYCNOS-01, post-transcriptionally regulates MYCN levels and affects growth in MYCN-amplified rhabdomyosarcoma and neuroblastoma cells.	29466962	RID00461	expression association
Neuroblastoma	MYCNOS-01	MYCN	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	TF	ENST00000641263	GRCh38_2:15936265-15941582	ENSG00000134323	NA	NA	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	The long non-coding RNA MYCNOS-02 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells;MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels;MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein level;Reduction of MYCNOS-01 or MYCN expression decreased cell growth	29466962	RID00462	expression association
Hepatocellular carcinoma	HNF1A	HNF1A-AS1	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000135100	NA	ENSG00000241388	GRCh38_12:120941728-120980965	6927	283460	HNF-1A|HNF1|HNF4A|IDDM20|LFB1|MODY3|TCF-1|TCF1	C12orf27|HAS1|NCRNA00262	The HNF1alpha-regulated lncRNA HNF1A-AS1 reverses the malignancy of hepatocellular carcinoma by enhancing the phosphatase activity of SHP-1;HNF1alpha activated the transcription of HNF1A-AS1 by directly binding to its promoter region;knockdown of HNF1A-AS1 reversed the suppressive effects of HNF1alpha on the migration and invasion of HCC cells	29466992	RID00463	transcriptional regulation
Hepatocellular carcinoma	HNF1A-AS1	PTPN6	interact	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000111679	NA	283460	5777	C12orf27|HAS1|NCRNA00262	NA	The HNF1alpha-regulated lncRNA HNF1A-AS1 reverses the malignancy of hepatocellular carcinoma by enhancing the phosphatase activity of SHP-1.HNF1A-AS1 directly bound to the C-terminal of SHP-1 with a high binding affinity and increased the phosphatase activity of SHP-1;Inhibition of SHP-1 enzymatic activity substantially reversed the HNF1alpha- or HNF1A-AS1-induced reduction on the metastatic property of HCC cells	29466992	RID00464	interact with protein
Breast cancer	UCA1	YAP1	positively-E	luciferase reporter assay;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-18a)	regulation	NA	trastuzumab	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000137693	NA	652995	10413	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	COB1|YAP|YAP2|YAP65|YKI	Long non-coding RNA UCA1 desensitizes breast cancer cells to trastuzumab by impeding miR-18a repression of Yes-associated protein 1;A luciferase reporter assay confirmed the association of miR-18a with wild-type UCA1 but not with UCA1 mutated at the predicted miR-18a-binding site. The direct targeting of YAP1 by miR-18a was verified by the observation that miR-18a mimic suppressed luciferase expression from a construct containing the YAP1 3' untranslated region.	29408336	RID00465	ceRNA or sponge
Hepatocellular carcinoma	LINC00261	HES1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000114315	NA	140828	3280	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	HES-1|HHL|HRY|bHLHb39	LINC00261 suppresses cell proliferation, invasion and Notch signaling pathway in hepatocellular carcinoma.upregulation of LINC00261 significantly inhibited Notch signaling by downregulating Notch1 and Hes-1 expression in HCC cells.	29278875	RID00466	expression association
Hepatocellular carcinoma	LINC00261	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000148400	NA	140828	4851	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	AOS5|AOVD1|TAN1|hN1	LINC00261 suppresses cell proliferation, invasion and Notch signaling pathway in hepatocellular carcinoma.upregulation of LINC00261 significantly inhibited Notch signaling by downregulating Notch1 and Hes-1 expression in HCC cells.	29278875	RID00467	expression association
Prostate cancer	CDKN2B-AS1	TGFB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105329	NA	100048912	7040	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;Knockdown of ANRIL significantly decreased the levels of TGF-beta1 and p-Smad2	29278879	RID00468	expression association
Prostate cancer	CDKN2B-AS1	SMAD2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000175387	NA	100048912	4087	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway	29278879	RID00469	expression association
Prostate cancer	CDKN2B-AS1	SMAD7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000101665	NA	100048912	4092	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CRCS3|MADH7|MADH8	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;Knockdown of ANRIL significantly decreased the levels of TGF-beta1 and p-Smad2,and increased the level of p-Smad7 in prostate cancer LNCap cells	29278879	RID00470	expression association
Prostate cancer	CDKN2B-AS1	let-7a	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta1/ Smad signaling pathway;knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells	29278879	RID00471	expression association
Glioblastoma	H19	NKD1	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000140807	NA	283120	85407	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Naked1	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter;by showing that its expression is inversely linked to that of NKD1, a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter	29643989	RID00472	epigenetic regulation
Osteosarcoma	CDKN2B-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL is associated with a poor prognosis of osteosarcoma and promotes tumorigenesis via PI3K/Akt pathway;knockdown of ANRIL could significantly decrease the expression level of phosphorylated PI3K and AKT in OS cells	29520337	RID00473	expression association
Osteosarcoma	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA ANRIL is associated with a poor prognosis of osteosarcoma and promotes tumorigenesis via PI3K/Akt pathway;knockdown of ANRIL could significantly decrease the expression level of phosphorylated PI3K and AKT in OS cells	29520337	RID00474	expression association
Cervical cancer	HOTAIR	MAPK1	positively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-23b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targetting miR-23b/MAPK1 axis;HOTAIR may competitively bind miR-23b and modulate the expression of MAPK1 indirectly in cervical cancer cells	29335299	RID00475	ceRNA or sponge
Malignant glioma	H19	miR-152	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 promotes proliferation and invasion in human glioma cells by downregulating miR-152;H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression;H19 and miR-152 directly regulated each other. Taken together, H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression, providing evidence for the potential application of H19 as a biomarker and therapy target for glioma.	29422115	RID00476	ceRNA or sponge
Cervical cancer	NCK1-DT	CDK1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	ceRNA(miR-6857)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000239213	GRCh38_3:136835345-136862618	ENSG00000170312	NA	101927597	983	NA	CDC2|CDC28A|P34CDC2	LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway;NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation	29416014	RID00477	ceRNA or sponge
Testicular germ cell cancer	SPRY4-IT1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Testicular cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000142208	NA	100642175	207	SPRIGHTLY	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours;Knockdown of SPRY4 and SPRY4-IT1 also led to a significant reduction in the phosphorylation of Akt;SPRY4 and SPRY4-IT1 may act as oncogenes in TGCTs via activation of the PI3K/Akt signalling pathway.	29410498	RID00478	expression association
Papillary thyroid carcinoma	CCND2-AS1	CDH2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000255920	GRCh38_12:4247981-4276252	ENSG00000170558	NA	103752584	1000	CCND2-AS2	CD325|CDHN|CDw325|NCAD	LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma;CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration	29366479	RID00479	expression association
Papillary thyroid carcinoma	CCND2-AS1	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000255920	GRCh38_12:4247981-4276252	ENSG00000026025	NA	103752584	7431	CCND2-AS2	NA	LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma;CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration	29366479	RID00480	expression association
Glioblastoma	SNHG7	miR-5059	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000233016	GRCh38_9:136721366-136728184	NA	NA	84973	NA	NCRNA00061	NA	Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095;we found that SNHG7 directly inhibited miR-5095, which targeted the 3' UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/beta-catenin signaling pathway in GBM;SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095. miR-5095 was a potential miRNA target for SNHG7. There are two putative binding sites for miR-5095 in SNHG7.	29360452	RID00481	ceRNA or sponge
Lung cancer	UCA1	HMGB1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000189403	NA	652995	3146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HMG-1|HMG1|HMG3|SBP-1	Long non-coding RNA UCA1 promotes lung cancer cell proliferation and migration via microRNA-193a/HMGB1 axis;UCA1 promoted the miR-193a expression and miR-193a could bind to the predicted binding site of UCA1. In summary, our study demonstrated that UCA1 exerts oncogenes activity in lung cancer, acting mechanistically by upregulating HMGB1 expression through 'sponging' miR-193a.	29355524	RID00482	ceRNA or sponge
Gastric cancer	BG981369	SOX4	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	NA	GRCh38_1:172885475-172885888	ENSG00000124766	NA	NA	6659	NA	EVI16	lncRNA BG981369 Inhibits Cell Proliferation, Migration, and Invasion, and Promotes Cell Apoptosis by SRY-Related High-Mobility Group Box 4 (SOX4) Signaling Pathway in Human Gastric Cancer;we found that SOX4 may act as a downstream mediator of BG981369, suggesting that BG981369 inhibits proliferation, migration, and invasion, and promotes apoptosis by targeting SOX4 in the GC cell lines	29398692	RID00483	expression association
Acute lymphocytic leukemia	LINC-PINT	HMOX1	positively-E	RNAi	downregulation	qPCR	NA	NA	chemoresistance(+);cell viability(-);cell proliferation(-)	NA	regulation	NA	panobinostat;curcumin	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000231721	GRCh38_7:130938963-131110176	ENSG00000100292	NA	378805	3162	LincRNA-Pint|MKLN1-AS1|PINT	HMOX1D|HO-1|HSP32|bK286B10	Deregulation of linc-PINT in acute lymphoblastic leukemia is implicated in abnormal proliferation of leukemic cells;linc-PINT induced the transcription of HMOX1 which reduced the viability of ALL cells. Intriguingly, we observed that treatment with anti-tumoral epigenetic drugs like LBH-589 (Panobinostat) and Curcumin induced the expression of linc-PINT and HMOX1 in ALL. These results indicate that the downregulation of linc-PINT plays a relevant role in the pathogenesis of ALL, and linc-PINT re-expression may be one of the mechanisms exerted by epigenetic drugs to reduce cell proliferation in ALL.	29560114	RID00484	expression association
Malignant glioma	DANCR	RAB1A	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-634)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000138069	NA	57291	5861	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	RAB1|YPT1	LncRNA DANCR functions as a competing endogenous RNA to regulate RAB1A expression by sponging miR-634 in glioma;DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression;DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma	29301870	RID00485	ceRNA or sponge
Non-small cell lung cancer	HNF1A-AS1	miR-17-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000241388	GRCh38_12:120941728-120980965	NA	NA	283460	NA	C12orf27|HAS1|NCRNA00262	NA	Long non-coding RNA HNF1A-AS1 promotes cell proliferation and invasion via regulating miR-17-5p in non-small cell lung cancer;Bioinformatics analysis and luciferase reporter assay revealed that HNF1A-AS1 interacted with miR-17-5p by directly targeting it.lncRNA HNF1A-AS1 promoted lung cancer cells proliferation and invasion via regulating miR-17-5p	29289833	RID00486	ceRNA or sponge
Colorectal cancer	HOTTIP	SGK1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000118515	NA	100316868	6446	HOXA-AS6|HOXA13-AS1|NCRNA00213	SGK	Knockdown of the long non-coding RNA HOTTIP inhibits colorectal cancer cell proliferation and migration and induces apoptosis by targeting SGK1;luciferase reporter assay suggested that knockdown of HOTTIP could target decreasing the expression of Serum- and glucocorticoid-inducible kinase 1 (SGK1) gene, and we subsequently verified that up-regulation of the SGK1 gene promoted cell proliferation and migration and inhibited cell apoptosis in HCT-116 and SW620 cell lines.up-regulation of the SGK1 emerged the opposite effect with knockdown of HOTTIP.	29274585	RID00487	transcriptional regulation
Cervical cancer	XLOC_008466	miR-216b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA		GRCh38_10:43323011-43327969	NA	NA	NA	NA	NA	NA	Bioinformatics analysis revealed that XLOC_008466 sponged miR-216b with the complementary binding sites at 3'-UTR;our study reveals the tumor promoting role of XLOC_008466 in cervical cancer carcinogenesis	29247951	RID00488	ceRNA or sponge
Lung adenocarcinoma	OIP5-AS1	BCL2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-448)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000171791	NA	729082	596	cyrano|linc-OIP5	Bcl-2|PPP1R50	Long non-coding RNA OIP5-AS1 functions as an oncogene in lung adenocarcinoma through targeting miR-448/Bcl-2. We also certified that OIP5-AS1 could sponge and regulate miR-448 to affect cell function in lung adenocarcinoma. MiR-448 could target Bcl-2 and affect the expression of Bcl-2.	29247949	RID00489	ceRNA or sponge
Thyroid cancer	SPRY4-IT1	TGFB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000105329	NA	100642175	7040	SPRIGHTLY	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA SPRY4-IT was concerned with the poor prognosis and contributed to the progression of thyroid cancer. silenced SPRY4-IT1 could increase the levels of transforming growth factor-beta1 (TGF-beta1) and p-Smad2/3 and function mediated by si-SPRY4-IT1 could be rescued by the interference of TGF-beta1;SPRY4-IT1 might become a novel prognostic factor in the clinical behaviors of TC patients and participated in the progression of TC through targeting TGF-beta/Smad signaling pathway	29234152	RID00490	expression association
Breast cancer	CCAT1	miR-148b	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Down-regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR-148b in breast cancer;CCAT1 could negatively regulate miR-148b expression;overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. Luciferase reporter assay was performed to confirm the interaction between CCAT1 and miR-148b in breast cancer cells	29024383	RID00491	ceRNA or sponge
Cervical cancer	HOTAIR	miR-206	negatively-E	RNAi;RNA-FISH	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells;These elucidates that the phenotypic effects of migration and invasion observed after HOTAIR inhibition, at least in part, through the regulation of MKL1 via inhibition of miR206 expression in HeLa cells. These data indicate the existence of a positive feedback loop between HOTAIR and MKL1.Luciferase reporter assays and CHIP were used to determine how MKL1 regulates HOTAIR. High level of MKL1 significantly correlate with HOTAIR expression in Cervical cancer patient.In this study, we further confirmed that knockdown HOTAIR could enhance miR206 RNA expression level in HeLa cells.	29391067	RID00492	expression association
Cervical cancer	HOTAIR	MRTFA	positively-E	western blot	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196588	NA	100124700	57591	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSAC|MAL|MKL|MKL1|MRTF-A	LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells;These elucidates that the phenotypic effects of migration and invasion observed after HOTAIR inhibition, at least in part, through the regulation of MKL1 via inhibition of miR206 expression in HeLa cells. These data indicate the existence of a positive feedback loop between HOTAIR and MKL1.Luciferase reporter assays and CHIP were used to determine how MKL1 regulates HOTAIR. High level of MKL1 significantly correlate with HOTAIR expression in Cervical cancer patient.In this study, we further confirmed that knockdown HOTAIR could enhance miR206 RNA expression level in HeLa cells.	29391067	RID00493	expression association
Nephroblastoma	LINC00473	CHUK	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000213341	NA	90632	1147	C6orf176|LNC473|bA142J11.1	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	LINC00473 antagonizes the tumour suppressor miR-195 to mediate the pathogenesis of Wilms tumour via IKKalpha;LINC00473 harboured binding sites for miR-195 and limited miR-195 availability in a dose-dependent manner;IKKalpha was the downstream of LINC00473/miR-195 signals and could be directly targeted by miR-195 to participate LINC00473-induced tumour progression;Loss-of-function of LINC00473 in vivo effectively promoted the regression of Wilms tumour via miR-195/IKKalpha-mediated growth inhibition	29159834	RID00494	ceRNA or sponge
Non-small cell lung cancer	SNHG7	FAIM2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-193b)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000135472	NA	84973	23017	NCRNA00061	LFG|LFG2|NGP35|NMP35|TMBIM2	miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer;oncogene SNHG7 predicted a poor clinical outcome and functioned as competitive endogenous RNA (ceRNA) antagonized microRNA-193b (miR-193b) to up-regulate the FAIM2 level in NSCLC;forced expression of SNHG7 could down-regulate miR-193b to elevate the FAIM2 level of tumour cells, leading to impaired miR-193b/FAIM2-induced tumour progression	29131440	RID00495	ceRNA or sponge
Malignant glioma	TP73-AS1	PPP1R13L	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000104881	NA	57212	10848	KIAA0495|PDAM	IASPP|NKIP1|RAI|RAI4	The Long Noncoding RNA TP73-AS1 Interacted with miR-124 to Modulate Glioma Growth by Targeting Inhibitor of Apoptosis-Stimulating Protein of p53;TP73-AS1 inhibited the brain glioma growth and metastasis as a competing endogenous RNA (ceRNA) through miR-124-dependent iASPP regulation	29412778	RID00496	ceRNA or sponge
Osteosarcoma	CERNA2	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000171791	NA	642934	596	HOST2|lncRNA-HOST2	Bcl-2|PPP1R50	Prognostic value of long non-coding RNA HOST2 expression and its tumor-promotive function in human osteosarcoma. we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells;the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000)	29509239	RID00497	expression association
Osteosarcoma	CERNA2	BAX	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000087088	NA	642934	581	HOST2|lncRNA-HOST2	BCL2L4	Prognostic value of long non-coding RNA HOST2 expression and its tumor-promotive function in human osteosarcoma. we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells;the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000)	29509239	RID00498	expression association
Hepatocellular carcinoma	AF119895	NXF3	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-6508-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:186618535-186621317	ENSG00000147206	NA	NA	56000	NA	NA	AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p;AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3'UTR;	29274323	RID00499	ceRNA or sponge
Osteosarcoma	CRNDE	NOTCH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000148400	NA	NA	4851	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	AOS5|AOVD1|TAN1|hN1	LncRNA, CRNDE promotes osteosarcoma cell proliferation, invasion and migration by regulating Notch1 signaling and epithelial-mesenchymal transition;Overexpression of CRNDE was found to enhance the activity of Notch1 signaling and promote epithelial-mesenchymal transition (EMT)	29246789	RID00500	expression association
Gastric cancer	HOTAIR	miR-34a	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+)	sponge;histone modification	binding/interaction	RNA-RNA	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/beta-catenin signaling pathways by up-regulating miR-34a;HOTAIR directly bound to miR-34a. LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer.	29080815;26136075	RID00501	ceRNA or sponge;epigenetic regulation
Hepatocellular carcinoma	CDKN2B-AS1	miR-122-5p	negatively-F	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Knockdown of LncRNA ANRIL suppresses cell proliferation, metastasis, and invasion via regulating miR-122-5p expression in hepatocellular carcinoma;ANRIL was demonstrated to directly bind to miR-122-5p and inhibit its expression	29127494	RID00502	ceRNA or sponge
Breast cancer	TP73-AS1	ZEB1	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-200a)	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000148516	NA	57212	6935	KIAA0495|PDAM	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;TP73-AS1 promoted ZEB1 expression via competing with ZEB1 3'UTR for miR-200a binding;ZEB1 could bind to the promoter region of TP73-AS1 to activate its expression	28857253	RID00503	ceRNA or sponge
Breast cancer	TP73-AS1	TWIST1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000122691	NA	57212	7291	KIAA0495|PDAM	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;Suppressing TP73-AS1 expression to rescue miR-200a expression, thus to inhibit ZEB1 and Twist expression and up-regulate E-cadherin might improve breast cancer cell invasion and migration	28857253	RID00504	expression association
Breast cancer	TP73-AS1	CDH1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000039068	NA	57212	999	KIAA0495|PDAM	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration;Suppressing TP73-AS1 expression to rescue miR-200a expression, thus to inhibit ZEB1 and Twist expression and up-regulate E-cadherin might improve breast cancer cell invasion and migration	28857253	RID00505	expression association
Lung adenocarcinoma	SPRY4-IT1	EZH2	negatively-F	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma;The interaction between SPRY4-IT1 and EZH2 was determined using a RNA pull-down assay and a RNA immunoprecipitation (RIP) assay. EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression	28796375	RID00506	interact with protein
Hepatocellular carcinoma	MALAT1	EGFR	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell motility(+);cell growth(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000146648	NA	378938	1956	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195;Malat1 acted as a circular endogenous RNA (ceRNA) for miR-195;Malat1 silence could not suppress HCC cell growth and motility when miR-195 was knocked down. EGFR was a direct target of miR-195. miR-195 overexpression could not suppress HCC cell growth and motility when the 3'UTR site of EGFR was overexpressed.	28722813	RID00507	ceRNA or sponge
Ovarian cancer	TDRG1	miR-196	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000204091	GRCh38_6:40334775-40387590	NA	NA	732253	NA	LINC00532|lincRNA-NR_024015	NA	The role of the long non-coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR-93/RhoC pathway; LncRNA TDRG1 downregulation upregulation miR-93 expression, while its overexpression reduced miR-93 expression; LncRNA TDRG1 has microRNA-93 (miR-93) binding sites	28984384	RID00508	ceRNA or sponge
Ovarian cancer	TDRG1	RHOC	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000204091	GRCh38_6:40334775-40387590	ENSG00000155366	NA	732253	389	LINC00532|lincRNA-NR_024015	ARH9|ARHC|H9|RHOH9	The role of the long non-coding RNA TDRG1 in epithelial ovarian carcinoma tumorigenesis and progression through miR-93/RhoC pathway;TDRG1 downregulation reduced the expression of Ras homolog gene family member C (RhoC)	28984384	RID00509	expression association
Cervical cancer	NEAT1	miR-101	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA-101;the expression of mircoRNA-101 (miR-101) target gene Fos was positively associated with NEAT1 expression due to NE1 competitive molecular sequestering of miR-101 via base pairing	29207151	RID00510	ceRNA or sponge
Gastric cancer	H19	ERBB2	positively-E	luciferase reporter assay;Immunoprecipitation;western blot;RT-qPCR;RNAi	upregulation	qPCR	NA	NA	prognosis(-)	ceRNA(let-7c)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141736	NA	283120	2064	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	H19 functions as a competing endogenous RNA to regulate human epidermal growth factor receptor expression by sequestering let-7c in gastric cancer;The results of the present study suggest that H19 may function as a competing endogenous RNA to regulate HER2 expression by sequestering let-7c in GC cells. Assessment of tumor diameter and pathological tumor stage suggested that increased H19 expression was associated with a poorer prognosis in patients with GC.	29207111;24055342;27660891	RID00511	ceRNA or sponge
Gastric cancer	SNHG12	miR-320	negatively-F	western blot;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	LncRNA SNHG12 regulates gastric cancer progression by acting as a molecular sponge of miR-320;miR-320 was directly regulated by SNHG12 and suppression of miR-320 expression reversed the inhibitory effects of SNHG12 siRNA on GC cell proliferation and invasion	29207106	RID00512	ceRNA or sponge
Pancreatic cancer	XLOC_000647	NLRP3	negatively-E	western blot;IHC;luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cancer progression(-);epithelial to mesenchymal transition(+);cell invasion(-)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_1:247332910-247393369	ENSG00000162711	NA	NA	114548	NA	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCAS1|FCU|KEFH|MWS|NALP3|PYPAF1	Long non-coding RNA XLOC_000647 suppresses progression of pancreatic cancer and decreases epithelial-mesenchymal transition-induced cell invasion by down-regulating LRP3;XLOC_000647 functions as a novel tumor suppressor of lncRNA and acts as an important regulator of NLRP3, inhibiting cell proliferation, invasion, and EMT in PC;a significantly negative correlation was observed between XLOC_000647 levels and its genomic nearby gene NLRP3, XLOC_000647 decreased NLRP3 by inhibiting its promoter activity.	29386037	RID00513	transcriptional regulation
Lung cancer	CAV1	HOTAIR	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000105974	NA	ENSG00000228630	GRCh38_12:53962308-53974956	857	100124700	BSCL3|CGL3|LCCNS|MSTP085|PPH3|VIP21	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Cav-1 promote lung cancer cell proliferation and invasion through lncRNA HOTAIR;CAV-1 could regulate the expression of HOTAIR;knockdown of the expression of HOAIR partially reverses the promotion of cell viability and invasion induced by CAV-1	29080835	RID00514	expression association
Endometrial cancer	HAND2-AS1	HAND2	positively-E	RNAi;western blot	downregulation	qPCR;microarray;sequencing	TCGA;GSE17025	UCEC.zip;GSE17025.zip	cell invasion(-);cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000164107	NA	79804	9464	DEIN|NBLA00301|UPH	DHAND2|Hed|Thing2|bHLHa26|dHand	Long non-coding RNA HAND2-AS1 inhibits invasion and metastasis in endometrioid endometrial carcinoma through inactivating neuromedin U;Down-regulation of HAND2-AS1 and HAND2 was correlated with tumor grade, lymph node metastasis and recurrence of EEC patients;Similarly, overexpression of HAND2 also inhibited migration and invasion EEC cells indicating that HAND2-AS1 and HAND2 had a concordant role in the progression of EEC. HAND2 was not regulated by HAND2-AS1 in EEC	29107108	RID00515	expression association
Endometrial cancer	HAND2-AS1	NMU	negatively-E	RNAi;western blot	downregulation	qPCR;microarray;sequencing	NA	NA	cell invasion(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000237125	GRCh38_4:173527270-173659696	ENSG00000109255	NA	79804	10874	DEIN|NBLA00301|UPH	NA	Long non-coding RNA HAND2-AS1 inhibits invasion and metastasis in endometrioid endometrial carcinoma through inactivating neuromedin U;the anti-tumorigenic effect of HAND2-AS1 was mediated by down-regulating NMU	29107108	RID00516	expression association
Gastric cancer	NEAT1	STAT3	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-506)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168610	NA	283131	6774	LINC00084|NCRNA00084|TncRNA|VINC	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA NEAT1-modualted miR-506 regulates gastric cancer development through targeting STAT3;it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer	29363783	RID00517	ceRNA or sponge
Malignant glioma	UCA1	miR-122	negatively-F	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells;UCA1 acted as an miR-122 sponge to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122	28548636	RID00518	ceRNA or sponge
Pancreatic ductal adenocarcinoma	FEZF1-AS1	FEZF1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE61166	GSE61166.zip	cancer progression(+)	ceRNA(miR-506)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000128610	NA	154860	389549	NA	FEZ|HH22|ZNF312B	FEZF1-AS1/miR-107/ZNF312B axis facilitates progression and Warburg effect in pancreatic ductal adenocarcinoma;FEZF1-AS1 may act as an endogenous sponge by competing for miR-107, thereby modulating the derepression of ZNF312B;Downregulation of FEZF1-AS1 or ZNF312B significantly inhibited proliferation, colony formation, migration, and invasion of PDAC cells in vitro, whereas the miR-107 inhibitor abrogated the effect of dow-regulation of FEZF1-AS1 or ZNF312B in reducing oncogenic capacities of PDAC cells	29348628	RID00519	ceRNA or sponge
Esophagus squamous cell carcinoma	NKILA	NFKBIA	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);cell metastasis(-)	phosphorylation	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	NKILA inhibits NF-kB signaling and suppresses tumor metastasis;NKILA could inhibit phosphorylation of IkBalpha, suppress p65 nuclear translocation and downregulate the expression of NF-kB target genes in ESCC cells. The long non-coding RNA (lncRNA) NKILA (nuclear transcription factor NF-kB interacting lncRNA) functions as a suppressor in human breast cancer and tongue cancer.	29348395	RID00520	interact with protein
Esophagus squamous cell carcinoma	NKILA	RELA	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000173039	NA	105416157	5970	NA	CMCU|NFKB3|p65	NKILA inhibits NF-kB signaling and suppresses tumor metastasis;NKILA could inhibit phosphorylation of IkBalpha, suppress p65 nuclear translocation and downregulate the expression of NF-kB target genes in ESCC cells	29348395	RID00521	expression association
Gastrointestinal stromal tumor	CCDC26	KIT	interact	RNA pull-down assay;RNAi	downregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	imatinib	NA	NA	Cancer	Gastrointestinal stromal tumor	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000157404	NA	137196	3815	RAM	C-Kit|CD117|MASTC|PBT|SCFR	CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT;CCDC26 can interact with c-KIT and that CCDC26 knockdown can upregulate c-KIT expression	29423012	RID00522	interact with protein
Lung cancer	PVT1-5	SLC7A5	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-126)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_8:127794533-128101252	ENSG00000103257	NA	NA	8140	NA	4F2LC|CD98|D16S469E|E16|LAT1|MPE16	Long non-coding RNA PVT1-5 promotes cell proliferation by regulating miR-126/SLC7A5 axis in lung cancer;knockdown of lncRNA-PVT1-5 in cells could down-regulate the expression of SLC7A5;lncRNA-PVT1-5 may function as a competing endogenous RNA (ceRNA) for miR-126 to promote cell proliferation by regulating the miR-126/SLC7A5 pathway, suggesting that lncRNA-PVT1-5 plays a crucial role in lung cancer progression and lncRNA-PVT1-5/miR-126/SLC7A5 regulatory network may shed light on tumorigenesis in lung cancer	29277611	RID00523	ceRNA or sponge
Gastric cancer	LOC101927497	miR-574-5p	negatively-F	RNA antisense purification	downregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000237819	GRCh38_7:92836483-92917187	NA	NA	101927497	NA	NA	NA	Functional role of lncRNA LOC101927497 in N-methyl-N'-nitro-N-nitrosoguanidine-induced malignantly transformed human gastric epithelial cells;LncRNA LOC101927497 functions as a suppressor by interacting with miR-574-5p, thus inhibiting the malignant phenotype of GES-1-T cells	29223541	RID00524	ceRNA or sponge
Gastric cancer	STAT3	HAGLROS	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor malignant transformation(+);cell autophagy(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000226363	GRCh38_2:176177717-176179008	6774	102800310	ADMIO|ADMIO1|APRF|HIES	NA	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy;Mechanistic investigations showed that HAGLROS was a direct target of transcriptional factor STAT3	29329543	RID00525	transcriptional regulation
Gastric cancer	HAGLROS	MTOR	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(+);cell autophagy(-)	ceRNA(miR-100-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179008	ENSG00000198793	NA	102800310	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition	29329543	RID00526	ceRNA or sponge
Gastric cancer	HAGLROS	RHEB	positively-F	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	NA	NA	tumor malignant transformation(+);cell autophagy(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226363	GRCh38_2:176177717-176179008	ENSG00000106615	NA	102800310	6009	NA	NA	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. HAGLROS interacted with mTORC1 components to activate mTORC1 signaling pathway which was known to be an important negative signal of autophagy. Here activation of mTORC1 signaling pathway by HAGLROS inhibited autophagy, thereby promoted excessive proliferation and maintained the malignant phenotype of GC cells.	29329543	RID00527	interact with protein
Malignant glioma	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00528	expression association
Malignant glioma	H19	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00529	expression association
Malignant glioma	H19	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	temozolomide	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway;silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1	29391808	RID00530	expression association
Nasopharynx carcinoma	LINC00460	IL6	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-149-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000233532	GRCh38_13:106374477-106384315	ENSG00000136244	NA	728192	3569	NA	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	LncRNA-LINC00460 facilitates nasopharyngeal carcinoma tumorigenesis through sponging miR-149-5p to up-regulate IL6;LINC00460 contributed to the progression of NPC through regulating miR-149-5p/IL6 signal pathway	28987345	RID00531	ceRNA or sponge
Osteosarcoma	SNHG12	NOTCH2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000134250	NA	85028	4853	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	AGS2|HJCYS|hN2	LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p;	29229388	RID00532	ceRNA or sponge
Breast cancer	SNHG15	miR-211-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983023-44986961	NA	NA	285958	NA	C7orf40|Linc-Myo1g|MYO1GUT	NA	Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p;SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration	29217194	RID00533	ceRNA or sponge
Ovarian cancer	SNHG20	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000168036	NA	654434	1499	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Up-regulation of long non-coding RNA SNHG20 promotes ovarian cancer progression via Wnt/beta-catenin signaling;lncRNA SNHG20 knockdown inhibited Wnt/beta-catenin signaling activity by suppressing beta-catenin expression and reversing the downstream target gene expression	29101241	RID00534	expression association
Hepatocellular carcinoma	LINC00176	miR-9	negatively-F	RNAi;MS2-tagged RNA purification	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000196421	GRCh38_20:64034344-64039962	NA	NA	NA	NA	NA	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00535	ceRNA or sponge
Hepatocellular carcinoma	LINC00176	miR-185	negatively-F	RNAi;MS2-tagged RNA purification	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000196421	GRCh38_20:64034344-64039962	NA	NA	NA	NA	NA	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00536	ceRNA or sponge
Hepatocellular carcinoma	MYC	LINC00176	positively-E	RNAi;ChIP	upregulation	microarray	GSE70178	GSE70178.zip	cell cycle(+);cell survival(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Liver cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000196421	GRCh38_20:64034344-64039962	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	NA	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs; Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185;Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185	28869604	RID00537	transcriptional regulation
Pancreatic ductal adenocarcinoma	KRAS	CCAT2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	MEK/ERK signaling pathway(+);oncogenic role(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000133703	NA	ENSG00000280997	GRCh38_8:127400399-127402150	3845	101805488	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	LINC00873|NCCP1	CCAT2 is an oncogenic long non-coding RNA in pancreatic ductal adenocarcinoma.CCAT2 was regulated by KRAS through MEK/ERK signaling pathway.Additionally, KRAS inhibition markedly decreased CCAT2 promoter activity by more than 60%, indicating that KRAS might regulate CCAT2 expression at transcriptional level.	29298720	RID00538	transcriptional regulation
Ovarian cancer	HAGLR	FZD4	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	OV.zip	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-608)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000174804	NA	401022	8322	HOXD-AS1|MIR7704HG|Mdgt	CD344|EVR1|FEVR|FZD4S|Fz-4|Fz4|FzE4|GPCR|hFz4	HOXD-AS1 promotes cell proliferation, migration and invasion through miR-608/FZD4 axis in ovarian cancer;HOXD-AS1 was detected to positively regulate the expression of frizzled family receptor 4 (FZD4) by competitively binding to miR-608	29416930	RID00539	ceRNA or sponge
Esophagus squamous cell carcinoma	miR-196a	GAS5	negatively-F	luciferase reporter assay;ChIRP-RT-qPCR	upregulation	qPCR	NA	NA	cell growth(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Negative regulation of lncRNA GAS5 by miR-196a inhibits esophageal squamous cell carcinoma growth;miR-196a could bind to the seventh exon of GAS5.Additionally, both GAS5 and miR-196a could bind to Ago2 which is a key component of the RNA-induced silencing complex (RISC). Together, these results suggest that GAS5 functions as a tumor suppressor gene in ESCC and is regulated by miR-196a involved in RISC.	29170131	RID00540	ceRNA or sponge
Osteosarcoma	LUCAT1	ABCB1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-200c)	regulation	NA	methotrexate	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000085563	NA	100505994	5243	SCAL1|SCAT5	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis;miR-200c both targeted the 3'-UTR of LUCAT1 and ABCB1 mRNA, suggesting the modulation of LUCAT1 on ABCB1 through sponging miR-200c;Rescue experiments confirmed the combined role of LUCAT1, miR-200c and ABCB1 on osteosarcoma proliferation, invasion and methotrexate resistance	29170124	RID00541	ceRNA or sponge
Colorectal cancer	CPS1-IT1	HIF1A	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-);cell autophagy(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000100644	NA	29034	3091	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA CPS1-IT1 suppresses EMT and metastasis of colorectal cancer by inhibiting hypoxia-induced autophagy through inactivation of HIF-1alpha;CPS1-IT1 suppresses EMT and autophagy by inhibiting the activation of HIF-1alpha in CRC	29017924	RID00542	expression association
Osteosarcoma	TUG1	FOXA1	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-212-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000129514	NA	55000	3169	LINC00080|NCRNA00080|TI-227H	HNF3A|TCF3A	LncRNA TUG1 promotes cell proliferation and suppresses apoptosis in osteosarcoma by regulating miR-212-3p/FOXA1 axis;FOXA1 was identified as a target of miR-212-3p and TUG1 functioned as a ceRNA to upregulate FOXA1 by sponging miR-212-3p in OS cells	29793327	RID00543	ceRNA or sponge
Triple-receptor negative breast cancer	CYTOR	BRCA1	negatively-E	RNAi;immunohistochemical staining	upregulation	qPCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000012048	NA	112597	672	C2orf59|LINC00152|NCRNA00152	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer;linc00152 partially enhanced breast cancer tumorigenesis by inactivation of the BRCA1/PTEN through DNA methyltransferases	29156515	RID00544	epigenetic regulation
Triple-receptor negative breast cancer	CYTOR	PTEN	negatively-E	RNAi;immunohistochemical staining	upregulation	qPCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171862	NA	112597	5728	C2orf59|LINC00152|NCRNA00152	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer;linc00152 partially enhanced breast cancer tumorigenesis by inactivation of the BRCA1/PTEN through DNA methyltransferases	29156515	RID00545	epigenetic regulation
Osteosarcoma	TP53COR1	miR-130b	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);PTEN/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	NA	GRCh38_6:36663392-36667296	NA	NA	102800311	NA	TRP53COR1|linc-p21|lincRNA-p21	NA	LncRNA-p21 inhibited the proliferation of osteosarcoma cells via the miR-130b/PTEN/AKT signaling pathway;lncRNA-p21 overexpression up-regulated the protein level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a well-known inhibitor of AKT signaling.Moreover, our gain and loss function assay showed that the promotion of PTEN by lncRNA-p21 was mediated by miR-130b, an oncogene overexpressed in OS tissue.PTEN expression was positively correlated with lncRNA-p21 expression in OS tissue (r = 0.630,p<0.0001), and PTEN expression was negatively correlated with miR-130b expression (r = 0.378,p= 0.0161)	29136769	RID00546	expression association
Osteosarcoma	TP53COR1	PTEN	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);PTEN/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000171862	NA	102800311	5728	TRP53COR1|linc-p21|lincRNA-p21	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-p21 inhibited the proliferation of osteosarcoma cells via the miR-130b/PTEN/AKT signaling pathway;lncRNA-p22 overexpression up-regulated the protein level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a well-known inhibitor of AKT signaling.Moreover, our gain and loss function assay showed that the promotion of PTEN by lncRNA-p21 was mediated by miR-130b, an oncogene overexpressed in OS tissue.PTEN expression was positively correlated with lncRNA-p21 expression in OS tissue (r = 0.630,p<0.0001), and PTEN expression was negatively correlated with miR-130b expression (r = 0.378,p= 0.0161)	29136769	RID00547	expression association
Malignant glioma	CASC2	MTOR	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+);cytotoxicity(+);cell autophagy(-)	ceRNA(miR-193a-5p)	regulation	NA	temozolomide	NA	Tumor Promoting Inflammation;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000198793	NA	255082	2475	C10orf5	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR-193a-5p and regulating mTOR expression;CASC2 is downregulated in gliomas, resulting in increased miR-193a-5p level and a decrease in mTOR expression, which further induces protective autophagy, leading to TMZ resistance	29136760	RID00548	ceRNA or sponge
Choriocarcinoma	MALAT1	FBXW8	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell proliferation(+)	ceRNA(miR-218)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000174989	NA	378938	26259	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FBW6|FBW8|FBX29|FBXO29|FBXW6	The long non-coding RNA MALAT1 interacted with miR-218 modulates choriocarcinoma growth by targeting Fbxw8;miR-218-mediated Fbxw8 regulation was required for MALAT1-induced choriocarcinoma cell proliferation	29096355	RID00549	ceRNA or sponge
Gastric cancer	DUXAP9	MMP9	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000100985	NA	503638	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long intergenic noncoding RNA 01296 aggravates gastric cancer cells progress through miR-122/MMP-9;LINC01296 sponged miR-122, which was proved to target MMP-9;LINC01296 was positively correlated with MMP-9 expression, while miR-122 was negatively correlated to it	29091895	RID00550	ceRNA or sponge
Malignant glioma	WSPAR	EPCAM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);self-renewal(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000119888	NA	105664404	4072	LncTCF7|TCONS_00009511	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	LncRNATCF7 promotes the growth and self-renewal of glioma cells via suppressing the miR-200c-EpCAM axis;lncTCF7 enhanced the self-renewal of glioma cells via up-regulating the expression of epithelial cell adhesion molecule (EpCAM);ncTCF7 bound to miR-200c and decreased the abundance of miR-200c	29091867	RID00551	ceRNA or sponge
Gastric cancer	GACAT3	miR-497	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	NA	104797537	NA	LINC01458|lncRNA-AC130710	NA	LncRNA GACAT3 promotes gastric cancer progression by negatively regulating miR-497 expression;GACAT3 directly binds to microRNA-497 (miR-497), and GACAT3 expression was inversely correlated with miR-497 expression	29091858	RID00552	ceRNA or sponge
Thyroid cancer	CCAT1	miR-143	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line;CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143;CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143	29791590	RID00553	ceRNA or sponge
Prostate cancer	HULC	BECN1	interact	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	radioresistance(-);cell autophagy(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000126581	NA	728655	8678	HCCAT1|LINC00078|NCRNA00078	ATG6|VPS30|beclin1	LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells;HULC knockdown promoted autophagy through interaction with Beclin-2 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.	29694502	RID00554	interact with protein
Prostate cancer	HULC	MTOR	positively-E	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	radioresistance(-);cell autophagy(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000198793	NA	728655	2475	HCCAT1|LINC00078|NCRNA00078	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells;HULC knockdown promoted autophagy through interaction with Beclin-2 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.	29694502	RID00555	expression association
Breast cancer	GACAT3	CCND2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236289	GRCh38_2:16013928-16087201	ENSG00000118971	NA	104797537	894	LINC01458|lncRNA-AC130710	KIAK0002|MPPH3	LncRNA GACAT3 predicts poor prognosis and promotes cell proliferation in breast cancer through regulation of miR-497/CCND2;GACAT3 and cyclin D2 (CCND2) contained a binding site of miR-497;GACAT3 may act as a ceRNA for miR-497, enhancing the expression of CCND2	29945347	RID00556	ceRNA or sponge
Urinary bladder cancer	H19	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression. Here we found that H19 levels are remarkably increased in bladder cancer tissues, and upregulated H19 promotes bladder cancer cell migration in vitro and in vivo. H19 is associated with enhancer of zeste homolog 2 (EZH2), and that this association results in Wnt/beta-catenin activation and subsequent downregulation of E-cadherin. A significant negative correlation is also observed between H19 levels and E-cad levels in vivo. These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression. Inhibition of E-cadherin expression by lnc-RNA H19 to facilitate bladder cancer metastasis;RNA interference is applied to knockdown H19 expression in bladder cancer cell, and found potentiated E-cadherin expression (p< 0.05), accompanied with weakened metastatic potency (p< 0.05)	23354591;29614625	RID00557	transcriptional regulation
Colorectal cancer	AB073614	JAK2	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);JAK/STAT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000096968	NA	NA	3717	NA	JTK10|THCYT3	LncRNA AB073614 induces epithelial-mesenchymal transition of colorectal cancer cells via regulating the JAK/STAT3 pathway;LncRNA AB073614 knockdown in SW480 and HCT116 cells significantly promoted the protein expression levels of E-cadherin and Occludin, and decreased the expressions of N-cadherin and Vimentin, then further decreased the cell migration and invasion ability. Interestingly, the expression of phosphorylated STAT3 was also down-regulated. Also, the Western blotting result326 showed that JAK inhibitor (AT9283) was able to block the STAT3 phosphorylation induced by lncRNA AB073614 overexpression. All these results indicate that lncRNA AB073614 can induce the expression of EMT cell markers and regulate the process of EMT of CRC cells through regulating the JAK/STAT3 pathway activation.	29439310	RID00558	expression association
Colorectal cancer	AB073614	STAT3	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);JAK/STAT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_3:149173591-149175492	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	LncRNA AB073614 induces epithelial- mesenchymal transition of colorectal cancer cells via regulating the JAK/STAT3 pathway;LncRNA AB073614 knockdown in SW480 and HCT116 cells significantly promoted the protein expression levels of E-cadherin and Occludin, and decreased the expressions of N-cadherin and Vimentin, then further decreased the cell migration and invasion ability. Interestingly, the expression of phosphorylated STAT3 was also down-regulated	29439310	RID00559	expression association
Lung cancer	DANCR	miR-216a	negatively-E	RIP;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712404-52720351	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	LncRNA DANCR Promotes Lung Cancer by Sequestering miR-216a;The miR-216a level in cancer cells was negatively correlated with DANCR expression;DANCR upregulation is a potential indicator of aggressive lung cancer	29651883	RID00560	ceRNA or sponge
Gastric cancer	TMEM238L	VIM	interact	RIP	downregulation	microarray	NA	NA	cancer progression(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000263429	GRCh38_17:10794913-10804099	ENSG00000026025	NA	100289255	7431	NA	NA	Long noncoding RNA LINC00675 enhances phosphorylation of vimentin on Ser83 to suppress gastric cancer progression;Mechanistic investigations revealed that LINC00675 interacted with vimentin, a protein involved in cell metastasis, and enhanced its phosphorylation level on Ser83 to result in the collapse of vimentin filament in GC cells	29107103	RID00561	interact with protein
Multiple myeloma	CCAT1	HOXA1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-181a-5p)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000105991	NA	100507056	3198	CARLO5|CARLo-5|onco-lncRNA-40	BSAS|HOX1|HOX1F	Long non-coding RNA CCAT1 promotes multiple myeloma progression by acting as a molecular sponge of miR-181a-5p to modulate HOXA1 expression;CCAT1 positively regulated HOXA1 expression through sponging miR-181a-5p in MM cells	29228867	RID00562	ceRNA or sponge
Breast cancer	GAS5	ATG3	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-23a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000144848	NA	60674	64422	NCRNA00030|SNHG2	APG3|APG3-LIKE|APG3L|PC3-96	Effect of the LncRNA GAS5-MiR-23a-ATG3 Axis in Regulating Autophagy in Patients with Breast Cancer;GAS5 was found to act as a microRNA sponge in a pathway that included miR-23a and its target gene ATG3	30007957	RID00563	ceRNA or sponge
Breast cancer	LINC00518	ABCC1	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-199a)	regulation	NA	adriamycin;vincristine;paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000183674	GRCh38_6:10429255-10435015	ENSG00000103222	NA	221718	4363	C6orf218	ABC29|ABCC|GS-X|MRP|MRP1	Linc00518 Contributes to Multidrug Resistance Through Regulating the MiR-199a/MRP1 Axis in Breast Cancer;linc00518 could act as a molecular sponge of miR-199a to repress MRP1 expression;MRP1 depletion increased the sensitivity of MCF-7/ADR cells to ADR, VCR and PTX, and this effect was attenuated following miR-199a inhibition or linc00518 overexpression	30001527	RID00564	ceRNA or sponge
Gastric cancer	RP11-789C1.1	CDH1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-5003)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000250266	GRCh38_4:170273919-170283079	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-Coding RNA RP11-789C1.1 Suppresses Epithelial to Mesenchymal Transition in Gastric Cancer Through the RP11-789C1.1/MiR-5003/E-Cadherin Axis;miR-5003 was the target of both RP11-789C1.1 and E-cadherin;at both the mRNA and protein level, silencing RP11-789C1.1 remarkably reduced the expression of E-cadherin and promoted EMT, which were reversed by knocking down miR-5003. LncRNA RP11-789C1.1 directly targets miR-5003-3p in gastric cancer;miR-5003-3p promotes migration, invasion, and EMT by directly targeting E-cadherin in gastric cancer	29991048	RID00565	ceRNA or sponge
Hepatocellular carcinoma	PVT1	INCENP	positively-E	RNAi;Tarbase;starBase;lncACTdb;TANRIC	upregulation	qPCR;microarray;sequencing	TCGA;GSE54236;GSE49515;GSE60502;GSE58208;GSE98269;GSE57957;GSE49713	LIHC.zip;GSE54236.zip;GSE49515.zip;GSE60502.zip;GSE58208.zip;GSE98269.zip;GSE57957.zip;GSE49713.zip	cell proliferation(+)	ceRNA(miR-424-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000149503	NA	5820	3619	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	A Preliminary Investigation of PVT1 on the Effect and Mechanisms of Hepatocellular Carcinoma: Evidence from Clinical Data, a Meta-Analysis of 840 Cases, and In Vivo Validation. The in silico prediction revealed that there were complementary sequences between PVT1 and miR-424-5p as well as between miR-424-5p and INCENP;whereas a positive correlation trend was found between PVT1 and INCENP based on data from TCGA; the upregulation of PVT1 could promote HCC cell proliferation in vitro and vivo	29975928	RID00566	ceRNA or sponge
Epithelial ovarian cancer	PCGEM1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000067560	NA	64002	387	LINC00071|NCRNA00071|PCAT9	ARH12|ARHA|RHO12|RHOH12	LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00567	expression association
Epithelial ovarian cancer	PCGEM1	YAP1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000137693	NA	64002	10413	LINC00071|NCRNA00071|PCAT9	COB1|YAP|YAP2|YAP65|YKI	LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00568	expression association
Epithelial ovarian cancer	PCGEM1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000087245	NA	64002	4313	LINC00071|NCRNA00071|PCAT9	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00569	expression association
Epithelial ovarian cancer	PCGEM1	BCL2L1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000171552	NA	64002	598	LINC00071|NCRNA00071|PCAT9	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00570	expression association
Epithelial ovarian cancer	PCGEM1	RPS6KB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000108443	NA	64002	6198	LINC00071|NCRNA00071|PCAT9	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.Upregulation of PCGEM1 induced cancer cell proliferation, migration, and invasion, but decreased cell apoptosis through upregulating RhoA, YAP (Yes-associated protein), MMP2 (matrix metalloproteinase 2), Bcl-xL, and P70S6K expression;LncRNA PCGEM1 Induces Ovarian Carcinoma Tumorigenesis and Progression Through RhoA Pathway.In conclusion, we suggest that PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP, P70S6K, MMP2, and Bcl-xL.	29949791	RID00571	expression association
Lung cancer	RCC2-AS1	RCC2	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell autophagy(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227751	GRCh38_1:17406760-17407382	ENSG00000179051	NA	114515514	55920	NA	TD-60	LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2;LCPAT1 was shown to bind to RCC2, and RCC2 mediated the effect of LCPAT1 on cell autophagy, migration, invasion and EMT in lung cancer	29913439	RID00572	interact with protein
Pancreatic cancer	LINC01121	GLP1R	negatively-E	luciferase reporter assay	upregulation	microarray	GSE14245;GSE27890;GSE16515	GSE14245.zip;GSE27890.zip;GSE16515.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cAMP/PKA signaling pathway(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000205054	GRCh38_2:45164816-45323397	ENSG00000112164	NA	400952	2740	UNQ6975	GLP-1|GLP-1-R|GLP-1R	LINC01121 Inhibits Cell Apoptosis While Facilitating proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R; GLP1R was indeed a target of LINC01121;the LINC01121 vector group exhibited increased expressions of LINC01121; decreased mRNA and protein levels of GLP1R, Bad, cAMP, and PKA; increased protein levels of CREB, Bcl-2, PCNA, p-PKA and p-CREB; increased cell proliferation, migration and invasion; and decreased cell apoptosis;LINC01121 functions as a tumor promoter by means of its involvement in the process of translational repression of the GLP1R and inhibition of the cAMP/PKA signaling pathway	29843149	RID00573	transcriptional regulation
Gastric cancer	MT1JP	RUNX3	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000020633	NA	4498	864	MT1|MT1J|MT1NP|MTB	AML2|CBFA3|PEBP2aC	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00574	ceRNA or sponge
Gastric cancer	MT1JP	CDKN1A	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000124762	NA	4498	1026	MT1|MT1J|MT1NP|MTB	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00575	expression association
Gastric cancer	MT1JP	BCL2L11	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000153094	NA	4498	10018	MT1|MT1J|MT1NP|MTB	NA	LncRNA MT1JP Suppresses Gastric Cancer Cell proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis;MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulation p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis;MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC	29742512	RID00576	expression association
Colorectal cancer	SH3PXD2A-AS1	CDKN1C	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000129757	NA	100505839	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID00577	epigenetic regulation
Colorectal cancer	SH3PXD2A-AS1	KLF2	negatively-E	RNAi;RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000127528	NA	100505839	10365	NA	LKLF	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID00578	epigenetic regulation
Colorectal cancer	HOTAIR	miR-203a-3p	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+);WNT/beta-catenin signaling pathway(+)	sponge	binding/interaction	RNA-RNA	cisplatin;paclitaxel	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR is a Prognostic Biomarker for the proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/beta-Catenin Signaling Pathway;HOTAIR interacts with miR-203a-3p.To analyze whether HOTAIR and miR-203a-3p could regulate drug-resistance of CRC cells, we treated CRC cells with CDDP after HOTAIR knockdown or miR-203a-3p overexpression. As expected, CDDP inhibited cell proliferation in a dose-dependent manner. HOTAIR knockdown or miR-203a-3p overexpression increased the sensitivity of CRC cells to CDDP. We confirmed these results with another chemotherapy drug, PTX. HOTAIR knockdown and miR-203a-3p overexpression increased the sensitivity of CRC cells to PTX.Therefore, these data suggested that HOTAIR could enhance the drug resistance of CRC cells.HOTAIR suppressed the expression of miR-203a-3p, thus inducing Wnt/beta-catenin signaling activation and CRC cell proliferation and chemoresistance enhancements.HOTAIR promotes the proliferation and chemoresistance of CRC cells through targeting miR-203a-3p-Wnt/beta-catenin signaling pathway.	29680837	RID00579	ceRNA or sponge
Hepatocellular carcinoma	LNCDQ	CDH1	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_1:155234457-155239960	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulation of LncDQ is Associated with Poor Prognosis and Promotes Tumor Progression via Epigenetic Regulation of the EMT Pathway in HCC;LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells	29669339	RID00580	epigenetic regulation
Malignant glioma	CYTOR	BMI1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-16)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000168283	NA	112597	648	C2orf59|LINC00152|NCRNA00152	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell proliferation and Invasion by Interacting with MiR-16;LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression.LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion	29669323	RID00581	ceRNA or sponge
Cervical cancer	SNHG12	miR-424-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000197989	GRCh38_1:28578538-28583132	NA	NA	85028	NA	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p;Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion	29533945	RID00582	ceRNA or sponge
Malignant glioma	SNHG16	PRMT5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-4518)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000100462	NA	100507246	10419	Nbla10727|Nbla12061|ncRAN	HRMT1L5|HSL7|IBP72|JBP1|SKB1|SKB1Hs	LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma;SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518;Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells	29529599	RID00583	ceRNA or sponge
Lung adenocarcinoma	LINC00707	CDC42	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000238266	GRCh38_10:6779549-6879450	ENSG00000070831	NA	100507127	998	NA	CDC42Hs|G25K|TKS	The Long Intergenic Noncoding RNA 00707 Promotes Lung Adenocarcinoma Cell proliferation and Migration by Regulating Cdc42;Microarray analysis and rescue assays suggested that Cdc42 is an important target gene involved in the carcinogenesis of LINC00707	29482190	RID00584	expression association
Lung cancer	EPEL	CCNB1	positively-E	RNAi	upregulation	microarray	GSE31210;GSE50081	GSE31210.zip;GSE50081.zip	cell proliferation(+);prognosis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_4:182138658-182144515	ENSG00000134057	NA	NA	891	NA	CCNB	The LncRNA EPEL Promotes Lung Cancer Cell proliferation Through E2F Target Activation;EPEL knockdown specifically down-regulated the expression of cell cycle-related E2F target genes, including Cyclin B1 (CCNB1), in lung cancer cells but not that of apoptosis- or metabolism-related E2F target genes. EPEL interacted with E2F1 and regulated the expression of the E2F target genes by changing the binding efficiency of E2F1 to the E2F target promoters.Moreover, the expression levels of EPEL and CCNB1 both alone and in combination were robust prognostic markers for lung cancer.	29448242	RID00585	expression association
Osteosarcoma	GAS5	TIMP2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-203a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000035862	NA	60674	7077	NCRNA00030|SNHG2	CSC-21K|DDC8	LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a;miR-203a was negatively regulated by lncRNA GAS5;TIMP2 was a target of miR-203a and the anti-growth and anti-metastasis actions of miR-203a suppression were reversed by TIMP2 silencel;lncRNA GAS5 silence, miR-203a overexpression, and TIMP2 silence could activate PI3K/AKT/GSK3beta signaling while block NF-kB signaling	29414815	RID00586	ceRNA or sponge
Clear cell renal cell carcinoma	DGCR5	EGFR	positively-F	RIP;mass spectrometry	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000146648	NA	26220	1956	LINC00037|NCRNA00037	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way.LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR	29393141	RID00587	interact with protein
Malignant glioma	HOXA-AS2	EGFR	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-373)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000146648	NA	285943	1956	HOXA3as	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis;HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways.	29310118	RID00588	ceRNA or sponge
Gastric cancer	ZEB1-AS1	miR-335-5p	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000237036	GRCh38_10:31206278-31320447	NA	NA	220930	NA	NA	NA	Downregulation of miR-335-5p by Long Noncoding RNA ZEB1-AS1 in Gastric Cancer Promotes Tumor proliferation and Invasion;miR-335-5p expression was downregulated and negatively correlated with ZEB1-AS1 expression in GC tissues;miR-335-5p expression was directly regulated by ZEB1-AS1	29215918	RID00589	ceRNA or sponge
Non-small cell lung cancer	PVT1	miR-497	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of LncRNA PVT1 inhibits tumorigenesis in non-small-cell lung cancer by regulating miR-497 expression;PVT1 could directly interact with miR-497;knockdown of PVT1 inhibited cell viability, invasion and induced apoptosis in NSCLC by regulating miR-497 expression	29133127	RID00590	ceRNA or sponge
Esophagus squamous cell carcinoma	miR-548k	NPTN-IT1	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000281183	GRCh38_15:73567012-73569294	NA	101241892	NA	lncRNA-LET	Up-regulated miR-548k promotes esophageal squamous cell carcinoma progression via targeting long noncoding RNA-LET;Mechanistically, we found that miR-548k directly targets and represses the expression of long noncoding RNA-LET (lncRNA-LET), and further down-regulates p53 and up-regulates NF90.	29126868	RID00591	ceRNA or sponge
Papillary thyroid carcinoma	BISPR	miR-21-5p	negatively-E	luciferase reporter assay;RNA pull-down assay	upregulation	microarray	NA	NA	cancer progression(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000282851	GRCh38_19:17405686-17419324	NA	NA	105221694	NA	lncBST2	NA	LncRNA BISPR promotes the progression of thyroid papillary carcinoma by regulating miR-21-5p;BISPR promoted the development of TPC cells by inhibiting miR-21-5p expression; BISPR stimulated propagation and invasiveness of TPC cells by depressing miR-21-5p	29856242	RID00592	expression association
Osteosarcoma	SNHG1	NOB1	positively-E	luciferase reporter assay	upregulation	microarray	GSE85537	GSE85537.zip	tumorigenesis(+);cell growth(+);cell migration(+);cell invasion(+)	ceRNA(miR-326)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000141101	NA	23642	28987	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ART-4|MST158|MSTP158|NOB1P|PSMD8BP1	Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma;SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS	29115574	RID00593	ceRNA or sponge
Multiple myeloma	NEAT1	MCL1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-193a)	regulation	NA	dexamethasone	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000143384	NA	283131	4170	LINC00084|NCRNA00084|TncRNA|VINC	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway;NEAT1 acts as a molecular sponge for miR-193a. The in-depth study revealed that during the development of DEX resistance in these cells, the miR-193a levels were decreased, which resulted in the increased expression of the target gene myeloid cell leukemia-1 (MCL1).MCL1,which acts as key determinants in cell proliferation,differentiation, and tumorigenesis, was identified as a downstream target of miR-193a.	29205703	RID00594	ceRNA or sponge
Pancreatic ductal adenocarcinoma	H19	E2F1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	The long noncoding RNA H19 promotes cell proliferation via E2F-1 in pancreatic ductal adenocarcinoma.In conclusion, H19 is overexpressed and plays oncogenic role in PDAC through promoting cancer cell proliferation via the upregulation of E2F-1.E2F-1 was overexpressed in PDAC tissues with possible correlation with H19 expression level. In conclusion, H19 is overexpressed and plays oncogenic role in PDAC through promoting cancer cell proliferation via the upregulation of E2F-1.Long noncoding RNA H19 derived miR-675 regulates cell proliferation by down-regulating E2F-1 in human pancreatic ductal adenocarcinoma;the suppressed cell proliferation caused by H19 knockdown could be rescued by inhibiting miR-675 expression	27573434;29344285	RID00595	expression association
Osteosarcoma	HULC	miR-122	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma;HULC functioned as an endogenous sponge for miR-122, and its silence functioned through upregulating miR-122	28688193	RID00596	ceRNA or sponge
Breast cancer	TP73-AS1	TFAM	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000108064	NA	57212	7019	KIAA0495|PDAM	MTDPS15|MTTF1|MTTFA|TCF6|TCF6L1|TCF6L2|TCF6L3	TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition;TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a	28639399	RID00597	ceRNA or sponge
Tongue cancer	Lnc-EGFR	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000258451	GRCh38_14:20693480-20707120	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long noncoding RNA Lnc-EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer;the oncogenic potential of Lnc-EGFR, which was achieved by positive regulation of EGFR in human tongue cancer	29138845	RID00598	expression association
Colorectal cancer	AC078922.1	miR-31	negatively-F	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(-)	sponge	binding/interaction	RNA-RNA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000257241	GRCh38_12:69946543-69947081	NA	NA	NA	NA	NA	NA	The long non-coding RNA ENST00000547547 reduces 5-fluorouracil resistance of colorectal cancer cells via competitive binding to microRNA-31;ENST00000547547 reduced the chemoresistance of 5-FU via competitive binding to miR-31 in 5-FU-resistant CRC cell lines	29115526	RID00599	ceRNA or sponge
Colorectal cancer	RP11-317J10.2	CCND1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_8:85442047-85464915	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Downregulation of LncRNA-RP11-317J10.2 promotes cell proliferation and invasion and predicts poor prognosis in colorectal cancer.This study reveals a crucial role for lncRNA-RP11-317J10.2 in CRC growth and invasion via upregulation of cyclin D1 expression. Cyclin D1 was upregulated by lncRNA-RP11-317J10.2 knockdown, and co-expression of cyclin D1-targeting siRNA abrogates the pro-tumorigenic effects of lncRNA-RP11-317J10.2 knockdown.	29073791	RID00600	expression association
Non-small cell lung cancer	PCAT7	miR-134-5p	negatively-F	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	prognosis(-);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000231806	GRCh38_9:94555054-94603990	NA	NA	101928099	NA	PCAN-R2	NA	Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC);Rescue assays were carried out to confirm the contribution of PCAT7 to the progression of NSCLC cells by targeting miR-134-5p.	29275424;28728844	RID00601	ceRNA or sponge
Non-small cell lung cancer	NPTN-IT1	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000148400	NA	101241892	4851	lncRNA-LET	AOS5|AOVD1|TAN1|hN1	Downregulation of long non-coding RNA LET predicts poor prognosis and increases Notch signaling in non-small cell lung cancer;highlight a novel lncRNA-LET/Notch axis in regulating NSCLC cell fate and tumor progression;we demonstrated that lncRNA-LET overexpression significantly reduced the expression of Notch1 intracellular Domain (NICD1) in H292 cells while knockdown of lncRNA-LET increased NICD1 expression in H1975 cells	29416684	RID00602	expression association
Breast cancer	SUMO1P3	miR-320a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000235082	GRCh38_1:160317403-160317706	NA	NA	474338	NA	NA	NA	The long non-coding RNA SUMO1P3 facilitates breast cancer progression by negatively regulating miR-320a;SUMO1P3 binds to miR-320a,which has been identified as a tumor suppressor in various cancers, including breast cancer	29312511	RID00603	ceRNA or sponge
Malignant glioma	PVT1	EZH2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2;exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion	29046366	RID00604	expression association
Esophagus squamous cell carcinoma	SNHG1	CDH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000039068	NA	23642	999	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00605	expression association
Esophagus squamous cell carcinoma	SNHG1	VIM	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000026025	NA	23642	7431	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00606	expression association
Esophagus squamous cell carcinoma	SNHG1	CDH2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000170558	NA	23642	1000	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CD325|CDHN|CDw325|NCAD	Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells	29081407	RID00607	expression association
Esophagus squamous cell carcinoma	SNHG1	NOTCH1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148400	NA	23642	4851	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AOS5|AOVD1|TAN1|hN1	knockdown of SNHG1 suppressed the Notch signaling pathway by reducing the Notch1 and Hes-1 expression levels in ESCC cells	29081407	RID00608	expression association
Esophagus squamous cell carcinoma	SNHG1	HES2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000069812	NA	23642	54626	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	bHLHb40	knockdown of SNHG1 suppressed the Notch signaling pathway by reducing the Notch1 and Hes-2 expression levels in ESCC cells	29081407	RID00609	expression association
Endometrial cancer	CCAT2	miR-216b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	Knockdown of lncRNA CCAT2 inhibits endometrial cancer cells growth and metastasis via sponging miR-216b;CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways	29036788	RID00610	ceRNA or sponge
Gastric cancer	CCAT1	miR-219-1	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	LncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miR-219-1.the roles of CCAT1 on cell proliferation, apoptosis and invasion were inhibited by miR-219-1;CAT1 promotes the tumorigenesis and progression of GC by negative-regulating miR-219-1.In addition, miR-219-1 was predicted and convinced a direct target of CCAT1.	29231252	RID00611	ceRNA or sponge
Urinary bladder cancer	HULC	ZIC2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000043355	NA	728655	7546	HCCAT1|LINC00078|NCRNA00078	HPE5	Long non-coding RNA HULC promotes bladder cancer cells proliferation but inhibits apoptosis via regulation of ZIC2 and PI3K/AKT signaling pathway; moreover, overexpression of HULC significantly up-regulated ZIC2 expression level	28946549	RID00612	expression association
Hepatocellular carcinoma	PVT1	miR-214	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes hepatocellular carcinoma progression through regulating miR-214.RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2).	28800314	RID00613	epigenetic regulation
Gastric cancer	SALL4	DANCR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101115	NA	ENSG00000226950	GRCh38_4:52712404-52720351	57167	57291	DRRS|HSAL4|ZNF797	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	Long noncoding RNA DANCR is activated by SALL4 and promotes the proliferation and invasion of gastric cancer cells;DANCR is activated by SALL4 in gastric cancer cells and exerted its oncogenic activities through the activation of beta-catenin pathway.	29416741	RID00614	transcriptional regulation
Pancreatic cancer	GAS5	PTEN	positively-E	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell metastasis(-)	ceRNA(miR-32-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA GAS5 suppresses pancreatic cancer metastasis through modulating miR-32-5p/PTEN axis;GAS5 positively regulated the expression of PTEN through miR-32-5p;GAS5 suppressed the proliferation, migration and invasion of PC cells through regulating miR-32-5p/PTEN axis.The interaction between GAS5 and miR-32-5p in PC cells	29225772	RID00615	ceRNA or sponge
Non-small cell lung cancer	CCAT1	SOX4	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-130a-3p)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000124766	NA	100507056	6659	CARLO5|CARLo-5|onco-lncRNA-40	EVI16	LncRNA CCAT1/miR-130a-3p axis increases cisplatin resistance in non-small-cell lung cancer cell line by targeting SOX4;CCAT1 directly interacted with miR-130a-3p and negatively regulated miR-130a-3p expression. CCAT1 contributed to DDP resistance of A549/DDP cells by down-regulating miR-130a-3p.miR-130a-3p was found to directly target SOX4 to suppress its expression.CCAT1/miR-130a-3p axis enhanced DDP resistance of NSCLC cells by targeting SOX4, providing potential targets to overcome DDP resistance and improve efficacy of chemotherapy for patients with NSCLC.	29020498	RID00616	ceRNA or sponge
Breast cancer	uc.38	PBX1	negatively-E	RIP;western blot	downregulation	qPCR	NA	NA	apoptosis process(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_1:161127332-161127555	ENSG00000185630	NA	NA	5087	NA	CAKUHED	uc.38 induces breast cancer cell apoptosis via PBX1;uc.38 negatively regulated the expression of the pre-B-cell leukaemia homeobox 1 (PBX1) protein and subsequently affected the expression of Bcl-2 family members, ultimately inducing breast cancer cell apoptosis	29312798	RID00617	interact with protein
Endometrial carcinoma	MEG3	PI3K	interact	RIP	downregulation	qPCR	NA	NA	tumorigenesis(-);cancer progression(-);PI3K signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 inhibit endometrial carcinoma tumorigenesis and progression through PI3K pathway; RNA immunoprecipitation assay (RIP) showed that MEG3 can combine directly with PI3K.	29094270	RID00618	interact with protein
Epithelial ovarian cancer	HAGLR	miR-133a-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	LncRNA HOXD-AS1 promotes epithelial ovarian cancer cells proliferation and invasion by targeting miR-133a-3p and activating Wnt/beta-catenin signaling pathway;HOXD-AS1 promoted cell proliferation, invasion, and EMT process through sponging miR-133a-3p in EOC cells	29239819	RID00619	ceRNA or sponge
Colorectal cancer	SOX21-AS1	MYO6	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000196586	NA	100507533	4646	NA	DFNA22|DFNB37	Long non-coding RNA SOX21-AS1 sponges miR-145 to promote the tumorigenesis of colorectal cancer by targeting MYO6;miR-145 was proved to be the target of SOX21-AS1;myosin VI (MYO6) was found to be one of the targets of miR-145	29217166	RID00620	ceRNA or sponge
Melanoma	FALEC	CDKN1A	negatively-E	RIP;western blot;ChIP;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000124762	NA	100874054	1026	FAL1|LINC00568|ncRNA-a1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21;we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21	29196104	RID00621	epigenetic regulation
Hepatocellular carcinoma	DLX6-AS1	MMP2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-203a)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000087245	NA	285987	4313	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA DLX6-AS1 aggravates hepatocellular carcinoma carcinogenesis by modulating miR-203a/MMP-2 pathway;miR-203a potentially targeted DLX6-AS1 3'-UTR, suggesting the interaction between miR-203a and DLX6-AS1. Furthermore, miR-203a also targeted MMP-2 mRNA 3'-UTR, which was validated by luciferase reporter assay;This results and findings provide a novel insight for HCC tumorigenesis	29145165	RID00622	ceRNA or sponge
Colorectal cancer	HNF1A-AS1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000168036	NA	283460	1499	C12orf27|HAS1|NCRNA00262	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00623	expression association
Colorectal cancer	HNF1A-AS1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000110092	NA	283460	595	C12orf27|HAS1|NCRNA00262	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00624	expression association
Colorectal cancer	HNF1A-AS1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000136997	NA	283460	4609	C12orf27|HAS1|NCRNA00262	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/beta-catenin signaling pathway;we found that decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/beta-catenin signaling pathway activity by downregulating the expression of beta-catenin,CCND1, and c-myc	29145164	RID00625	expression association
Urinary bladder cancer	ZEB2-AS1	miR-27b	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000238057	GRCh38_2:144517978-144521477	NA	NA	100303491	NA	ZEB2-AS|ZEB2AS|ZEB2NAT	NA	LncRNA ZEB2-AS1 promotes bladder cancer cell proliferation and inhibits apoptosis by regulating miR-27b;ZEB2-AS1 promoted tumorigenesis and development of BC through down-regulating tumor-suppressive miR-27b.According to the sequences of predicted binding sites be-tween ZEB2-AS1 and miR-27b, mutant (mut) and wild type (wt) frag-ment of ZEB2-AS1 were designed. relative luciferase activity of ZEB2-AS1-wt was significantly reduced by miR-27b mimic; while the relative luciferase activity of ZEB2-AS1-mut wasnot affected by the changes in miR-27b expression	28992472	RID00626	ceRNA or sponge
Triple-receptor negative breast cancer	CDKN2B-AS1	miR-199a	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL promotes carcinogenesis via sponging miR-199a in triple-negative breast cancer;miR-199a targeted ANRIL at 3'-UTR;Rescue experiments showed that miR-199a inhibitor could reverse the tumor-suppressing role of ANRIL knockdown on TNBC proliferation and apoptosis;ANRIL overexpression modulated TNBC tumorigenesis through acting as molecular 'sponge' for miR-199a	28961506	RID00627	ceRNA or sponge
B-cell acute lymphocytic leukemia	ZEB1-AS1	STAT3	positively-E	western blot	upregulation	qPCR	NA	NA	prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000168610	NA	220930	6774	NA	ADMIO|ADMIO1|APRF|HIES	LncRNA ZEB1-AS1 contributes to STAT3 activation by associating with IL-11 in B-lymphoblastic leukemia;ZEB1-AS1 could bind to IL-11 and promote IL-11 stability;ZEB1-AS1 promotes the activation of IL-11/STAT3 signaling pathway by associating with IL-11 in B-ALL;a high level of ZEB1-AS1 predicted poor prognosis of B-ALL patients	28861713	RID00628	expression association
Pancreatic cancer	HOTTIP	HOXA9	positively-E	RNAi	upregulation	qPCR;microarray	GSE61166	GSE61166.zip	cell stemness(+)	NA	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000078399	NA	100316868	3205	HOXA-AS6|HOXA13-AS1|NCRNA00213	ABD-B|HOX1|HOX1.7|HOX1G	LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9; HOTTIP mediated HOXA9 to enhance the Wnt/beta-catenin pathway by binding to WDR5 in PCSCs;the HOTTIP/WDR5/HOXA9/Wnt axis contributes to PCSC stemness and is a potential therapeutic target for PDAC.	28947139	RID00629	expression association
Colon cancer	HNF1A-AS1	SIRT1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000096717	NA	283460	23411	C12orf27|HAS1|NCRNA00262	SIR2|SIR2L1|SIR2alpha	Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA;HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway. These results suggested that HNF1A-AS1 regulate coloncancer cell apoptosis in part by modulating p53 expression.	28943452	RID00630	ceRNA or sponge
Colon cancer	HNF1A-AS1	TP53	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Colon cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000141510	NA	283460	7157	C12orf27|HAS1|NCRNA00262	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA;HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway. These results suggested that HNF1A-AS1 regulate coloncancer cell apoptosis in part by modulating p53 expression.	28943452	RID00631	expression association
Oral squamous cell carcinoma	UCA1	SF1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);chemoresistance(+)	ceRNA(miR-184)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168066	NA	652995	7536	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BBP|D11S636|MBBP|ZCCHC25|ZFM1|ZNF162	LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression;Mechanisms investigation indicated that UCA1 could interact with miR-184 to repress its expression.The OSCC nude mice model experiments demonstrated that depletion of UCA1 further boosted CDDP-mediated repression effect on tumor growth. UCA1 accelerated proliferation, increased CDDP chemoresistance and restrained apoptosis partly through modulating SF1 via sponging miR-184 in OSCC cells, suggesting that targeting UCA1 may be a potential therapeutic strategy for OSCC patients.	29125238	RID00632	ceRNA or sponge
Clear cell renal cell carcinoma	H19	E2F1	negatively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	Long non-coding RNA H19 regulates E2F1 expression by competitively sponging endogenous miR-29a-3p in clear cell renal cell carcinoma;down-regulated lncRNA-H19 could affect the expression of miR-29a-3p targeting E2F1 with competitively binding miR-29a-3p;Over expression of E2F1 could rescue lncRNA-H19 siRNA induced suppression on cell migration and invasion in ccRCC cells	29214011	RID00633	ceRNA or sponge
Prostate cancer	TP53COR1	PKM	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-);cell proliferation(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Prostate cancer	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000067225	NA	102800311	5315	TRP53COR1|linc-p21|lincRNA-p21	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	LincRNA-p21 suppresses development of human prostate cancer through inhibition of PKM2;We also found that the proliferation and tumorigenesis of lincRNA-p21-silenced prostate cancer cells were significantly inhibited after knocking down PKM2;We demonstrated that lincRNA-p21 blunted the prostate cancer cell proliferation and tumorigenic capacity through down-regulation of PKM2	28994148	RID00634	expression association
Chordoma	MIR31HG	miR-31	negatively-E	RIP;luciferase reporter assay;RNA pull-down assay;RNAi;qRT-PCR	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID00635	epigenetic regulation
Chordoma	MIR31HG	RNF144B	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-31)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000137393	NA	554202	255488	LncHIFCAR|hsa-lnc-31	IBRDC2|PIR2|bA528A10.3|p53RFP	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID00636	ceRNA or sponge
Pancreatic cancer	CRNDE	IRS1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-384)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000169047	NA	NA	3667	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HIRS-1	Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1;We identified miR-384 as a direct target for CRNDE; CRNDE positively regulated IRS1 expression through sponging miR-384	28940804	RID00637	ceRNA or sponge
Gastric cancer	GAS5	miR-222	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	The GAS5/miR-222 Axis Regulates proliferation of Gastric Cancer Cells Through the PTEN/Akt/mTOR Pathway; GAS5 directly targeted and suppressed miR-222 expression.GAS5 regulated GC cell proliferation through the PTEN/Akt/mTOR pathway by negatively regulating miR-222.	29098549	RID00638	ceRNA or sponge
Osteosarcoma	MIR210HG	miR-503	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000247095	GRCh38_11:565660-568457	NA	NA	100506211	NA	NA	NA	Long Noncoding RNA miR210HG Sponges miR-503 to Facilitate Osteosarcoma Cell Invasion and Metastasis;miR-503 was verified to be the target miRNA of miR210HG using bioinformatics online program and luciferase assayl;miR-503 could reverse the role of miR210HG on osteosarcoma cells	28972855	RID00639	ceRNA or sponge
Breast cancer	NEAT1	HMGA2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);cell growth(+);cell invasion(+)	ceRNA(miR-211)	regulation	NA	5-fluorouracil	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000149948	NA	283131	8091	LINC00084|NCRNA00084|TncRNA|VINC	BABL|HMGI-C|HMGIC|LIPO|STQTL9	The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer;LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis;the EMT-inducer HMGA2 was identified as a downstream target of miR-211. The interaction between NEAT1 and miR-211.	28720546	RID00640	ceRNA or sponge
Melanoma	BANCR	NOTCH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000134250	NA	100885775	4853	LINC00586	AGS2|HJCYS|hN2	BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR-204; We identified that miR 204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR 204;BANCR may promote melanoma cell growth through inhibition of miR 204, leading to the activation of Notch2 pathway;Our results suggest the BANCR/miR 204/Notch2 axis mediates melanoma cell proliferation and tumor progression	29075789	RID00641	ceRNA or sponge
Hepatocellular carcinoma	MALAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-143-3p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Non-Coding RNA MALAT1 Regulates ZEB1 Expression by Sponging miR-143-3p and Promotes Hepatocellular Carcinoma Progression;ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1;MALAT1 may regulate ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression;The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p	28543721	RID00642	ceRNA or sponge
Thyroid cancer	MALAT1	FGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138685	NA	378938	2247	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BFGF|FGF-2|FGFB|HBGF-2	LncRNA-MALAT1 Promotes Angiogenesis of Thyroid Cancer by Modulating Tumor-Associated Macrophage FGF2 Protein Secretion;overexpression of FGF2 blocked the effects of MALAT1 siRNAs on cell migration, invasion, and angiogenesis;MALAT1-mediated FGF2 protein secretion from TAMs inhibits inflammatory cytokines release, promotes proliferation, migration, and invasion of FTC133 cells and induces vasculature formation	28543663	RID00643	expression association
Osteosarcoma	GAS5	DIRAS3	positively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);epithelial to mesenchymal transition(-)	ceRNA(miR-221)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000162595	NA	60674	9077	NCRNA00030|SNHG2	ARHI|NOEY2	Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway.GAS5 could directly bind to miR-221 to decrease miR-221 expression and enhance ARHI expression;lncRNA GAS5 functions as a competing endogenous RNA for miR-221 to suppress cell growth and EMT in osteosarcoma by regulating the miR-221/ARHI pathway;Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway	28519068	RID00644	ceRNA or sponge
Medulloblastoma	CDKN2B-AS1	BRI3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-323)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164713	NA	100048912	25798	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	I3	Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on proliferation and Migration by Targeting miR-323;ANRIL acted as a sponge of miR-323 and its silence functioned through up-regulating miR-323;BRI3 and CDK6 were target genes of miR-323 and the effect of BRI3 on DAOY cells was the same as ANRIL;ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3;ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR-323-mediated regulation of BRI3, which could activate p38 MAPK, ERK, and AKT as well as Wnt signaling pathway	28513871	RID00645	ceRNA or sponge
Papillary thyroid carcinoma	PTCSC3	SCAI	positively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-574-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000173611	NA	100886964	286205	NA	C9orf126|NET40	LncRNA PTCSC3/miR-574-5p Governs Cell proliferation and Migration of Papillary Thyroid Carcinoma via Wnt/beta-Catenin Signaling; RNA Pull-down assay verified the bound of PTCSC3 and miR-574-5p; PTCSC3/miR-574-5p regulated the activity of Wnt/beta-catenin via SCAI and mediated cell proliferation and migration of PTC-1.	28513866	RID00646	ceRNA or sponge
Malignant glioma	CCAT1	FGFR3	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-181b)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000068078	NA	100507056	2261	CARLO5|CARLo-5|onco-lncRNA-40	ACH|CD333|CEK2|HSFGFR3EX|JTK4	lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b;Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process,and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b;CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRalpha.In conclusion,CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRalpha, which provides a potential therapeutic target for glioma treatment	28475287	RID00647	ceRNA or sponge
Malignant glioma	CCAT1	PDGFRA	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-181b)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000134853	NA	100507056	5156	CARLO5|CARLo-5|onco-lncRNA-40	CD140A|PDGFR-2|PDGFR2	lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b;Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process,and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b;CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRalpha.In conclusion,CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRalpha, which provides a potential therapeutic target for glioma treatment	28475287	RID00648	ceRNA or sponge
Hepatocellular carcinoma	LNCARSR	PTEN	negatively-F	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+)	interact with mRNA	binding/interaction	RNA-RNA	doxorubicin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000171862	NA	112577459	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA lncARSR Promotes Doxorubicin Resistance in Hepatocellular Carcinoma via Modulating PTEN-PI3K/Akt Pathway. lncARSR physically associates with PTEN mRNA, promotes PTEN mRNA degradation, decreases PTEN expression, and activates PI3K/Akt pathway;the effects of lncARSR overexpression on doxorubicin resistance could be reversed by PI3K/Akt pathway inhibitor, and lncARSR knockdown-induced doxorubicin sensitivity could be reversed by PTEN depletion	28464252	RID00649	interact with mRNA
Breast cancer	Lnc-BM	JAK2	positively-E	RIP;RNAi	upregulation	qPCR;microarray	GSE79540	GSE79540.zip	cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_14:62110875-62112546	ENSG00000096968	NA	NA	3717	NA	JTK10|THCYT3	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis;Lnc-BM increased JAK2 kinase activity to mediate oncostatin M- and IL-6-triggered STAT3 phosphorylation. In breast cancer cells, Lnc-BM promoted STAT3-dependent expression of ICAM1 and CCL2, which mediated vascular co-option and recruitment of macrophages in the brain, respectively. Recruited macrophages in turn produced oncostatin M and IL-6, thereby further activating the Lnc-BM/JAK2/STAT3 pathway and enhancing breast cancer brain metastases (BCBM).	29130936	RID00650	interact with protein
Breast cancer	Lnc-BM	STAT3	positively-E	RIP;RNAi	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:62110875-62112546	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis;Lnc-BM increased JAK2 kinase activity to mediate oncostatin M- and IL-6-triggered STAT3 phosphorylation. In breast cancer cells, Lnc-BM promoted STAT3-dependent expression of ICAM1 and CCL2, which mediated vascular co-option and recruitment of macrophages in the brain, respectively. Recruited macrophages in turn produced oncostatin M and IL-6, thereby further activating the Lnc-BM/JAK2/STAT3 pathway and enhancing breast cancer brain metastases (BCBM).	29130936	RID00651	expression association
Acute lymphocytic leukemia	WT1	MEG3	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000184937	NA	ENSG00000214548	GRCh38_14:100779410-100861031	7490	55384	AWT1|GUD|NPHS4|WAGR|WIT-2|WT33	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MEG3 is proven to be transcriptionally activated by Wilms' tumor 1 (WT1), dysregulation of which by epigenetic silencing or mutations is causally involved in AML;MEG3 is identified as a novel target of the WT1 molecule;Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways	28400619	RID00652	transcriptional regulation
Renal cell carcinoma	LINC-ROR	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000141510	NA	100885779	7157	ROR|lincRNA-RoR|lincRNA-ST8SIA3	BCC7|BMFS5|LFS1|P53|TRP53	lncRNA ROR promotes the proliferation of renal cancer and is negatively associated with favorable prognosis.The suppression of lncRNA ROR also induced an increase in the expression of p53 and a decrease in the expression of c-Myc in vitro;lncRNA ROR was expressed at high levels in RCC tissue and cell lines, and was associated with the proliferation ability of RCC cells	29039528	RID00653	expression association
Renal cell carcinoma	LINC-ROR	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136997	NA	100885779	4609	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MRTL|MYCC|bHLHe39|c-Myc	lncRNA ROR promotes the proliferation of renal cancer and is negatively associated with favorable prognosis.The suppression of lncRNA ROR also induced an increase in the expression of p53 and a decrease in the expression of c-Myc in vitro;lncRNA ROR was expressed at high levels in RCC tissue and cell lines, and was associated with the proliferation ability of RCC cells	29039528	RID00654	expression association
Non-small cell lung cancer	XIST	ATG7	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);cell autophagy(-)	ceRNA(miR-17)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000197548	NA	7503	10533	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	APG7-LIKE|APG7L|GSA7	Knockdown of lncRNA-XIST enhances the chemosensitivity of NSCLC cells via suppression of autophagy;knockdown of lncRNA-XIST significantly decreased autophagy by regulation of ATG7 as determined by qPCR and by western blotting;Knockdown of lncRNA-XIST restored the chemosensitivity of cisplatin-resistant A549 cells to cisplatin, which was reversed by miR-17 inhibitor and overexpression of ATG7 as determined by CCK8 assays.Dual-Luciferase reporter assays indicated that miRNA-17 can directly target ATG7; This study provides evidence that lncRNA-XIST may be a potential marker of poor response to cisplatin chemotherapy in NSCLC patients and the pathway 'lncRNA-XIST/miR-17/autophagy' may be a promising target for patients with chemoresistant NSCLC.	29130102	RID00655	ceRNA or sponge
Gastric cancer	MIAT	HDAC4	positively-E	RNAi;Targetscan;qRT-PCR;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-29a-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000068024	NA	440823	9759	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	AHO3|BDMR|HA6116|HD4|HDAC-4|HDAC-A|HDACA	lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis.our results demonstrated that MIAT competitively binds to miR-29a-3p and consequently upregulates the expression of HDAC4, which is a downstream target of miR-29a-3p;lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis;the present study highlighted the involvement of the MIAT/miR-29a-3p/HDAC4 axis in the development of GC	29039602	RID00656	ceRNA or sponge
Gastric cancer	MALAT1	ATG12	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	chemosensitivity(+);cell autophagy(+)	ceRNA(miR-23b-3p)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000145782	NA	378938	9140	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG12|APG12L|FBR93|HAPG12	Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer;MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells.In the functional aspect, we found that knockdown of MALAT1 sensitized SGC7901/VCR cells to cisplatin as illustrated by decreased IC50 concentration	29162158	RID00657	ceRNA or sponge
Pancreatic cancer	XIST	PPP1R13L	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-140;miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000104881	NA	7503	10848	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	IASPP|NKIP1|RAI|RAI4	The lncRNA XIST interacts with miR-140/miR-124/iASPP axis to promote pancreatic carcinoma growth; Further, the interaction between XIST and miR-140/miR-124, between miR-140/miR-124 and iASPP was validated using RNA immunoprecipitation assays with the AGO2 antibody. XIST positively correlated with iASPP and CDK1, inversely correlated with miR-140 and miR-124,respectively; XIST might be an oncogenic lncRNA that promoted proliferation of PC cell line through inhibiting miR-140/miR-124 expression and promoting cell cycle-related factor expression, and could be regarded as a therapeutic target in human pancreatic carcinoma	29371940	RID00658	ceRNA or sponge
Glioblastoma	lncHERG	miR-940	negatively-F	luciferase reporter assay	upregulation	microarray	GSE90598	GSE90598.zip	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA		GRCh38_7:66904120-66906297	NA	NA	NA	NA	NA	NA	Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma;Mechanistically, we found that lncHERG can serve as a sponge for miR-940 which is a tumor suppressor in cervical cancer;LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend	29296221	RID00659	ceRNA or sponge
Pancreatic cancer	NORAD	RHOA	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;microarray	GSE15471;GSE16515	GSE15471.zip;GSE16515.zip	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-125a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000067560	NA	647979	387	LINC00657	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer; NORAD may function as a ceRNA to regulate the expression of the small GTP binding protein RhoA through competition for hsa-miR-125a-3p, thereby promoting EMT	29121972	RID00660	ceRNA or sponge
Gastric cancer	DANCR	NPTN-IT1	negatively-E	RIP;RNAi;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	lncRNA	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000281183	GRCh38_15:73567012-73569294	57291	101241892	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	lncRNA-LET	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID00661	epigenetic regulation
Melanoma	ILF3-DT	miR-200b	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00662	epigenetic regulation
Melanoma	ILF3-DT	miR-200a	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00663	epigenetic regulation
Melanoma	ILF3-DT	miR-429	negatively-E	RNA pull-down assay;ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000267100	GRCh38_19:10651862-10653844	NA	NA	147727	NA	ILF3-AS1	NA	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID00664	epigenetic regulation
Breast cancer	SOX2	PVT1	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000181449	NA	ENSG00000249859	GRCh38_8:127794526-128187101	6657	5820	ANOP3|MCOPS3	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion;a transcriptional factor binding site was found between SOX2 and PVT1 promoter and the interaction between each other was further verified by chromatin immunoprecipitation (ChIP) analysis;These data suggest that elevated expression of SOX2 can activate lncRNA PVT1 expression promoted breast cancer tumorigenesis and progression.	28882595	RID00665	transcriptional regulation
Non-small cell lung cancer	NEAT1	MAPK6	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-98-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000069956	NA	283131	5597	LINC00084|NCRNA00084|TncRNA|VINC	ERK3|HsT17250|PRKM6|p97MAPK	NEAT1/hsa-mir-98-5p/MAPK6 axis is involved in non-small-cell lung cancer development;We speculated that NEAT1 may act as a competing endogenous lncRNA to upregulate MAPK6 by attaching hsa-mir-98-5p in lung cancers;NEAT1/hsa-mir-98-5p/MAPK6 is involved in the development and progress in NSCLC;Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa-mir-98-5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa-mir-98-5p	29095526	RID00666	ceRNA or sponge
Pancreatic cancer	UCA1	miR-135a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer by Sponging miR-135a;miR-135a reversed the effect of UCA1 on cell apoptosis rate and cell viability in SW1990 cells	28315290	RID00667	ceRNA or sponge
Uveal melanoma	FTH1P3	miR-224-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	miRNA	ENSG00000213453	GRCh38_2:27392784-27393367	NA	NA	2498	NA	FTHL3|FTHL3P	NA	Long non-coding RNA FTH1P3 facilitates uveal melanoma cell growth and invasion through miR-224-5p;Elevated expression of FTH1P3 enhanced uveal melanoma cell proliferation and migration by inhibiting miR-224-5p expression. Moreover, we found that FTH1P3 was a direct target gene of miR-224-5p in uveal melanoma cell.	29095823	RID00668	ceRNA or sponge
Cervical cancer	LINC00473	ILF2	positively-F	RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000143621	NA	90632	3608	C6orf176|LNC473|bA142J11.1	NF45|PRO3063	The long noncoding RNA LINC00473, a target of microRNA 34a, promotes tumorigenesis by inhibiting ILF2 degradation in cervical cancer;LINC00473 directly interacted with ILF2 and suppressed its degradation	29218240	RID00669	interact with mRNA
Malignant glioma	HOXA11-AS	EZH2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Regulation of HOXA11-AS/miR-214-3p/EZH2 axis on the growth, migration and invasion of glioma cells;HOXA11-AS functioned as a competing endogenous RNA (ceRNA) for miR-214-3p, which in turn positively regulated the expression of its direct target EZH2	28946213	RID00670	ceRNA or sponge
Hepatocellular carcinoma	PCAT1	HMGB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000189403	NA	100750225	3146	PCA1|PCAT-1	HMG-1|HMG1|HMG3|SBP-1	Long noncoding RNA PCAT-1 promotes invasion and metastasis via the miR-129-5p-HMGB1 signaling pathway in hepatocellular carcinoma;PCAT-1 could act as an endogenous RNA by directly binding to miR-129-5p;PCAT-1 repressed inhibitory effect of miR-129-5p and reverse high mobility group box 1 (HMGB1) expression, a target gene of miR-129-5p	28931210	RID00671	ceRNA or sponge
Prostate cancer	PCAT1	FSCN1	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000075618	NA	100750225	6624	PCA1|PCAT-1	FAN1|HSN|SNL|p55	Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer;PCAT-1 could act as a miR-145-5p sponge to modulate FSCN1 expression;PCAT-1 accelerated PC cell proliferation, migration, invasion and suppressed apoptosis by up-regulating FSCN1 mediated via miR-145-5p;Rescue experiments demonstrated that miR-145-5p restoration attenuated the promotive effects of PCAT1 on PC progression, while Fascin-1 (FSCN1) upregulation relieved the anti-cancer role of miR-145-5p in PC	28922730	RID00672	ceRNA or sponge
Triple-receptor negative breast cancer	MALAT1	miR-129-5p	negatively-F	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer;we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p.MALAT1 regulated miR-129-5p expression by directly binding to it.	28915533	RID00673	ceRNA or sponge
Malignant glioma	HOTTIP	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000148516	NA	100316868	6935	HOXA-AS6|HOXA13-AS1|NCRNA00213	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA HOTTIP promotes hypoxia-induced epithelial-mesenchymal transition of malignant glioma by regulating the miR-101/ZEB1 axis;HOTTIP sponged endogenous miR-101 and inhibited its activity, which resulted in increased ZEB1 expression and promoted process of EMT	28886531	RID00674	ceRNA or sponge
Non-small cell lung cancer	FEZF1-AS1	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000039068	NA	154860	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID00675	epigenetic regulation
Gastric cancer	UCA1	GRK2	negatively-F	RNA pull-down assay;RIP;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000173020	NA	652995	156	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADRBK1|BARK1|BETA-ARK1	Long noncoding RNA UCA1 promotes tumour metastasis by inducing GRK2 degradation in gastric cancer;we report that the lncRNA UCA1 increases the metastatic ability of gastric cancer (GC) cells by regulating GRK2 protein stability by promoting Cbl-c-mediated GRK2 ubiquitination and degradation;This process then activates the ERK-MMP9 signalling pathway. LncRNA UCA1 interacts with GRK2 and promotes GRK2 degradation via ubiquitination.	28843497	RID00676	interact with protein
Lung cancer	LINC00963	PGK1	positively-F	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+);AKT/mTOR signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000204054	GRCh38_9:129476946-129513687	ENSG00000102144	NA	100506190	5230	MetaLnc9	HEL-S-68p|MIG10|PGKA	MetaLnc9 Facilitates Lung Cancer Metastasis via a PGK1-Activated AKT/mTOR Pathway;Mechanistic investigations showed that LINC00963 (MetaLnc9) interacted with the glycolytic kinase PGK1 and prevented its ubiquitination in NSCLC cells, leading to activation of the oncogenic AKT/mTOR signaling pathway.	28923857	RID00677	interact with protein
Intrahepatic cholangiocarcinoma	CCAT1	miR-152	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	LncRNA-CCAT1 Promotes Migration, Invasion, and EMT in Intrahepatic Cholangiocarcinoma Through Suppressing miR-152.bioinformatics analysis and luciferase reporter assay revealed that CCAT1 directly bound to the miR-152, which has been reported to serve as a tumor suppressor in variety cancers.	28921383	RID00678	ceRNA or sponge
Lung cancer	YY1	PVT1	positively-E	ChIP;luciferase reporter assay;DNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lung cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000249859	GRCh38_8:127794526-128187101	7528	5820	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Transcription Factor YY1 Modulates Lung Cancer Progression by Activating lncRNA-PVT1;we showed that YY1 could directly bind to the promoter region of (long noncoding RNA-plasmacytoma variant translocation 1 [lncRNA-PVT1]) and activated its transcription through the consensus YY1 motif	28972861	RID00679	transcriptional regulation
Nasopharynx carcinoma	HOTAIR	FASN	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000169710	NA	100124700	2194	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FAS|OA-519|SDR27X1	LncRNA HOTAIR contributes to the tumorigenesis of nasopharyngeal carcinoma via up-regulating FASN;Knockdown of HOTAIR led to downregulation of FASN in NPC cells, thus suppressing cell proliferation and invasion;We suggest that HOTAIR is important in the progression and recurrence of NPC, perhaps through upregulating FASN	29228426	RID00680	expression association
Hepatocellular carcinoma	NORAD	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000171862	NA	647979	5728	LINC00657	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression;we identified that both LINC00657 and PTEN mRNA were targets of miR-106a-5p by using dual-luciferase reporter assay	28919047	RID00681	ceRNA or sponge
Osteosarcoma	XIST	PDCD4	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-21-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000150593	NA	7503	27250	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	H731	Long non-coding RNA XIST regulates PDCD4 expression by interacting with miR-21-5p and inhibits osteosarcoma cell growth and metastasis;we affirmed that XIST regulated PDCD4 expression by competitively binding to miR-21-5p. XIST inhibited cell proliferation and cell mobility by competitively binding to miR-21-5p and upregulating PDCD4 in OS	29048648	RID00682	ceRNA or sponge
Osteosarcoma	SOX2-OT	SOX2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell motility(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000181449	NA	347689	6657	NCRNA00043|SOX2OT	ANOP3|MCOPS3	LncRNA SOX2-OT is a novel prognostic biomarker for osteosarcoma patients and regulates osteosarcoma cells proliferation and motility through modulating SOX2;LncRNA SOX2-OT positively regulated SOX2 expression in osteosarcoma cells and positively associated with SOX2 expression in osteosarcoma tissues. The rescued-function studies suggested that SOX2 is necessary for lncRNA SOX2-OT induced osteosarcoma cells migration, invasion, and expression of cancer stem cell biomarkers	28960757	RID00683	expression association
Hepatocellular carcinoma	MEG3	ADH4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-664)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000198099	NA	55384	127	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ADH-2|HEL-S-4	Overexpression of Long Non-Coding RNA MEG3 Inhibits proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA-664;MEG3 over-expression imposes another level of post-transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR-664 target gene, ADH4, through competitive sponging miR-664;MEG3 overexpression inhibited the proliferation of HCC cells, at least in part by affecting miR-664 mediated regulation of ADH4.	28374914	RID00684	ceRNA or sponge
Ovarian cancer	DLEU1	CDK1	positively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-490-3p)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000176124	GRCh38_13:50082169-50906856	ENSG00000170312	NA	10301	983	BCMS|BCMS1|DLB1|DLEU2|LEU1|LEU2|LINC00021|NCRNA00021|XTP6	CDC2|CDC28A|P34CDC2	DLEU1 contributes to ovarian carcinoma tumourigenesis and development by interacting with miR-490-3p and altering CDK1 expression;Short interfering RNA silencing of DLEU1 produced opposite results, where qRT-PCR showed increased miR-490-3p expression;The dual-luciferase reporter assay revealed a direct interaction between DLEU1 and miR-490-3p;we suggest that through interaction with miR-490-3p, DLEU1 may influence the expression of CDK1, CCND1 and SMARCD1 protein, subsequently promoting the development and progression of EOC. MiR-490-3p plays a tumour suppressor role in epithelial ovarian cancer by targeting CDK1 regulation and influencing SMARCD1 and cyclin D1 (CCND1) expressions.	28598010	RID00685	ceRNA or sponge
Colorectal cancer	PCAT1	MYC	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000136997	NA	100750225	4609	PCA1|PCAT-1	MRTL|MYCC|bHLHe39|c-Myc	Down regulation of the long non-coding RNA PCAT-1 induced growth arrest and apoptosis of colorectal cancer cells;Our study revealed a tumorigenic effect of lncRNA PCAT-1 in CRC cells, and this effect is partly dependent on the inhibition of c-myc	28855110	RID00686	expression association
Malignant glioma	PWAR5	EZH2	interact	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-);cancer progression(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000279192	GRCh38_15:24985053-24988232	ENSG00000106462	NA	8123	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA PAR5 inhibits the proliferation and progression of glioma through interaction with EZH2;in vitro restoration of PAR5 expression inhibited human glioma cell proliferation, invasion and migration by binding to EZH2 and regulating oncogene expression	29048683	RID00687	interact with protein
Malignant glioma	SNHG15	VEGFA	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-153)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000112715	NA	285958	7422	C7orf40|Linc-Myo1g|MYO1GUT	MVCD1|VEGF|VPF	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis.According to the bioinformatic database (RNAhybrid), we predicted that SNHG15 may be associated with the miR-153 binding sites. Furthermore, dual-luciferase gene reporter assay proved that SNHG15 could bind to miR-153 at the predicted binding sites.miR-153 binds to the 3'-UTR of VEGFA and Cdc42.	29048682	RID00688	ceRNA or sponge
Malignant glioma	SNHG15	CDC42	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(-)	ceRNA(miR-153)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000070831	NA	285958	998	C7orf40|Linc-Myo1g|MYO1GUT	CDC42Hs|G25K|TKS	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation;knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis	29048682	RID00689	ceRNA or sponge
Breast cancer	AP000439.3	CCND1	positively-E	western blot;RNAi	downregulation	sequencing	GSE64590;TCGA	GSE64590.zip;BRCA.zip	cell cycle(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000261347	GRCh38_11:69467598-69469705	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Silencing one of most prominent lncRNA, AP000439.3, resulted in inhibition of cell cycle progression and proliferation. Further study revealed AP000439.3 can regulate expression of CCND1 through enhancing estrogen receptor induction of CCND1;Genome-wide study of ER-regulated lncRNAs shows AP000439.3 may function as a key regulator of cell cycle in breast cancer	29048636	RID00690	expression association
Non-small cell lung cancer	MIAT	ZEB1	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000148516	NA	440823	6935	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer;the knockdown of MIAT significantly downregulated the expression of the zinc finger E-box binding homeobox 1 (ZEB1), that was upregulation in NSCLC and that promoted cell invasion;we found that MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner;MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ZEB1 pathway	28843520	RID00691	ceRNA or sponge
Gastric cancer	MT1DP	MT1F	positively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000205361	GRCh38_16:56643705-56644786	ENSG00000198417	NA	326343	4494	MTM	MT1	Decreased long non-coding RNA MTM contributes to gastric cancer cell migration and invasion via modulating MT1F;we found a positive correlation between the expression level of MTM and MT1F both in cell and tissue samples;MT1F overexpression decreased GC cell migration and invasion, while knockdown of MT1F restored cell migration and invasion in MTM-overexpressing GC cells, suggesting MT1F as a key target of MTM	29228617	RID00692	expression association
Renal cell carcinoma	RP11-436H11.5	BCL2L2	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-335-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000105618	GRCh38_5:124734618-124735175	ENSG00000129473	NA	NA	599	NA	BCL-W|BCL2-L-2|BCLW|PPP1R51	LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma;Luciferase reporter assay results demonstrated that lncRNA RP11-436H11.5 enhanced BCL-W expression by regulating miR-335-5p expression. LncRNA RP11-436H11.5 could function as a miR-335-5p decoy to derepress expression of BCL-W	29070041	RID00693	ceRNA or sponge
Colorectal cancer	SNHG17	CDKN1C	negatively-E	RIP;ChIP;RNAi	upregulation	microarray	GSE21510	GSE21510.zip	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000196756	GRCh38_20:38419638-38435409	ENSG00000129757	NA	388796	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long non-coding RNA SNHG17 is an unfavourable prognostic factor and promotes cell proliferation by epigenetically silencing P57 in colorectal cancer;Mechanistic studies revealed the capability of lncRNA SNHG17 to epigenetically suppress P57 by binding to enhancer of zeste homolog 2 (a key component of polycomb repressive complex 2) in CRC cells, and quantitative real-time polymerase chain reaction assays demonstrated that SNHG17 expression levels were inversely correlated with those of P57 in CRC tissues	28933484	RID00694	epigenetic regulation
Urinary bladder cancer	MALAT1	BCL2	positively-E	CRISPR;qRT-PCR;RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells;the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes (Bcl-2 and MMP-13).MALAT1 may suppress miR-125b by acting as a molecular sponge in bladder cancer. All together, these data suggest that the MALAT1-miR-125b-Bcl-2/MMP-13 axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	29151968	RID00695	ceRNA or sponge
Urinary bladder cancer	MALAT1	MMP13	positively-E	CRISPR;qRT-PCR;RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell invasion(+)	ceRNA(miR-125b)	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137745	NA	378938	4322	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG3|MANDP1|MDST|MMP-13	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells;the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes (Bcl-2 and MMP-13).MALAT1 may suppress miR-125b by acting as a molecular sponge in bladder cancer. All together, these data suggest that the MALAT1-miR-125b-Bcl-2/MMP-13 axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	29151968	RID00696	ceRNA or sponge
Colorectal cancer	UICLM	ZEB2	positively-E	IHC;RIP;luciferase reporter assay	upregulation	microarray	NA	NA	cell metastasis(+)	ceRNA(miR-215)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000233392	GRCh38_2:240954617-240967451	ENSG00000169554	NA	NA	9839	NA	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA UICLM promotes colorectal cancer liver metastasis by acting as a ceRNA for microRNA-215 to regulate ZEB2 expression;Mechanistic investigations revealed that UICLM induced its biological effects by regulating ZEB2, as the oncogenesis facilitated by UICLM was inhibited by ZEB2 depletion	29187907	RID00697	ceRNA or sponge
Hepatocellular carcinoma	Lnc-Myd88	MYD88	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:38103490-38122445	ENSG00000172936	NA	NA	4615	NA	MYD88D	Long non-coding RNA Myd88 promotes growth and metastasis in hepatocellular carcinoma via regulating Myd88 expression through H3K27 modification;we confirmed a new long non-coding RNA Myd88 aberrant upregulation in HCC located upstream of Myd88 and verified a positive regulation relationship between them indicating that Lnc-Myd88 might participate in the enhanced expression of Myd88 in HCC;ChIP assays demonstrated that Lnc-Myd88 might increase Myd88 expression through enhancing H3K27Ac in the promoter of Myd88 gene, thus resulting in the activation of both NF-kB and PI3K/AKT signal pathways	29022910	RID00698	epigenetic regulation
Epithelial ovarian cancer	HULC	ATG7	negatively-F	RIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000197548	NA	728655	10533	HCCAT1|LINC00078|NCRNA00078	APG7-LIKE|APG7L|GSA7	The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma;our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1;RIP indicated that ATG7 interacted with HULC	29022892	RID00699	interact with protein
Epithelial ovarian cancer	HULC	ITGB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000150093	NA	728655	3688	HCCAT1|LINC00078|NCRNA00078	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma;our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1;We found that ITGB1 siRNA co-transfection with HULC reversed the function of HULC in inducing ovarian cancer cell migration and invasive ability	29022892	RID00700	expression association
Renal cell carcinoma	PVT1	MCL1	positively-E	western blot;RNAi	upregulation	qPCR;sequencing	TCGA	KIRC.zip	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000143384	NA	5820	4170	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Long noncoding RNA PVT1 inhibits renal cancer cell apoptosis by up-regulating Mcl-1. PVT1 knockdown promoted apoptosis, inhibited renal cancer cell proliferation, decreased Mcl-1, and increased cleaved caspase-3 and cleaved PARP. PVT1 increased Mcl-1 mRNA levels in renal cancer cells by promoting mRNA stability without influencing its transcription.	29254209	RID00701	expression association
Colon cancer	CCAT1	ITPKB	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(-)	ceRNA(miR-410)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colon cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000143772	NA	100507056	3707	CARLO5|CARLo-5|onco-lncRNA-40	IP3-3KB|IP3K|IP3K-B|IP3KB|PIG37	Long noncoding RNA CCAT1 functions as a ceRNA to antagonize the effect of miR-410 on the down-regulation of ITPKB in human HCT-116 and HCT-8 cells;In summary, these data demonstrated that miR-410 could promote cell proliferation and reduce apoptosis by inhibiting ITPKB expression and the expression of lnc CCAT1 antagonized the effect of miR-410.	29190961	RID00702	ceRNA or sponge
Nasopharynx carcinoma	XIST	miR-29c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	radioresistance(-);cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Downregulation of lncRNA X Inactive Specific Transcript (XIST) Suppresses Cell proliferation and Enhances Radiosensitivity by Upregulating mir-29c in Nasopharyngeal Carcinoma Cells;Knockdown of XIST and miR-29c overexpression both resulted in a dramatic suppression of cell proliferation, a marked enhancement of radiosensitivity, and an obvious increase of gamma-H2AX foci formation in NPC cells;Luciferase reporter assay and qRT-PCR analysis demonstrated that XIST interacts with miR-29c and negatively regulates its expression	28985197	RID00703	ceRNA or sponge
Non-small cell lung cancer	SNHG20	CDKN1A	negatively-E	RIP;RNAi;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000124762	NA	654434	1026	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA SNHG20 promotes non-small cell lung cancer cell proliferation and migration by epigenetically silencing of P21 expression;SNHG20 could interact with EZH2 (enhancer of zeste homolog 2), thereby repressing P21 expression	28981099	RID00704	epigenetic regulation
Osteosarcoma	FOXC2-AS1	MMP2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-3182)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000087245	NA	103752587	4313	ODRUL	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA ODRUL Contributes to Osteosarcoma Progression through the miR-3182/MMP2 Axis;ODRUL knockdown significantly inhibits OS cell proliferation, migration, invasion, and tumor growth in vitro and in vivo by decreasing matrix metalloproteinase (MMP) expression;ODRUL could directly interact with miR-3182 and upregulate MMP2 expression via its competing endogenous RNA activity on miR-3182 at the posttranscriptional level.	28750740	RID00705	ceRNA or sponge
Nasopharynx carcinoma	MALAT1	CAPNS1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000126247	NA	378938	826	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1/miR-124/Capn4 axis regulates proliferation, invasion and EMT in nasopharyngeal carcinoma cells; MALAT1 promoted proliferation, invasion and EMT of NPC cells through de-repressing Capn4 by sponging miR-124	28857668	RID00706	ceRNA or sponge
Urinary bladder cancer	H19	DNMT3B	positively-E	luciferase reporter assay;IHC;IF;RNA pull-down assay;RIP	upregulation	qPCR;microarray	GSE89006	GSE89006.zip	epithelial to mesenchymal transition(+);cell metastasis(+)	ceRNA(miR-29b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000088305	NA	283120	1789	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ICF|ICF1|M.HsaIIIB	lncRNA H19 regulates epithelial-mesenchymal transition and metastasis of bladder cancer by miR-29b-3p as competing endogenous RNA;Mechanistically, we proved that H19 could directly bind to miR-29b-3p (miR-29b) and derepress the expression of target DNMT3B;we demonstrated for the first time that H19 might function as ceRNA (competing endogenous RNA) for miR-29b-3p and relieve the suppression for DNMT3B, which led to EMT and metastasis of BC	28779971	RID00707	ceRNA or sponge
Malignant glioma	GAS5	FOXO1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell stemness(-);tumor malignant transformation(-)	ceRNA(miR-196a-5p)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Brain glioma	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150907	NA	60674	2308	NCRNA00030|SNHG2	FKH1|FKHR|FOXO1A	GAS5 suppresses malignancy of human glioma stem cells via a miR-196a-5p/FOXO1 feedback loop;We demonstrate that GAS5 suppresses GSC malignancy by binding to miR-196a-5p. miR-196a-5p, an onco-miRNA, stimulates GSC proliferation, migration, and invasion, in addition to reducing levels of apoptosis;miR-196a-5p specifically downregulates the expression of forkhead box protein O1 (FOXO1) by targeting its 3' untranslated region (3'-UTR);we also show that FOXO1 promotes GAS5 transcription, thus forminga positive feedback loop	28666797	RID00708	ceRNA or sponge
Hepatocellular carcinoma	NEAT1	miR-613	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1 promotes cell proliferation and invasion in hepatocellular carcinoma by negative regulating miR-613 expression;we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression;lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1.miR-613 isa target of NEAT1 in HCC cells.	28783584	RID00709	ceRNA or sponge
Hepatocellular carcinoma	GHET1	ATF1	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000123268	NA	102723099	466	lncRNA-GHET1	EWS-ATF1|FUS/ATF-1|TREB36	LncRNA GHET1 activated by H3K27 acetylation promotes cell tumorigenesis through regulating ATF1 in hepatocellular carcinoma;RNA pull-down assays supported that GHET1 could bind to ATF1 protein; overexpression of ATF1 almost completely reversed the GHET1 knockdown mediated inhibition on the proliferation, migration, invasion and EMT of HCC cells	28772210	RID00710	interact with protein
Cholangiocarcinoma	PCAT1	WNT1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cancer progression(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000125084	NA	100750225	7471	PCA1|PCAT-1	BMND16|INT1|OI15	Long noncoding RNA PCAT1 regulates extrahepatic cholangiocarcinoma progression via the Wnt/beta-catenin-signaling pathway;PCAT1 is a competing endogenous for microRNA (miR)-122, with bioinformatics analysis and luciferase-reporter assay results demonstrating that PCAT1 regulated WNT1 expression via miR-122;PCAT1 silencing inhibited ECC progression by reducing Wnt/beta-catenin signaling through miR-122 repression and WNT1 expression	28753454	RID00711	ceRNA or sponge
Endometrial cancer	HOTAIR	BECN1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000126581	NA	100124700	8678	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ATG6|VPS30|beclin1	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00712	expression association
Endometrial cancer	HOTAIR	ABCB1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000085563	NA	100124700	5243	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00713	expression association
Endometrial cancer	HOTAIR	ABCB4	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000005471	NA	100124700	5244	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells;It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression;RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR	28721581	RID00714	expression association
Osteosarcoma	DANCR	AXL	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);cell stemness(+)	ceRNA(miR-33a-5p)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000167601	NA	57291	558	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	ARK|JTK11|Tyro7|UFO	lncRNA DANCR promotes tumor progression and cancer stemness features in osteosarcoma by upregulating AXL via miR-33a-5p inhibition;pull-down assays and luciferase reporter assays indicated that DANCR upregulation expression of the receptor tyrosine kinase AXL by competitively binding to miR-33a-5p;DANCR increases CSCs function by upregulating AXL via competitively binding to miR-33a-5p, and this function is sequentially performed through the PI3K-Akt signaling pathway	28642170	RID00715	ceRNA or sponge
Non-small cell lung cancer	BLACAT1	miR-144	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000281406	GRCh38_1:205434885-205457091	NA	NA	101669762	NA	LINC00912|linc-UBC1|onco-lncRNA-30	NA	Long Noncoding RNA Bladder Cancer Associated Transcript 1 Promotes the proliferation, Migration, and Invasion of Nonsmall Cell Lung Cancer Through Sponging miR-144; Bioinformatics methods and luciferase reporter assay revealed the close link within miR-144 and BLACAT1 3'-untranslated region (UTR)	28885863	RID00716	ceRNA or sponge
Malignant glioma	HOXA11-AS	miR-140-5p	negatively-F	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Long Noncoding RNA HOXA11-AS Functions as miRNA Sponge to Promote the Glioma Tumorigenesis Through Targeting miR-140-5p;Bioinformatics prediction forecast that miR-140-5p directly targeted HOXA11-AS at 3'-UTR, which was confirmed by luciferase reporter assay;In vitro rescue experiment assays, miR-140-5p inhibitor transfection, could reverse the function of HOXA11-AS knockdown on the proliferation, cell cycle arrest, and apoptosis	28832185	RID00717	ceRNA or sponge
Uveal melanoma	HOXA11-AS	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124762	NA	221883	1026	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID00718	epigenetic regulation
Uveal melanoma	HOXA11-AS	miR-124	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID00719	ceRNA or sponge
Lung adenocarcinoma	CASC2	SOX4	negatively-E	RNAi	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000124766	NA	255082	6659	C10orf5	EVI16	Long noncoding RNA CASC2 inhibits metastasis and epithelial to mesenchymal transition of lung adenocarcinoma via suppressing SOX4;epithelial to mesenchymal transition (EMT) process of LAC cells and SOX4 expression was suppressed by upregulating CASC2	29131257	RID00720	expression association
Gastric cancer	SNHG7	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000147883	NA	84973	1030	NCRNA00061	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of gastric cancer cells by repressing the P15 and P16 expression;Relative expression of SNHG7 is upregulation in gastric cancer tissues and cells, and partially contributes to the development and progression of gastric cancer through regulation of p15 and p16 expressions	29131253	RID00721	expression association
Gastric cancer	SNHG7	CDKN2A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000147889	NA	84973	1029	NCRNA00061	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of gastric cancer cells by repressing the P15 and P16 expression;Relative expression of SNHG7 is upregulation in gastric cancer tissues and cells, and partially contributes to the development and progression of gastric cancer through regulation of p15 and p16 expressions	29131253	RID00722	expression association
Gastric cancer	MEG3	TP53	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	lncRNA MEG3 inhibit proliferation and metastasis of gastric cancer via p53 signaling pathway;overexpression of lncRNA MEG3 could also increase the expression of p53	28975980	RID00723	expression association
Multiple myeloma	MALAT1	HMGB1	positively-E	RIP	upregulation	qPCR	NA	NA	cell autophagy(+);apoptosis process(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	LncRNA MALAT-1 Elevates HMGB1 to Promote Autophagy Resulting in Inhibition of Tumor Cell Apoptosis in Multiple Myeloma; MALAT-1 knockdown facilitated the degradation of HMGB1 at the post-translational level via increase of the ubiquitination of HMGB1 in MM cells. MALAT-1 was shown to promote autophagy in MM through upregulation of HMGB1; LncRNA MALAT-1 increases the expression level of HMGB1 in MM thereby promotes autophagy resulting in the inhibition of apoptosis.	28295550	RID00724	interact with protein
Pancreatic cancer	XIST	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-133a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000146648	NA	7503	1956	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LncRNA XIST Promotes Pancreatic Cancer proliferation Through miR-133a/EGFR;as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting;XIST was positively correlated with EGFR	28295543	RID00725	ceRNA or sponge
Oral squamous cell carcinoma	HAS2-AS1	HAS2	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;microarray	GSE84807	GSE84807.zip	epithelial to mesenchymal transition(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000248690	GRCh38_8:121639293-121994185	ENSG00000170961	NA	594842	3037	HAS2-AS|HAS2AS|HASNT|NCRNA00077	NA	Long noncoding RNA HAS2-AS1 mediates hypoxia-induced invasiveness of oral squamous cell carcinoma; the hypoxia-induced HAS2-AS1 expression is dependent on HIF-1alpha which directly binds to and activates the transcription of HAS2-AS1;HAS2-AS1 mediates hypoxia-induced epithelial mesenchymal transition of OSCC cells via stabilizing HAS2.	28485478	RID00726	expression association
Malignant glioma	MEG3	miR-93	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);PI3K/AKT signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long non-coding RNA MEG3 inhibits cell growth of gliomas by targeting miR-93 and inactivating PI3K/AKT pathway; miR-93 was predicted a direct target of lncRNA-MEG3 by bioinformatics analysis;Overexpressed MEG3 counteracted the role of miR-93 in facilitating proliferation and inhibiting apoptosis in U-251 cells	28791407	RID00727	ceRNA or sponge
Non-small cell lung cancer	HOXA11-AS	SP1	positively-E	RIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000185591	NA	221883	6667	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non-small cell lung cancer cells;HOXA11-AS functions as a competing endogenous RNA to regulate transcriptional factor Sp1 expression via sponging miR-124	29034803	RID00728	ceRNA or sponge
Gastric cancer	SNHG1	DNMT1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000130816	NA	23642	1786	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	LncRNA-SNHG1 contributes to gastric cancer cell proliferation by regulating DNMT1;LncRNA-SNHG1 accelerated the proliferation of gastric cancer cells obviously and increased the expression of DNMT1	28754593	RID00729	expression association
Non-small cell lung cancer	HAGLR	miR-147a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	HOXD-AS1 functions as an oncogenic ceRNA to promote NSCLC cell progression by sequestering miR-147a;We found that lncRNA HOXD-AS1 was specifically upregulation (P<0.001) in NSCLC tissues and promoted cancer cell growth by targeting miR-147a;The dual-luciferase reporter assay showed that HOXD-AS1 could negatively regulate the expression of miR-147a	29033588	RID00730	ceRNA or sponge
Hepatocellular carcinoma	NNT-AS1	CDK6	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA(miR-363)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000248092	GRCh38_5:43571594-43603230	ENSG00000105810	NA	100652772	1021	NA	MCPH12|PLSTIRE	Long noncoding RNA NNT-AS1 promotes hepatocellular carcinoma progression and metastasis through miR-363/CDK6 axis;Bioinformatics analysis and luciferase reporter assay validated that miR-363 targeted NNT-AS1 and CDK6 3'-UTR;NNT-AS1 competed with CDK6 for miR-363 binding and could increase CDK6 expression	29179477	RID00731	ceRNA or sponge
Lung cancer	IGFBP4-1	IGFBP4	negatively-E	RNAi	upregulation	qPCR	NA	NA	energy metabolic process(+);cancer progression(+)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_17:40439467-40439917	ENSG00000141753	NA	NA	3487	NA	BP-4|HT29-IGFBP|IBP4|IGFBP-4	Overexpression of lncRNA IGFBP4-1 reprograms energy metabolism to promote lung cancer progression;lnc-IGFBP4-1 was observed to negatively correlate with gene IGFBP4, and lower expression level of IGFPB4 was found after lnc-IGFBP4-1-overexpression was transfected into PC9 cells, higher expression level of IGFPB4 was also found after lnc-IGFBP4-1-downregulation was transfected into GLC-82 cells, which indicates that IGFBP4 may exert its targeting function regulated by lnc-IGFBP4-1	28946875	RID00732	expression association
Esophagus squamous cell carcinoma	HOTTIP	HOXA13	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-30b);histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells;harboring a miR-30b-binding site, HOTTIP as a molecular sponge mainly regulated miR-30b level in the nucleus and modulated the repression of HOXA13 mediated by miR-30b in the cytoplasm, resulting in the positive HOTTIP/HOXA13 correlation;HOTTIP upregulation snail1 by competitively binding miR-30b, subsequently promoting epithelial-mesenchymal transition (EMT) and invasion.HOTTIP recruits WDR5 to the HOXA13 promoter and activatesHOXA13 transcription.HOTTIP directly bound the adaptor protein WDR5 and drove histone H3 lysine 4 trimethylation and HOXA13 gene transcription in ESCC cells.	28534516	RID00733	ceRNA or sponge;epigenetic regulation
Cervical cancer	PVT1	miR-424	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA PVT1 Facilitates Cervical Cancer Progression via Negative Regulating of miR-424;lowered expression of miR-424 could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines. Our results reveal a tumor-promoting role for PVT1, acting as a competing endogenous RNA (ceRNA) or a molecular sponge in negatively modulating miR-424	28276314	RID00734	ceRNA or sponge
Non-small cell lung cancer	GAS5	miR-135b	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Inhibits Tumorigenesis and Enhances Radiosensitivity by Suppressing miR-135b Expression in Non-Small Cell Lung Cancer; Luciferase reporter assay confirmed that GAS5 could directly target miR-135b and negatively regulate its expression;GAS5 inhibits tumorigenesis and enhances radiosensitivity by suppressing miR-135b expression in NSCLC cells	28117028	RID00735	ceRNA or sponge
Breast cancer	H19	CUL4A	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139842	NA	283120	8451	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway;we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down;we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression. CUL4A was greatly decreased by knockdown of H19 lncRNA in MCF-7/Dox1600/shH19 cells	29190892	RID00736	expression association
Breast cancer	H19	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	doxorubicin	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway;we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down;we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression	29190892	RID00737	expression association
Osteosarcoma	PARTICL	WWOX	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(+)	NA	association	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000286532	GRCh38_2:85537462-85538666	ENSG00000186153	NA	100630918	51741	PARTICLE	D16S432E|EIEE28|FOR|FRA16D|HHCMA56|PRO0128|SCAR12|SDR41C1|WOX1	The long non-coding RNA PARTICLE is associated with WWOX and the absence of FRA16D breakage in osteosarcoma patients;PARTICLE over-expression ameliorated WWOX promoter activity in U2OS harboring FRA16D non-breakage;It can be concluded that the lncRNA PARTICLE influences the WWOX tumor suppressor and in the absence of WWOX FRA16D breakage, it is associated with OS metastasis-free survival	29152092	RID00738	expression association
Nasopharynx carcinoma	PCAT7	ELF2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-134-5p)	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000231806	GRCh38_9:94555054-94603990	ENSG00000109381	NA	101928099	1998	PCAN-R2	"EU32|NERF|NERF-1A|NERF-1B|NERF-1a,b|NERF-2"	Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma;These results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p.CAT7 accelerates NPC cell growth partially by spongeing miR-134-5p, and then up-regulating ELF2.	28728844	RID00739	ceRNA or sponge
Colorectal cancer	TUG1	CPEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-186)	regulation	NA	methotrexate	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000137449	NA	55000	132864	LINC00080|NCRNA00080|TI-227H	CPE-BP2|CPEB-2|hCPEB-2	TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis;bioinformatics analysis showed that miR-186 could directly bind to TUG1, suggesting TUG1 might worked as a ceRNA to sponge miR-186;our study also showed that CPEB2 was the direct target of miR-186 in colorectal cancer cells.	28302487	RID00740	ceRNA or sponge
Liver cancer	HULC	HMGA2	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000149948	NA	728655	8091	HCCAT1|LINC00078|NCRNA00078	BABL|HMGI-C|HMGIC|LIPO|STQTL9	The long noncoding RNA HULC promotes liver cancer by increasing the expression of the HMGA2 oncogene via sequestration of the microRNA-186;microRNA-186 inhibited HMGA2 expression by targeting the 3'-untranslated region (3'-UTR) of HMGA2 mRNA;HULC acted as a competing noncoding RNA to sequester miR-186 and thereby relieved miR-186-mediated HMGA2 repression;We conclude that the long noncoding RNA HULC increases HMGA2 expression by sequestering miR-186 post-transcriptionally and thereby promotes liver cancer growth	28765279	RID00741	ceRNA or sponge
Colorectal cancer	DPP10-AS1	TIMP3	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	microarray	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000235026	GRCh38_2:115126622-115161384	ENSG00000100234	NA	NA	7078	NA	HSMRK222|K222|K222TA2|SFD	Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3;BC032913 enhanced the mRNA and protein expression of TIMP3 and inhibited Wnt/beta-catenin pathway activity, thus suppressing CRC metastasis in vitro and in vivo;the obtained data show that BC032913 plays an inhibitory role in CRC aggression by upregulating TIMP3, followed by inactivation of the Wnt/beta-catenin pathway	28918047	RID00742	expression association
Gastric cancer	TRERNA1	SNAI1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	as enhancer	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000124216	NA	100887755	6615	LINC00651|treRNA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition;we demonstrate that lncRNA TRERNA1 acts like an enhancer of SNAI1 to promote cell invasion and migration and to contribute to metastasis of gastric cancer (GC)	28918030	RID00743	expression association
Gastric cancer	TRERNA1	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000039068	NA	100887755	999	LINC00651|treRNA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition. TRERNA1 functions as a scaffold to recruit EZH2 to epigenetically silence epithelial-mesenchymal transition marker CDH1 by H3K27me3 of its promoter region;our findings indicated that TRERNA1 serves as a critical effector in GC progression by regulating CDH1 at the transcription level	28918030	RID00744	epigenetic regulation
Ovarian cancer	MALAT1	miR-200c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell viability(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Noncoding RNA MALAT1 Functions as a Sponge of MiR-200c in Ovarian Cancer;bioinformatics analysis suggested that3'-UTR of lncRNA MALAT1 and miR-200c have a complementarity region;luciferase assays verified the existence of direct binding between miR-200c and lncRNA MALAT1;lncRNA MALAT1 is a oncogene in ovarian cancer, involved in the regulation of cell viability, migration and invasion abilities of ovarian cancer cells, which achieved its biological function by regulating miR-200c expression; miR-200c expression was significantly decreased in ovarian cancer, which is negatively correlated with MALAT1 expression	28899458	RID00745	ceRNA or sponge
Hepatocellular carcinoma	MVIH	ARID1A	interact	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_10:78038556-78040701	ENSG00000117713	NA	NA	8289	NA	B120|BAF250|BAF250a|BM029|C1orf4|CSS2|ELD|MRD14|OSA1|P270|SMARCF1|hELD|hOSA1	ARID1A represses hepatocellular carcinoma cell proliferation and migration through lncRNA MVIH;we reveal that ARID1A interacts with lncRNA MVIH through some region(s) or domain(s) including ARID domain and C-terminal ARID1A protein binding domain;ARID1A upregulates its downstream target CDKN1A and suppresses HCC cell proliferation and migration through inhibiting MVIH	28716731	RID00746	interact with protein
Osteosarcoma	XIST	CDKN1A	negatively-E	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000124762	NA	7503	1026	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21;mechanistic analysis revealed that Xist can repress P21 expression to regulate OS cell cycle and proliferation by binding to EZH2	29254174	RID00747	epigenetic regulation
Malignant glioma	XIST	miR-29c	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	Genome Instability and Mutation	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with PS1, positively related with MGMT	28831025	RID00748	ceRNA or sponge
Malignant glioma	XIST	SP1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	NA	association	NA	temozolomide	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000185591	NA	7503	6667	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with PS1, positively related with MGMT	28831025	RID00749	expression association
Malignant glioma	XIST	MGMT	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);DNA repair(+)	NA	association	NA	temozolomide	NA	Genome Instability and Mutation	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000170430	NA	7503	4255	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway;Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT;XIST can inhibit miR-29c expression by directly targetting TMZ-resistant glioma cells.XIST was inversely correlated with miR-29c, positively correlated with SP1, positively related with MGMT	28831025	RID00750	expression association
Breast cancer	NEAT1	miR-128	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1 negatively regulates miR-218 expression and promotes breast cancer progression;NEAT1 promoted cell invasion and proliferation by negatively regulating miR-218 in breast cancer.miR-218 was shown to be a direct target of NEAT1 in breast cancer cells	28946559	RID00751	ceRNA or sponge
Non-small cell lung cancer	GAS5	PTEN	positively-E	RIP;western blot;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-21)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	GAS5 knockdown reduces the chemo-sensitivity of non-small cell lung cancer (NSCLC) cell to cisplatin (DDP) through regulating miR-21/PTEN axis;GAS5 could compete with PTEN for miR-21 binding;We further verified that the interaction between GAS5 and miR-21 was required in the regulation of NSCLC chemo-sensitivity to DDP through PTEN pathway	28686971	RID00752	ceRNA or sponge
Renal cell carcinoma	LncRNA-SARCC	miR-143-3p	negatively-E	RIP;ChIP;RNAi	downregulation	qPCR	NA	NA	cancer progression(-);chemoresistance(-)	transcriptional regulation	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENST00000460407	GRCh38_3:152834693-152841439	NA	NA	NA	NA	NA	NA	LncRNA-SARCC suppresses renal cell carcinoma (RCC) progression via altering the androgen receptor(AR)/miRNA-143-3p signals;LncRNA-SARCC bound and destabilized AR protein with an inhibition of AR function, which led to transcriptionally de-repress miR-143-3p expression, thus inhibition of its downstream signals including AKT, MMP-13, K-RAS and P-ERK.Notably, treating with Sunitinib, the multi-targeted receptor tyrosine kinase inhibitor, increased the expression of LncRNA-SARCC, which decreased RCC cells resistance to Sunitinib. AR could directly decrease miR-143-3p expression by binding to the potential androgen response elements (AREs) in its promoter.	28644440	RID00753	transcriptional regulation
Non-small cell lung cancer	PVT1	MMP9	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-200a);ceRNA(miR-200b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000100985	NA	5820	4318	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CLG4B|GELB|MANDP2|MMP-9	lncRNA-PVT1 Facilitates Invasion Through Upregulation of MMP9 in Nonsmall Cell Lung Cancer Cell;Specifically, lncRNA-PVT1 directly interacted with miR-200a and miR-200b, which suppressed MMP9 expression;lncRNA-PVT1 functions as a competitive endogenous RNA to regulate MMP9 expression through competitively binding the common microRNAs, miR-200a and miR-200b	28731781	RID00754	ceRNA or sponge
Hepatocellular carcinoma	HCG11	IGF2BP1	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228223	GRCh38_6:26521709-26527404	ENSG00000159217	NA	493812	10642	CTA-14H9.3|bK14H9.3	CRD-BP|CRDBP|IMP-1|IMP1|VICKZ1|ZBP1	Modulation of IGF2BP1 by long non-coding RNA HCG11 suppresses apoptosis of hepatocellular carcinoma cells via MAPK signaling transduction;Knockdown of both indicators led to decreased cell viability, proliferation, and migration ability in HepG2 cells while the cell apoptosis and G1 cell cycle arrest were induced after knockdown of HCG11 and IGF2BP1; HCG11 exerted its effect on HCC via interaction with IGF2BP1, leading to activation of MAPK signaling, which eventually promoted the progression of HCC	28677801	RID00756	interact with protein
Breast cancer	H19	DNMT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-152)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000130816	NA	283120	1786	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152;A negative correlation between H19 and miR-152 and positive correlation between H19 and DNMT1 mRNA were observed	28544374	RID00757	ceRNA or sponge
Non-small cell lung cancer	HOXA5	LINC00312	positively-E	ChIP;IHC	downregulation	qPCR;microarray	GSE10072;GSE19804;GSE66654	GSE10072.zip;GSE19804.zip;GSE66654.zip	cell proliferation(-);apoptosis process(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	TF	lncRNA	ENSG00000106004	NA	NA	GRCh38_3:8571782-8574668	3202	29931	HOX1|HOX1.3|HOX1C	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	Long non-coding RNA 00312 regulated by HOXA5 inhibits tumour proliferation and promotes apoptosis in Non-small cell lung cancer;we found that HOXA5 could bind in the promoter of linc00312 and up-regulated the expression of it.	28338293	RID00758	transcriptional regulation
Esophagus squamous cell carcinoma	MALAT1	CKS1B	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	radioresistance(+)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000173207	NA	378938	1163	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 affects the efficacy of radiotherapy for esophageal squamous cell carcinoma by regulating Cks1 expression;MALAT1 acted as one positive regulator of the radioresistance of ESCC, at least partly due to its promotion on Cks1 expression;Cks1 expression was also downregulated by MALAT1 siRNA, while Cks1 siRNA strongly recovered MALAT1-induced radioresistance in vitro	27935117	RID00759	expression association
Acute myeloid leukemia	H19	ID2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-19a);ceRNA(miR-19b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000115738	NA	283120	3398	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GIG8|ID2A|ID2H|bHLHb26	LncRNA H19 regulates ID2 expression through competitive binding to hsa-miR-19a/b in acute myelocytic leukemia;the results of the bioinformatic analysis revealed potential hsa-miR-19a/b-3p binding sites in lncRNA H19 and ID2;it was demonstrated that the knockdown of lncRNA H19 resulted in increased expression of hsa-microRNA (miR)-19a/b and decreased expression of inhibitor of DNA binding 2 (ID2) in AML cells;the results of the present study suggest that lncRNA H19 regulates the expression of ID2 through competitive binding to hsa-miR-19a and hsa-miR-19b, which may serve a role in AML cell proliferation	28765931	RID00760	ceRNA or sponge
Non-small cell lung cancer	RP11-713B9.1	CADM1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_11:115174977-115175324	ENSG00000182985	NA	NA	23705	NA	NA	Down-regulation of long noncoding RNA RP11-713B9.1 contributes to the cell viability in non-small cell lung cancer (NSCLC);the overexpression of RP11-713B9.1 resulted in significant upregulation of TSLC1 and inhibition of H460 cell viability, while the opposite effects were observed following the knockdown of RP11-713B9.1 in A549 cells	28765887	RID00761	expression association
Gastric cancer	TUG1	SOX4	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124766	NA	55000	6659	LINC00080|NCRNA00080|TI-227H	EVI16	MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4;the results of the current study indicate that the downregulation of miR-381 by lncRNA-TUG1 promoted the metastasis of GC cells by inhibiting SOX4	28927144	RID00762	expression association
Hepatocellular carcinoma	HOTAIR	SLC2A1	positively-E	RIP;western blot;RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+);mTOR signaling pathway(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism;Evading Apoptosis;Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000117394	NA	100124700	6513	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling;HOTAIR promoted glycolysis by upregulating glucose transporter isoform 1 (GLUT1) and activating mammalian target of rapamycin (mTOR) signaling	28731193	RID00763	interact with protein
Colorectal cancer	SNHG3	MYC	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	COAD.zip	cancer progression(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000136997	NA	8420	4609	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	MRTL|MYCC|bHLHe39|c-Myc	The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer;Mechanistic investigations demonstrated that SNHG3 functioned as a competing endogenous RNA (ceRNA) to 'sponge' miR-182-5p, thus leading to the release of c-Myc from miR-182-5p and modulating the expression of c-Myc;SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes	28731158	RID00764	ceRNA or sponge
Gastric cancer	PCAT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000124762	NA	100750225	1026	PCA1|PCAT-1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA PCAT-1 over-expression promotes proliferation and metastasis in gastric cancer cells through regulating CDKN1A;PCAT-1 knockdown through shRNA in AGS and MGC-803 cells inhibited cell proliferation, migration and invasion by regulating CDKN1A	28571676	RID00765	expression association
Hepatocellular carcinoma	LOC90784	BAX	positively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000087088	NA	NA	581	NA	BCL2L4	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00766	expression association
Hepatocellular carcinoma	LOC90784	CDK4	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00767	expression association
Hepatocellular carcinoma	LOC90784	CCND1	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00768	expression association
Hepatocellular carcinoma	LOC90784	MMP2	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00769	expression association
Hepatocellular carcinoma	LOC90784	MMP9	negatively-E	RNAi;western blot	upregulation	qPCR;microarray	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_2:86020216-86023868	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	upregulation long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC;Knockdown of lncRNA LOC90784 expression inhibited proliferation and induced apoptosis and cell cycle arrest by promoting Bax and repressing CDK4 and Cyclin D1 protein expression; it also inhibited invasion and migration by repressing MMP2 and MMP9 expression in HCC cells	28651931	RID00770	expression association
Hepatocellular carcinoma	HULC	COX2	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	cell growth(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	4513	HCCAT1|LINC00078|NCRNA00078	COII|MTCO2	lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein;HULC promoted the growth of HCC cells through elevating COX-2 protein;knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells	28634076	RID00771	interact with protein
Colorectal cancer	XIST	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148516	NA	7503	6935	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long noncoding RNA XIST expedites metastasis and modulates epithelial-mesenchymal transition in colorectal cancer.luciferase activity assay indicated that lncRNA XIST could bind directly with miR-200b-3p;knockdown of lncRNA XIST significantly reduced the expression of ZEB1, which was the direct target of miR-200b-3p, and the tumor suppressive effects caused by knockdown of lncRNA XIST could be rescued by re-expression of ZEB1 in CRC cells;our study demonstrated how lncRNA XIST regulates CRC progression and metastasis by competing for miR-200b-3p to modulate the expression of ZEB1	28837144	RID00772	ceRNA or sponge
Prostate cancer	ZEB1-AS1	ZEB1	positively-E	RIP;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long noncoding RNA ZEB1-AS1 epigenetically regulates the expressions of ZEB1 and downstream molecules in prostate cancer;we found that RNAi-mediated downregulation of ZEB1-AS1 induced significant ZEB1 inhibition while artificial overexpression of ZEB1-AS1 rescued ZEB1 expression, which means that ZEB1-AS1 promotes ZEB1 expression;ZEB1-AS1 bound and recruited histone methyltransferase MLL1 to the promoter region of ZEB1, induced H3K4me3 modification therein, and activated ZEB1 transcription;Biologically, ZEB1-AS1 promoted proliferation and migration of prostate cancer cells	28830551	RID00773	epigenetic regulation
Osteosarcoma	PVT1	HK2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+);cancer progression(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000159399	NA	5820	3099	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HKII|HXK2	Long non-coding RNA PVT1 promotes glycolysis and tumor progression by regulating miR-497/HK2 axis in osteosarcoma;PVT1 acted as molecular sponge to repress miR-497; HK2 was a direct target of miR-497 and overexpression of HK2 attenuated the suppressive effect of miR-497 on glycolysis;these findings suggested that PVT1 contributes to OS cell glucose metabolism, cell proliferation, and motility through the miR-497/HK2 pathway	28602700	RID00774	ceRNA or sponge
Epithelial ovarian cancer	ABHD11-AS1	RHOC	positively-F	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000155366	NA	171022	389	LINC00035|NCRNA00035|WBSCR26	ARH9|ARHC|H9|RHOH9	Role of the lncRNA ABHD11-AS1 in the tumorigenesis and progression of epithelial ovarian cancer through targeted regulation of RhoC; Overexpression of ABHD11-AS1 upregulation the expression of RhoC and its downstream molecules P70s6k, MMP2 and BCL-xL; lncRNA ABHD11-AS1 could directly combine with RhoC; RhoC is a direct target of the lncRNA ABHD11-AS1.	28818073	RID00775	interact with protein
Liver cancer	HAGLR	SOX4	positively-E	RIP;RNA pull-down assay;ChIP	upregulation	qPCR;microarray	GSE84402	GSE84402.zip	cell metastasis(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000124766	NA	401022	6659	HOXD-AS1|MIR7704HG|Mdgt	EVI16	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4;STAT3 could specifically interact with the promoter of HOXD-AS1 and activate HOXD-AS1 transcription;Overexpression of HOXD-AS1 competitively bound to miR-130a-3p that prevented SOX4 from miRNA-mediated degradation, thus activated the expression of EZH2 and MMP2 and facilitated HCC metastasis	28810927	RID00776	ceRNA or sponge
Liver cancer	STAT3	HAGLR	positively-E	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE84402	GSE84402.zip	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000224189	GRCh38_2:176164051-176188958	6774	401022	ADMIO|ADMIO1|APRF|HIES	HOXD-AS1|MIR7704HG|Mdgt	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4;STAT3 could specifically interact with the promoter of HOXD-AS1 and activate HOXD-AS1 transcription.HOXD-AS1 is regulated by the transcriptional factor STAT3, it significantly upregulation in HCC and can be used as a prognosis biomarker for HCC patients. HOXD-AS1 functions as a ceRNA that competitively binds to miR-130a-3p, then upregulates SOX4 and promotes HCC cell metastasis.	28810927	RID00777	transcriptional regulation
Colorectal cancer	CRNDE	DUSP5	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE21510	GSE21510.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000138166	NA	NA	1847	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	DUSP|HVH3	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID00778	epigenetic regulation
Colorectal cancer	CRNDE	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE21511	GSE21511.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000124762	NA	NA	1026	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID00779	epigenetic regulation
Malignant glioma	LINC00461	TOP2A	positively-E	starBase;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-411-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245526	GRCh38_5:88507546-88691057	ENSG00000131747	NA	645323	7153	NA	TOP2|TP2A	Oncogenic effects of evolutionarily conserved noncoding RNA ECONEXIN on gliomagenesis. Functional analysis of ECONEXIN in glioma cell lines, U87 and U251, showed it was dominantly located in the cytoplasm and interacted with miR-411-5p via two binding sites within ECONEXIN;Inhibition of ECONEXIN upregulation miR-411-5p together with the downregulation of its target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, resulting in decreased cell proliferation;Our data demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in glioma	28368417	RID00780	ceRNA or sponge
Gastric cancer	XIAP-AS1	XIAP	positively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000237331	GRCh38_X:123872626-123873932	ENSG00000101966	NA	106480735	331	NA	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	The long noncoding RNA XIAP-AS1 promotes XIAP transcription by XIAP-AS1 interacting with Sp1 in gastric cancer cells;XIAP-AS1 knockdown promoted tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in gastric tumor cells, as cleaved caspase-3 and caspase-9 was detected;tumor cell proliferation was inhibited by XIAP-AS1 knockdown in response to TRAIL administration; XIAP-AS1 is a potential target for TRAIL-induced apoptosis in gastric cancer cells	28792527	RID00781	transcriptional regulation
Nasopharynx carcinoma	LINC0086	miR-214	negatively-F	luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000178947	GRCh38_X:135421943-135428074	NA	NA	NA	NA	NA	NA	Long Noncoding RNA LINC0086 Functions as a Tumor Suppressor in Nasopharyngeal Carcinoma by Targeting miR-214;upregulation of LINC0086 dramatically decreased the expression of miR-214, an oncogene in several cancers, in C666-1 and HK-1 cells;An miR-214 binding site was found in the 3'-UTR of LINC0086;the suppressive effects of LINC0086 on NPC cell growth were reversed by overexpression of miR-214 in vitro and in vivo	28245169	RID00782	ceRNA or sponge
Oral squamous cell carcinoma	LINC00668	VEGFA	positively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-297)	regulation	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000112715	NA	400643	7422	NA	MVCD1|VEGF|VPF	Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma;Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression	28564590	RID00783	ceRNA or sponge
Non-small cell lung cancer	H19	miR-21	negatively-F	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Association of long non-coding RNA H19 and microRNA-21 expression with the biological features and prognosis of non-small cell lung cancer;Increased expression of H19 and miR-21 was positively correlated with advanced tumor-node-metastasis stage and tumor size;H19 and miR-21 interact in the regulation of NSCLC, and with greater expression of both H19 and miR-21, overall survival decreased	(<ce><de><U+02B5><d1><e9><U+05A4><U+02B5>)28799568	RID00784	ceRNA or sponge
Peripheral primitive neuroectodermal tumor	MYC	MALAT1	positively-E	ChIP	upregulation	qPCR;microarray	GSE93677	GSE93677.zip	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Sarcoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000251562	GRCh38_11:65497688-65506516	4609	378938	MRTL|MYCC|bHLHe39|c-Myc	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Identification of a Novel SYK/c-MYC/MALAT1 Signaling Pathway and Its Potential Therapeutic Value in Ewing Sarcoma. Ectopic expression of SYK rescued the cytotoxicity triggered by SYK-depletion associated with the reactivation of both AKT and MYC; MALAT1, was identified to be dependent on SYK-mediated signaling;c-MYC, a SYK-promoted gene, bound to the promoter of MALAT1 and transcriptionally activated MALAT1, which further promoted the proliferation of EWS cells	28336564	RID00785	transcriptional regulation
Hepatocellular carcinoma	HOXA11-AS	LATS1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000131023	NA	221883	9113	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	WARTS|wts	Promotion of LncRNA HOXA11-AS on the proliferation of hepatocellular carcinoma by regulating the expression of LATS1;RIP and CHIP experiments showed that HOXA11-AS inhibited the expression of LATS1 genes by binding enhancer of zeste homolog 2 (EZH2) proteins	28829501	RID00786	epigenetic regulation
Thyroid cancer	H19	let-7a	negatively-E	bioinformatics	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Effects of long non-coding RNA H19 and microRNA let7a expression on thyroid cancer prognosis;This study demonstrated that increased lncRNA H19 and decreased miRNA let7a expression levels are associated with poor prognosis in TC patients. An inverse relationship between lncRNA H19 and miRNA let7a expression levels was exhibited	28655518	RID00787	expression association
Epithelial ovarian cancer	ERLNC1	CDK4	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000135446	NA	101929441	1019	ElncRNA1|TC0101441	CMM3|PSK-J3	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00788	expression association
Epithelial ovarian cancer	ERLNC1	CDK6	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000105810	NA	101929441	1021	ElncRNA1|TC0101441	MCPH12|PLSTIRE	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00789	expression association
Epithelial ovarian cancer	ERLNC1	CCND1	NA	western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000110092	NA	101929441	595	ElncRNA1|TC0101441	BCL1|D11S287E|PRAD1|U21B31	ElncRNA1, a long non-coding RNA that is transcriptionally induced by oestrogen, promotes epithelial ovarian cancer cell proliferation.This pro-proliferation effect of ElncRNA1 was partially mediated by the regulation of CDK4, CDK6 and cyclin D1	28714515	RID00790	expression association
Esophagus squamous cell carcinoma	HNF1A-AS1	SOX4	positively-E	bioinformatics;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-214)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000124766	NA	283460	6659	C12orf27|HAS1|NCRNA00262	EVI16	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4;The result of luciferase activity assay showed that luciferase activity was strongly weakened by the combination of LncR-HAS1 WT and miR-214 mimic;the expression of SOX-4, a predicted target gene of miR-214, was suppressed by HAS1-siRNA and was increased by miR-214 inhibitor	28656277	RID00791	ceRNA or sponge
Osteosarcoma	ZEB1-AS1	miR-200s	negatively-F	western blot;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000237036	GRCh38_10:31206278-31320447	NA	NA	220930	NA	NA	NA	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell proliferation and Migration;Our results showed that ZEB1-AS1 functions as a molecular sponge for miR-200s and relieves the inhibition of ZEB1 caused by miR-200s;Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration	28075045	RID00792	ceRNA or sponge
Cervical cancer	PVT1	miR-195	negatively-E	western blot;RNA pull-down assay;RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(-)	histone modification;sponge	regulation	NA	paclitaxel	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells;PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195;PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region;PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells;Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX;Based on these findings, we infer that PVT1 could decrease miR-195 expression via enhancing histone H3K27me3 in the miR-195 promoter region and also via direct sponging of miR-195	28296507	RID00793	epigenetic regulation;ceRNA or sponge
Malignant glioma	MALAT1	RAP1B	positively-E	Targetscan;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-101)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127314	NA	378938	5908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	K-REV|RAL1B	Long non-coding RNA MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101;MALAT1 and Rap1B knockdown could inhibit proliferation and induce apoptosis of glioma cells;MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. Rap1B is a target of miR-101.	28551849	RID00794	ceRNA or sponge
Colorectal cancer	LL22NC03-N64E9.1	KLF2	negatively-E	RIP;western blot;ChIP	upregulation	qPCR;microarray;sequencing	TCGA;GSE9348;GSE41328	COAD.zip;GSE9348.zip;GSE41328.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_22:15796959-15798346	ENSG00000127528	NA	NA	10365	NA	LKLF	A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer; Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2;We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2.	28938648	RID00795	epigenetic regulation
Hepatocellular carcinoma	FER1L4	miR-106a-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	prognosis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	C20orf124	NA	Long non-coding RNA Fer-1-like protein 4 acts as a tumor suppressor via miR-106a-5p and predicts good prognosis in hepatocellular carcinoma;We found that down-regulated FER1L4 increased the expression of miR-106a-5p significantly and there was a reciprocal repression between FER1L4 and miR-106a-5p;we identified FER1L4 as a target of miR-106a-5p by using dual-luciferase reporter assay; FER1L4, as well as miR-106a-5p, can predict the clinical prognosis of HCC alone or combined.	28759956	RID00796	ceRNA or sponge
Hepatocellular carcinoma	HAGLR	ARHGAP11A	positively-E	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	ceRNA(miR-19a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000198826	NA	401022	9824	HOXD-AS1|MIR7704HG|Mdgt	GAP (1-12)	The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma. we identified that HOXD-AS1 upregulation the Rho GTPase activating protein 11A (ARHGAP11A) by competitively binding to microRNA-19a (miR19a), resulting in induced metastasis	28724429	RID00797	ceRNA or sponge
Hepatocellular carcinoma	HAGLR	RGS3	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000138835	NA	401022	5998	HOXD-AS1|MIR7704HG|Mdgt	C2PA|RGP3	The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma.the regulator of G-protein signaling 3 (RGS3), a potential inhibitor of the MEK-ERK1/2 signaling axis, was also found to be downregulated by ectopic HOXD-AS1 overexpression, leading to a remarkably reduced apoptotic effect.	28724429	RID00798	expression association
Osteosarcoma	SNHG15	miR-141	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell autophagy(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000232956	GRCh38_7:44983023-44986961	NA	NA	285958	NA	C7orf40|Linc-Myo1g|MYO1GUT	NA	LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141;SNHG15 knockdown and miR-141 overexpression significantly suppressed cell proliferation, invasion, migration and autophagy while SNHG15 overexpression and miR-141 repression exhibited the opposite effects on OS cells;SNHG15 could directly interact with miR-141 and regulate its expression;Our data showed that SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141	28720111	RID00799	ceRNA or sponge
Hepatocellular carcinoma	CPS1-IT1	HIF1A	negatively-E	RNAi	downregulation	qPCR;sequencing	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000100644	NA	29034	3091	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Melatonin suppresses hepatocellular carcinoma progression via lncRNA-CPS1-IT-mediated HIF-1alpha inactivation;We observed that melatonin significantly inhibited the proliferation, migration, and invasion of HCC cells and significantly induced the expression of the transcription factor FOXA2 in HCC cells. This increase in FOXA2 expression resulted in upregulation of lncRNA-CPS1 intronic transcript 1 (CPS1-IT1), which reduced HIF-1alpha activity and consequently resulted in the suppression of epithelial-mesenchymal transition (EMT) progression and HCC metastasis.	29137263	RID00800	expression association
Gallbladder cancer	UCA1	CDKN1A	negatively-E	western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID00801	epigenetic regulation
Gallbladder cancer	UCA1	CDH1	negatively-E	western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000039068	NA	652995	999	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID00802	epigenetic regulation
Osteosarcoma	MALAT1	EZH2	interact	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID00803	interact with protein
Malignant glioma	AB073614	SOX7	negatively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	NA	GRCh38_3:149173591-149175492	ENSG00000171056	NA	NA	83595	NA	NA	Long noncoding RNA AB073614 promotes the malignance of glioma by activating Wnt/beta-catenin signaling through downregulating SOX7;The level of AB073614 was found to correlate inversely with sex-determining region Y-box 7 (SOX7) expression but correlate positively with Wnt/beta-catenin signaling activity;the results indicated that AB073614 induced Wnt/beta-catenin signaling activity by repressing SOX7 expression;the findings demonstrated that AB073614 promoted the progression of glioma by targeting SOX7 to activate the Wnt/beta-catenin signaling pathway	29029454	RID00804	expression association
Non-small cell lung cancer	LINC00673	miR-150-5p	negatively-F	miRanda;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000227036	GRCh38_17:72403322-72592804	NA	NA	100499467	NA	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p;Overexpression of miR-150-5p suppressed lin00673's expression while inhibition of miR-150-5p led to significant upregulation of lin00673, suggesting that linc00673 could be negatively regulated by miR-150-5p, which was further confirmed by the inverse correlation between linc00673 and miR-150-5p in NSCLC patients' specimen;miR-150-5p could directly target linc00673 through luciferase assay, so linc00673 could sponge miR-150-5p and modulate the expression of a key EMT regulator ZEB1 indirectly;miR-150-5p inhibition abrogated linc00673 silence mediated proliferation, migration, invasion and EMT suppressing effect	28697764	RID00805	ceRNA or sponge
Breast cancer	HOXA-AS2	miR-520c-3p	negatively-F	starBase;OncomiRDB;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000253552	GRCh38_7:27107777-27134302	NA	NA	285943	NA	HOXA3as	NA	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge;microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells.	28545023	RID00806	ceRNA or sponge
Gastric cancer	TINCR	PDK1	negatively-E	RNAi;luciferase reporter assay;RNAhybrid	upregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-375)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000152256	NA	257000	5163	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	NA	The long noncoding RNA, TINCR, functions as a competing endogenous RNA to regulate PDK1 expression by sponging miR-375 in gastric cancer;the low expression of TINCR increased cell apoptosis and inhibited the proliferation of GC cells, while the downregulation of miR-375 reversed the function;TINCR could negatively regulate the miR-375 expression and increased the PDK1 expression in GC cells. The ceRNA regulatory network of TINCR/miR-375/PDK1 allows us to better understand the pathogenesis of GC and facilitate the development of long noncoding RNA (lncRNA)-directed diagnostics in GC.	28744139	RID00807	ceRNA or sponge
Osteosarcoma	ANCR	CDKN1A	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000124762	NA	282	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID00808	epigenetic regulation
Osteosarcoma	ANCR	CDKN1B	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000111276	NA	282	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID00809	epigenetic regulation
Non-small cell lung cancer	GAS5	miR-23a	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long Noncoding RNA GAS5 Suppresses Tumorigenesis by Inhibiting miR-23a Expression in Non-Small Cell Lung Cancer;Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a and reversely regulated its expression;miR-23a overexpression significantly abolished GAS5 overexpression-induced inhibition of proliferation and invasion, as well as promotion of apoptosis in NSCLC cells	28059053	RID00810	ceRNA or sponge
Bladder urothelial carcinoma	CCEPR	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_10:59173963-59176464	ENSG00000132646	NA	105682749	5111	CCHE1|lncRNA-CCHE1	ATLD2	Increased expression of long non-coding RNA CCEPR is associated with poor prognosis and promotes tumorigenesis in urothelial bladder carcinoma. we found CCEPR upregulates the expression of PCNA in mRNA and protein level to promote cancer growth.	28574830	RID00811	expression association
Cervical cancer	RSU1P2	MYC	positively-E	RegRNA;Targetscan;PicTar;RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(let-7a)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000232554	GRCh38_10:45099487-45154606	ENSG00000136997	NA	100133308	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells;We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a;The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity	27487126	RID00812	ceRNA or sponge
Colorectal cancer	lnc-Sox5	IDO1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cytotoxicity(-)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000115934	GRCh38_12:23181334-23251499	ENSG00000131203	NA	NA	3620	NA	IDO|IDO-1|INDO	Long noncoding RNA lnc-sox5 modulates CRC tumorigenesis by unbalancing tumor microenvironment. Our results also showed that the expression of indoleamine 2,3-dioxygenase 1 (IDO1) was significantly reduced by lnc-sox5 knock-down and therefore modulated the infiltration and cytotoxicity of CD3+CD8+T cells	28632999	RID00813	expression association
Papillary thyroid carcinoma	TUG1	miR-145	negatively-F	western blot;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA TUG1 influences papillary thyroid cancer cell proliferation, migration and EMT formation through targeting miR-145;These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145, and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells	28645161	RID00814	ceRNA or sponge
Hepatocellular carcinoma	MIR4435-2HG	YBX1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111036776-111523376	ENSG00000065978	NA	541471	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker;Mechanistically, lncRNA-AWPPH interacts with YBX1, promotes YBX1-mediated activation of SNAIL1 translation, and upregulates SNAIL1 expression;Furthermore, lncRNA-AWPPH promotes YBX1-mediated activation of PIK3CA transcription, upregulates PIK3CA expression, and activates PI3K/AKT pathway.this study identifies a novel lncRNA termed lncRNA-AWPPH which is highly expressed in HCC, indicates poor prognosis of HCC patients, and promotes HCC cell proliferation, migration, and in vivo tumor growth and metastasis via a novel regulatory mechanism of interacting with YBX1	28428004	RID00815	interact with protein
Breast cancer	CCAT2	CDKN2B	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000147883	NA	101805488	1030	LINC00873|NCCP1	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer;we confirmed that CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells	28531944	RID00816	epigenetic regulation
Breast cancer	MEG3	CDH1	positively-E	western blot;RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-421)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer;We further revealed that endogenous miR-421 expression was negatively regulated by MEG3 in breast cancer cells and MEG3 regulated E-cadherin expression by sponging to miR-421 in breast cancer cells	28463794	RID00817	ceRNA or sponge
Nasopharynx carcinoma	HULC	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000141510	NA	728655	7157	HCCAT1|LINC00078|NCRNA00078	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA Highly upregulation in Liver Cancer Activates p53-p21 Pathway and Promotes Nasopharyngeal Carcinoma Cell Growth. Downregulation of HULC activated p53 and induced the increased expression of p21, which finally caused cell cycle arrest and cell apoptosis	28445086	RID00818	expression association
Nasopharynx carcinoma	HULC	CDKN1A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124762	NA	728655	1026	HCCAT1|LINC00078|NCRNA00078	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA Highly upregulation in Liver Cancer Activates p53-p21 Pathway and Promotes Nasopharyngeal Carcinoma Cell Growth. Downregulation of HULC activated p53 and induced the increased expression of p21, which finally caused cell cycle arrest and cell apoptosis	28445086	RID00819	expression association
Epithelial ovarian cancer	MALAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	LncRNA MALAT1 promotes proliferation and metastasis in epithelial ovarian cancer via the PI3K-AKT pathway. silencing of MALAT1 hindered the expression of epithelial-to-mesenchymal transition (EMT)-related genes and MMPS. The evidence showed that MALAT1 induce EMT via PI3K/AKT pathway; Moreover, matrix metalloproteases (MMPs) such as MMP2 and MMP9, which are involved in migration/invasion, were also reduced.	28770968	RID00820	expression association
Epithelial ovarian cancer	MALAT1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	LncRNA MALAT1 promotes proliferation and metastasis in epithelial ovarian cancer via the PI3K-AKT pathway. silencing of MALAT1 hindered the expression of epithelial-to-mesenchymal transition (EMT)-related genes and MMPS. The evidence showed that MALAT1 induce EMT via PI3K/AKT pathway; Moreover, matrix metalloproteases (MMPs) such as MMP2 and MMP9, which are involved in migration/invasion, were also reduced.	28770968	RID00821	expression association
T-cell lymphoblastic lymphoma	MEG3	AIFM2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-214)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Lymphoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000042286	NA	55384	84883	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AMID|PRG3	The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma;Luciferase activity assay further confirmed the targeting relationship between MEG3 and miR-214;AIFM2 protein was predicted as a target of miR-214;The expression of AIFM2 was increased by MEG3 and was downregulated by miR-214 mimic	28534937	RID00822	ceRNA or sponge
Nasopharynx carcinoma	CDKN2B-AS1	let-7a	negatively-F	starBase;RNAhybrid;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);tumorigenesis(+);cytotoxicity(-)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Tumor Promoting Inflammation	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL represses tumorigenicity and enhances cisplatin-induced cytotoxicity via regulating microRNA let-7a in nasopharyngeal carcinoma;Luciferase assay revealed that ANRIL could negatively regulate miR-let-7a expression;ANRIL directly interacts with let-7a and regulates its expression. these data indicated that knockdown of ANRIL represses tumorigenicity and enhances DDP-induced cytotoxicity via regulating microRNA let-7a in NPC cells.In this study,the main purpose of this study was to investigate the role of ANRIL in NPC tumorigenesis,the association between ANRIL and cisplatin sensitivity and their underlying mechanism in NPC.	28117929	RID00823	ceRNA or sponge
Malignant glioma	CASC2	miR-181a	negatively-F	RNAi;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	chemoresistance(-);cell growth(-)	sponge	binding/interaction	RNA-RNA	temozolomide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway;CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ;CASC2 could inhibit the miR-181a expression by direct targeting in TMZ-resistant glioma cells. Results showed that CASC2 was inversely correlated with miR-181a, positively correlated with PTEN; miR-181a was inversely related with PTEN	28121023	RID00824	ceRNA or sponge
Malignant glioma	CASC2	PTEN	positively-E	RNAi;luciferase reporter assay;RIP	downregulation	qPCR	NA	NA	chemoresistance(-);cell growth(-)	ceRNA(miR-181a)	regulation	NA	temozolomide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway;CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ;CASC2 could inhibit the miR-181a expression by direct targeting in TMZ-resistant glioma cells. Results showed that CASC2 was inversely correlated with miR-181a, positively correlated with PTEN; miR-181a was inversely related with PTEN	28121023	RID00825	ceRNA or sponge
Esophagus squamous cell carcinoma	MEG3	CDH1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay;	downregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer. MEG3 acts as a ceRNA to regulate expression of E-cadherin and FOXO1 by competitively binding miR-9 and may be used as a potential biomarker in predicting ESCC patients' progression and prognosis	28539329	RID00826	ceRNA or sponge
Esophagus squamous cell carcinoma	MEG3	FOXO1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay;	downregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-9)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000150907	NA	55384	2308	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	FKH1|FKHR|FOXO1A	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer. MEG3 acts as a ceRNA to regulate expression of E-cadherin and FOXO1 by competitively binding miR-9 and may be used as a potential biomarker in predicting ESCC patients' progression and prognosis	28539329	RID00827	ceRNA or sponge
Prostate cancer	GAS5	CDKN1B	positively-E	RIP;western blot;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000111276	NA	60674	1027	NCRNA00030|SNHG2	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA GAS5 Inhibits Cellular proliferation by Targeting P27Kip1;Subsequent analysis demonstrated that P27Kip1, a known regulator of cell cycle, was positively regulated by GAS5 and upregulation of GAS5 increased its promoter activity	28396462	RID00828	transcriptional regulation
Cervical cancer	XLOC_006390	KMT5A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000106031	GRCh38_7:27187247-27192686	ENSG00000183955	NA	NA	387893	NA	NA	Long non-coding RNA XLOC_006390 promotes cervical cancer proliferation and metastasis through the regulation of SET domain containing 8;SET8 was also increased in cervical cancer tissues and its expression was positively associated with XLOC_006390, and XLOC_006390 regulated SET8 expression;lncRNA XLOC_006390 promotes cervical cancer cell growth and metastasis through the regulation of SET8.	28534991	RID00829	expression association
Laryngeal squamous cell carcinoma	RP11-169D4.1	CDH1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Larynx cancer	lncRNA	PCG	NA	GRCh38_11:72570660-72573229	ENSG00000039068	NA	NA	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Functional significance of the long non-coding RNA RP11-169D4.1 as a metastasis suppressor in laryngeal squamous cell carcinoma by regulating CDH1;We further verified that miR-205-5p had binding sites with RP11 169D4.1 and that RP11-169D4.1 could regulate the expression of CDH1.a positive correlation between the expression of RP11-169D4.1 and CDH1.	28534968	RID00830	expression association
Colorectal cancer	SPRY4-IT1	miR-101-3p	negatively-F	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	NA	GRCh38_5:142317636-142318322	NA	NA	100642175	NA	SPRIGHTLY	NA	Long non-coding RNA SPRY4-IT1 promotes proliferation and invasion by acting as a ceRNA of miR-101-3p in colorectal cancer cells;SPRY4-IT1 could negatively regulate the expression of miR-101-3p in colorectal carcinoma cells. The bioinformatics prediction revealed putative miR-101-3p binding sites within SPRY4-IT1 transcripts	28720069	RID00831	ceRNA or sponge
Thyroid cancer	LINC00312	PI3K	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);PI3K/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	Long Noncoding RNA LINC003121 Inhibits proliferation and Invasion of Thyroid Cancer Cells by Suppression of the Phosphatidylinositol-3-Kinase (PI3K)/Akt Signaling Pathway;LINC00312-mediated tumor suppression in TC cells may occur via suppression of activation of the PI3K/Akt signaling pathway and expression of MMP-9, and the role of MMP-9 expression induced by overexpressed LINC00312 or si-LINC00312 could be weakened by LY294002 (PI3K inhibitor). Results revealed that overexpression of LINC00312 significantly decreased the expressions of PI3K and p-Akt (both P<0.05), low expression of LINC00312 significantly increased the expressions of PI3K and p-Akt (both P<0.05)	29969438	RID00832	expression association
Thyroid cancer	LINC00312	AKT1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-);PI4K/AKT signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Thyroid cancer	lncRNA	PCG	NA	GRCh38_3:8571782-8574668	ENSG00000142208	NA	29931	207	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Noncoding RNA LINC003121 Inhibits proliferation and Invasion of Thyroid Cancer Cells by Suppression of the Phosphatidylinositol-3-Kinase (PI3K)/Akt Signaling Pathway;LINC00312-mediated tumor suppression in TC cells may occur via suppression of activation of the PI3K/Akt signaling pathway and expression of MMP-9, and the role of MMP-9 expression induced by overexpressed LINC00312 or si-LINC00312 could be weakened by LY294002 (PI3K inhibitor). Results revealed that overexpression of LINC00312 significantly decreased the expressions of PI3K and p-Akt (both P<0.05), low expression of LINC00312 significantly increased the expressions of PI3K and p-Akt (both P<0.05)	29969438	RID00833	expression association
Breast cancer	JMJD6	HOTAIR	positively-E	luciferase reporter assay;ChIP;electromobility shift assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000070495	NA	ENSG00000228630	GRCh38_12:53962308-53974956	23210	100124700	PSR|PTDSR|PTDSR1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	JMJD6 induces HOTAIR, an oncogenic lincRNA, by physically interacting with its proximal promoter;In ChIP assays, JMJD6 bound this region suggesting that JMJD6 may be directly recruited to the HOTAIR promoter;concurrent high expression of both genes correlated with poor survival when individual expression of either gene showed no significant association in TCGA datasets. We propose that high JMJD6 expression may achieve higher levels of HOTAIR in breast tumors. Further, since high levels of HOTAIR promote metastasis and death, blocking JMJD6 may be useful in preventing such events.	29229759	RID00834	transcriptional regulation
Colon cancer	LINC00261	CTNNB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000168036	NA	140828	1499	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy. LINC00261 might down-regulate nuclear beta-catenin through restraining beta-catenin from cytoplasm into nuclei or it could also promote beta-catenin degradation and inhibit activation of Wnt pathway;LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight	29267503	RID00835	expression association
Breast cancer	TUG1	CCND1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000110092	NA	55000	595	LINC00080|NCRNA00080|TI-227H	BCL1|D11S287E|PRAD1|U21B31	Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer;In vitro experiments revealed that TUG1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells, while TUG1 knockdown caused increased cell growth via promoting cell cycle progression and regulating the expression of CCND1 and CDK4	28950664	RID00836	expression association
Breast cancer	TUG1	CDK4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000135446	NA	55000	1019	LINC00080|NCRNA00080|TI-227H	CMM3|PSK-J3	Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer;In vitro experiments revealed that TUG1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells, while TUG1 knockdown caused increased cell growth via promoting cell cycle progression and regulating the expression of CCND1 and CDK4	28950664	RID00837	expression association
Colorectal cancer	MIR100HG	miR-100	positively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	host	regulation	NA	cetuximab	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00838	expression association
Colorectal cancer	MIR100HG	miR-125b	positively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	host	regulation	NA	cetuximab	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00839	expression association
Colorectal cancer	GATA6	MIR100HG	negatively-E	western blot;ChIP	upregulation	qPCR;sequencing	TCGA	COAD.zip	chemoresistance(+);WNT/beta-catenin signaling pathway(-)	transcriptional regulation	regulation	protein-DNA	cetuximab	NA	NA	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000141448	NA	ENSG00000255248	GRCh38_11:122028325-122556721	2627	399959	NA	AGD1|linc-NeD125|lncRNA-N2	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/beta-catenin signaling;miR-100 and miR-125b coordinately repressed five Wnt/beta-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness;Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6	29035371	RID00840	transcriptional regulation
Hepatocellular carcinoma	miR-215	PCAT1	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	100750225	NA	PCA1|PCAT-1	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma;We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays;We also found that post-transcriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 up-regulated PCAT-1 expression and promoted cell viability.Of note, gene profiling assays suggested that the kinase CRK-like proto-oncogene, adaptor protein (CRKL), is a potential downstream target of the miR-215-PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation.	28887306	RID00841	ceRNA or sponge
Hepatocellular carcinoma	PCAT1	CRKL	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000099942	NA	100750225	1399	PCA1|PCAT-1	NA	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma;We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays;We also found that post-transcriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 up-regulated PCAT-1 expression and promoted cell viability.Of note, gene profiling assays suggested that the kinase CRK-like proto-oncogene, adaptor protein (CRKL), is a potential downstream target of the miR-215-PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation.	28887306	RID00842	expression association
Breast cancer	LINC-ROR	DUSP7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000164086	NA	100885779	1849	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MKPX|PYST2	Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer;linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation;Taken together, these results suggest that linc-RoR promotes estrogen-independent growth and activation of MAPK/ERK pathway of breast cancer cells by regulating the ERK-specific phosphatase DUSP7	29041978	RID00843	expression association
Renal cell carcinoma	FILNC1	MYC	positively-E	western blot;RNA pull-down assay	upregulation	qPCR;sequencing	TCGA	KIRC.zip	energy metabolic process(-)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Kidney cancer	lncRNA	TF	ENSG00000231426	GRCh38_6:139677639-139860476	ENSG00000136997	NA	100132735	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Energy stress-induced lncRNA FILNC1 represses c-Myc-mediated energy metabolism and inhibits renal tumor development;We show that FILNC1 deficiency leads to enhanced glucose uptake and lactate production through upregulation of c-Myc;Upon energy stress, FILNC1 interacts with AUF1, a c-Myc mRNA-binding protein, and sequesters AUF1 from binding c-Myc mRNA, leading to downregulation of c-Myc protein; the authors show that upon energy stress FoxOs induce the expression of the long non-coding RNA FILNC1, which inhibits survival of RCC by downregulating c-Myc and c-Myc-dependent metabolic rewiring	28978906	RID00844	expression association
Osteosarcoma	FENDRR	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000087245	NA	400550	4313	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Antisense lncRNA FOXF1-AS1 Promotes Migration and Invasion of Osteosarcoma Cells Through the FOXF1/MMP-2/-9 Pathway;FOXF1-AS1 as well as FOXF1 silencing significantly inhibited cell proliferation, migration, invasion of OS cells and tumor growth both in vitro and vivo through decreasing the expression of MMP2 and MMP9, whereas enhanced expression of FOXF1-AS1 had the opposite effects;we concluded that FOXF1-AS1 may promote migration and invasion of OS cells through the FOXF1/MMP-2/-9 pathway	29104509	RID00845	expression association
Osteosarcoma	FENDRR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000100985	NA	400550	4318	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4B|GELB|MANDP2|MMP-9	Antisense lncRNA FOXF1-AS1 Promotes Migration and Invasion of Osteosarcoma Cells Through the FOXF1/MMP-2/-9 Pathway;FOXF1-AS1 as well as FOXF1 silencing significantly inhibited cell proliferation, migration, invasion of OS cells and tumor growth both in vitro and vivo through decreasing the expression of MMP2 and MMP9, whereas enhanced expression of FOXF1-AS1 had the opposite effects;we concluded that FOXF1-AS1 may promote migration and invasion of OS cells through the FOXF1/MMP-2/-9 pathway	29104509	RID00846	expression association
Gallbladder cancer	NMRAL2P	TWIST1	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000122691	NA	344887	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00847	expression association
Gallbladder cancer	NMRAL2P	VIM	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000026025	NA	344887	7431	NA	NA	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00848	expression association
Gallbladder cancer	NMRAL2P	CDH2	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000170558	NA	344887	1000	NA	CD325|CDHN|CDw325|NCAD	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00849	expression association
Gallbladder cancer	NMRAL2P	CDH1	negatively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000171658	GRCh38_3:185959943-185980872	ENSG00000039068	NA	344887	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype	28245089	RID00850	expression association
Esophageal cancer	TPM1-AS	TPM1	negatively-E	western blot;immunoprecipitation	downregulation	qRT-PCR	NA	NA	cell migration(-)	alternative splicing	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000259498	GRCh38_15:63046034-63049387	ENSG00000140416	NA	111064646	7168	TPM1-AS1	C15orf13|CMD1Y|CMH3|HEL-S-265|HTM-alpha|LVNC9|TMSA	Natural antisense transcript TPM1-AS regulates the alternative splicing of tropomyosin I through an interaction with RNA-binding motif protein 4; Mechanismly, the interaction of TPM1-AS with RBM4 hindered binding of RBM4 to TPM1 pre-mRNA and inhibited RBM4 to promote endogenous exon 2a inclusion of TPM1; Taken together, the results suggest that a natural antisense TPM1-AS regulates the alternative splicing of TPM1 through an interaction with RBM4 and involves in TPM1-mediated filopodium formation and migration of cancer cells	28754317	RID00851	interact with mRNA
Gastric cancer	AFAP1-AS1	AKT1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000142208	NA	84740	207	AFAP1-AS|AFAP1AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells;AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.	28451917	RID00852	expression association
Gastric cancer	AFAP1-AS1	PTEN	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000171862	NA	84740	5728	AFAP1-AS|AFAP1AS	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells;AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.	28451917	RID00853	expression association
Atherosclerosis	RP11-714G18.1	LRP2BP	positively-E	western blot;luciferase reporter assay;FISH	downregulation	qPCR;microarray	GSE97210	GSE97210.zip	cell migration(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000250410	GRCh38_4:185370725-185390928	ENSG00000109771	NA	NA	55805	NA	NA	LncRNA-RP11-714G18.1 suppresses vascular cell migration via directly targeting LRP2BP. Mechanistically, RP11-714G18.1 could directly bind to its nearby gene LRP2BP and increased the expression of LRP2BP.	29363163	RID00854	transcriptional regulation
Pre-eclampsia	MVIH	JUNB	positively-E	mass spectrometry	upregulation	qRT-PCR	NA	NA	cell growth(+);angiogenesis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cardiovascular system disease	Eclampsia	lncRNA	TF	NA	GRCh38_10:78038556-78040701	ENSG00000171223	NA	NA	3726	NA	AP-1	Promotion of trophoblast invasion by lncRNA MVIH through inducing Jun-B. Mass spectrometry analysis revealed that MVIH could modulate Jun-B protein expression, which has been reported to potentially regulate cell growth and angiogenesis	29083110	RID00855	expression association
Urinary bladder cancer	LINC00958	VEGFC	positively-E	RIP;ChIP;RNAi;IHC	upregulation	qPCR;microarray	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000150630	NA	100506305	7424	BLACAT2	Flt4-L|LMPH1D|LMPHM4|VRP	Long noncoding RNA BLACAT2 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. we demonstrate that BLACAT2 epigenetically upregulation VEGF-C expression by directly associating with WDR5, a core subunit of human H3K4 methyltransferase complexes.	29355840	RID00856	epigenetic regulation
Intervertebral disc degeneration	FAF1	MAPK1	positively-E	RNAi	upregulation	RT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000185104	GRCh38_1:50437028-50960267	ENSG00000100030	NA	NA	5594	CGI-03|HFAF1s|UBXD12|UBXN3A|hFAF1	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA FAF1 promotes intervertebral disc degeneration by targeting the Erk signaling pathway. The results of the present study demonstrated that the expression of FAF1 was upregulated in patients with disc bulging, herniation and IDD, and the expression of FAF1 was positively correlated with the grade of disc degeneration according to the patients' Pfirrmann score. The expression of phosphorylated extracellular signal-regulated kinase (Erk), a possible target of FAF1, was consistent with the expression of FAF1. In addition, it was elucidated that inactivation of the Erk signaling pathway by PD98059 reversed the effect of FAF1 on NP cell proliferation. Taken together, these results demonstrated that FAF1 was vital in the proliferation of NP cells by modulating the Erk signaling pathway, which suggests that FAF1 may be a novel marker in the early diagnosis of IDD and a therapeutic target for patients.	29257270	RID00857	expression association
Myocardial ischemia	TUG1	BNIP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000176171	NA	55000	664	LINC00080|NCRNA00080|TI-227H	NIP3	LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR-145-5p-Binp3 axis.	29207102	RID00858	expression association
Myocardial ischemia	TUG1	miR-145-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR-145-5p-Binp3 axis.In addition, miR-145-5p was negatively regulated by TUG1, and TUG1 overexpression aggravated hypoxia-induced injury via the downregulation of miR-145-5p.	29207102	RID00859	expression association
Osteosarcoma	MEG3	MDM2	positively-E	RNAi	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000135679	NA	55384	4193	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ACTFS|HDMX|hdm2	MEG3 inhibits proliferation and invasion and promotes apoptosis of human osteosarcoma cells. Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis.It was demonstrated that the upregulation of MEG3 significantly increased the transactivation of p53 and induced downstream changes in protein expression	29434890	RID00860	expression association
Osteosarcoma	MEG3	TP53	positively-E	RNAi	downregulation	RT-PCR	NA	NA	cell proliferation(-);cell invasion(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	MEG3 inhibits proliferation and invasion and promotes apoptosis of human osteosarcoma cells. Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis.It was demonstrated that the upregulation of MEG3 significantly increased the transactivation of p53 and induced downstream changes in protein expression	29434890	RID00861	expression association
Prostate cancer	SCHLAP1	MAPK1	positively-E	western blot;northern blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-198)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000281131	GRCh38_2:180692104-180916939	ENSG00000100030	NA	101669767	5594	LINC00913|PCAT11|PCAT114	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Noncoding RNA SChLAP1 Accelerates the proliferation and Metastasis of Prostate Cancer via Targeting miR-198 and Promoting the MAPK1 Pathway. Furthermore, our results showed that SChLAP1 interacted with miR-198 and subsequently modulated the MAPK1 signaling pathway in prostate cancer. miR-198 and MAPK1 had a targeted correlation	28492138	RID00862	ceRNA or sponge
Pulmonary hypertension	MEG3	PTEN	positively-E	RNAi;western blot;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Hypertension	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Down-regulation of lncRNA MEG3 promotes hypoxia-induced human pulmonary artery smooth muscle cell proliferation and migration via repressing PTEN by sponging miR-21. dual-luciferase reporter assay was applied to dissect the binding between PTEN and miR-21 and the results showed a decrease of luciferase activity in PASMCs co-transfected with wild-type PTEN and miR-21 mimics while restoration of luciferase activity was observed in cells co-transfected with mutant PTEN and miR-21 mimics.	29198701	RID00863	ceRNA or sponge
Osteosarcoma	RAB11B-AS1	RAB11B	negatively-F	luciferase reporter assay;western blot;IHC	downregulation	qRT-PCR	NA	NA	cancer progression(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000269386	GRCh38_19:8374373-8390685	ENSG00000185236	NA	100507567	9230	MIR4999HG	H-YPT3|NDAGSCW	Long non-coding RNA RAB11B-AS1 prevents osteosarcoma development and progression via its natural antisense transcript RAB11B. RAB11B-AS1 expression correlates negatively with RAB11B expression in OS tissues. Luciferase reporter assay illuminated that RAB11B-AS1 regulates RAB11B expression through antisense pairing. Thus our findings revealed that lnc-RAB11B-AS1 prevents osteosarcoma development and progression via inhibiting RAB11B expression, indicating lnc-RAB11B-AS1 as a potential therapeutic target for osteosarcoma.	29928484	RID00864	interact with mRNA
Hypertrophic scar	COL1A2-AS1	SMAD7	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	TF	NA	GRCh38_7:94367212-94392192	ENSG00000101665	NA	101927525	4092	TCONS_00013888|lncRNA8975-1	CRCS3|MADH7|MADH8	LncRNA COL1A2-AS1 inhibits the scar fibroblasts proliferation via regulating miR-21/Smad7 pathway. we found that miR-21 was involved in lncRNA COL1A2-AS1-induced expression of Smad7, by which COL1A2-AS1 acted as endogenous sponge to adsorb miR-21 and in turn regulated Smad7 and a cascade of molecular to play a protective role in hypertrophic scar	29117538	RID00865	ceRNA or sponge
Hypertrophic scar	COL1A2-AS1	miR-21	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Other	Hypertrophic scar	lncRNA	miRNA	NA	GRCh38_7:94367212-94392192	NA	NA	101927525	NA	TCONS_00013888|lncRNA8975-1	NA	LncRNA COL1A2-AS1 inhibits the scar fibroblasts proliferation via regulating miR-21/Smad7 pathway. we found that miR-21 was involved in lncRNA COL1A2-AS1-induced expression of Smad7, by which COL1A2-AS1 acted as endogenous sponge to adsorb miR-21 and in turn regulated Smad7 and a cascade of molecular to play a protective role in hypertrophic scar	29117538	RID00866	ceRNA or sponge
Heart failure	FTX	BCL2L2	negatively-E	Targetscan;RNAhybrid;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-29b-1-5p)	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000129473	NA	100302692	599	LINC00182|MIR374AHG|NCRNA00182	BCL-W|BCL2-L-2|BCLW|PPP1R51	Long noncoding RNA FTX regulates cardiomyocyte apoptosis by targeting miR-29b-1-5p and Bcl2l2. We then found that FTX functions as endogenous sponge for miR-29b-1-5p and regulates the activity of miR-29b-1-5p.Bcl2l2 was found to harboring a potential target site for miR-29b-1-5p.	29117536	RID00867	ceRNA or sponge
Osteosarcoma	SNHG1	WNT2B	positively-E	starBase;RegRNA;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-577)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000134245	NA	23642	7482	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	WNT13	Up-regulated lnc-SNHG1 contributes to osteosarcoma progression through sequestration of miR-577 and activation of WNT2B/Wnt/beta-catenin pathway. we also found that miR-577 could act as a ceRNA of SNHG1 in OS cells and the promotion of OS progression induced by lnc-SNHG1 overexpression required the inactivity of miR-577	29108989	RID00868	ceRNA or sponge
Gastric cancer	CYTOR	PRKAA1	positively-E	Targetscan;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glucose metabolic process(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000132356	NA	112597	5562	C2orf59|LINC00152|NCRNA00152	AMPK|AMPKa1	LINC00152/miR-139-5p regulates gastric cancer cell aerobic glycolysis by targeting PRKAA1. We also found that miR-139-5p was down-regulated by long intergenic non-coding RNA 152 (LINC00152) in gastric cancer cells.It is reported that miR-139-5p is a target miRNA of long non-codingRNA LINC00152. PRKAA1 was a target gene of miR-139-5p in gastric cancer cells	29156518	RID00869	ceRNA or sponge
Atherosclerosis	MIAT	STAT3	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-181b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000168610	NA	440823	6774	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	ADMIO|ADMIO1|APRF|HIES	MIAT promotes proliferation and hinders apoptosis by modulating miR-181b/STAT3 axis in ox-LDL-induced atherosclerosis cell models. Moreover, MIAT enhanced STAT3 expression through sequestering miR-181b as a molecular sponge. Furthermore, MiR-181b hindered cell growth, induced cell cycle arrest and promoted apoptosis by directly targeting STAT3.	29136944	RID00870	ceRNA or sponge
Colorectal cancer	TP73-AS1	TGFA	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-194)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000163235	NA	57212	7039	KIAA0495|PDAM	TFGA	Long non-coding RNA TP73-AS1 sponges miR-194 to promote colorectal cancer cell proliferation, migration and invasion via up-regulating TGFalpha. Bioinformatics analysis and luciferase reporter assay indicated that TP73-AS1 could bind directly with miR-194, and TP73-AS1 negatively regulated the expression of miR-194 in CRC cells. TGFalpha is a direct target of miR-194	30010111	RID00871	ceRNA or sponge
Ovarian cancer	SNHG3	GSK3B	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	oncogenic role(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000082701	NA	8420	2932	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	NA	Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer. SNHG3 functioned as an oncogene by regulating GSK3beta/beta-catenin signaling activity in ovarian cancer	29758922	RID00872	expression association
Ovarian cancer	SNHG3	CTNNB1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	oncogenic role(+)	NA	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000242125	GRCh38_1:28505980-28510892	ENSG00000168036	NA	8420	1499	NCRNA00014|RNU17C|RNU17D|U17HG|U17HG-A|U17HG-AB	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer. SNHG3 functioned as an oncogene by regulating GSK3beta/beta-catenin signaling activity in ovarian cancer	29758922	RID00873	expression association
Ovarian cancer	MYC	DANCR	positively-E	RNAi;ChIP	upregulation	qRT-PCR;sequencing	GSE51010;TCGA	GSE51010.zip;OV.zip	cell proliferation(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000226950	GRCh38_4:52712404-52720351	4609	57291	MRTL|MYCC|bHLHe39|c-Myc	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	MYC Targeted Long Noncoding RNA DANCR Promotes Cancer in Part by Reducing p21 Levels. Here, we report that MYC stimulates the transcription of DANCR, a long noncoding RNA (lncRNA) that is widely overexpressed in human cancer. Our observations expand knowledge of how MYC drives cancer cell proliferation by identifying DANCR as a critical lncRNA widely overexpressed in human cancers.	29180471	RID00874	transcriptional regulation
Ovarian cancer	DANCR	CDKN1A	negatively-E	RNAi	upregulation	qRT-PCR;sequencing	TCGA	OV.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000124762	NA	57291	1026	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	MYC Targeted Long Noncoding RNA DANCR Promotes Cancer in Part by Reducing p21 Levels. Mechanistic investigations indicated that DANCR limited the expression of cell-cycle inhibitor p21 (CDKN1A) and that the inhibitory effects of DANCR loss on cell proliferation could be partially rescued by p21 silencing.	29180471	RID00875	expression association
Aortic valve disease	TUG1	RUNX2	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell differentiation(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000124813	NA	55000	860	LINC00080|NCRNA00080|TI-227H	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 in aortic valve calcification.human Runx2 3'-UTRfragments containing putative binding sites for the miR-204-5p reportervector and the Runx2 promoter reporter vector were used in Dual-luciferase Reporter Assays.	29016735	RID00876	ceRNA or sponge
Osteoarthritis	KLF3-AS1	GIT1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000231160	GRCh38_4:38602438-38664914	ENSG00000108262	NA	79667	28964	NA	NA	MSC-derived exosomes promote proliferation and inhibit apoptosis of chondrocytes via lncRNA-KLF3-AS1/miR-206/GIT1 axis in osteoarthritis. Results also demonstrated that KLF3-AS1 acted as a competitive endogenous RNA (ceRNA) by sponging miR-206 to facilitate GIT1 expression	30324848	RID00877	ceRNA or sponge
Hirschsprung's disease	LOC100507600	BMI1	negatively-E	western blot;RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-128-1-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000226806	GRCh38_2:135820191-135823087	ENSG00000168283	NA	100507600	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long non-coding RNA LOC100507600 functions as a competitive endogenous RNA to regulate BMI1 expression by sponging miR128-1-3p in Hirschsprung's disease. Downregulation of LOC100507600 repressed cell migration and proliferation and didn't affect cell apoptosis or cycle. In sum, our study researches the potential diagnostic value of LOC100507600 in HSCR and deduces that LOC100507600 can contributes to HSCR as a competitive endogenous RNA to regulate BMI1 expression by sponging miR128-1-3p.	29429387	RID00878	ceRNA or sponge
Non-small cell lung cancer	GAPLINC	EEF2K	positively-E	western blot;luciferase reporter assay;FISH	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(miR-661)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000103319	NA	100505592	29904	LINC01540	CaMKIII|HSU93850|eEF-2K	Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway. Bioinformatic analysis and luciferase reporter confirmed that miR-661 targeted GAPLINC and eEF2K 3'-UTR and was negatively correlated with the expression of GAPLINC and eEF2K. Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.	30522114	RID00879	ceRNA or sponge
Acute myeloid leukemia	HOXA-AS2	S100A4	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-520c-3p)	regulation	NA	adriamycin	NA	Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000196154	NA	285943	6275	HOXA3as	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	Knockdown of Long Noncoding RNA HOXA-AS2 Suppresses Chemoresistance of Acute Myeloid Leukemia via the miR-520c-3p/S100A4 Axis. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay and anti-Ago2 RIP assay.HOXA-AS2 could negatively regulate the expression of miR-520c-3p in ADR cells. S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay.	30466095	RID00880	ceRNA or sponge
Osteosarcoma	SNHG16	ZEB1	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+)	ceRNA(miR-205)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000148516	NA	100507246	6935	Nbla10727|Nbla12061|ncRAN	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long Noncoding RNA SNHG16 Promotes Cell proliferation by Sponging MicroRNA-205 and Upregulating ZEB1 Expression in Osteosarcoma. ZEB1 was the target gene of miR-205	30453308	RID00881	ceRNA or sponge
Hepatocellular carcinoma	CERNA2	JAK2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000096968	NA	642934	3717	HOST2|lncRNA-HOST2	JTK10|THCYT3	Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway.The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.	30453302	RID00882	expression association
Hepatocellular carcinoma	CERNA2	STAT3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000168610	NA	642934	6774	HOST2|lncRNA-HOST2	ADMIO|ADMIO1|APRF|HIES	Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway.The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.	30453302	RID00883	expression association
Colorectal cancer	XIST	SGK1	positively-E	luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-124)	regulation	NA	doxorubicin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000118515	NA	7503	6446	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	SGK	Knockdown of Long Non-Coding RNA XIST Inhibited Doxorubicin Resistance in Colorectal Cancer by Upregulation of miR-124 and Downregulation of SGK1.XIST positively regulated SGK1 expression by interacting with miR-124 in DOX-resistant CRC cells. binding sites of miR-124 were identified in the 3'UTR of SGK1 mRNA.XIST exerted regulatory function in resistance of DOX possibly through miR-124/SGK1 axis, shedding new light on developing promising therapeutic strategy to overcome chemoresistance in CRC patients.	30439718	RID00884	ceRNA or sponge
Hepatocellular carcinoma	CRNDE	IRX5	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	oncogenic role(+)	ceRNA(miR-136-5p)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000176842	NA	NA	10265	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HMMS|IRX-2a|IRXB2	Long-Noncoding RNA Colorectal Neoplasia Differentially Expressed Gene as a Potential Target to Upregulate the Expression of IRX5 by miR-136-5P to Promote Oncogenic Properties in Hepatocellular Carcinoma. CRNDE acted as a tumor oncogene by exhibiting oncogenic properties of human HCC and revealed a novel CRNDE-miR-136-5P-IRX5 regulatory network in HCC .Using a bioinformatics databases (Starbase, RNAhybrid), miR-136-5P is a putative target of CRNDE in several miRNAs. MiR-136-5P inhibited the expression of IRX5 by targeting its 3'UTR and miR-136-5P was involved in the CRNDE-regulated expression of IRX5.	30423553	RID00885	ceRNA or sponge
Ischemic stroke	MALAT1	MDM2	positively-E	western blot;FISH	upregulation	qRT-PCR	NA	NA	p53 signaling pathway(+)	NA	regulation	NA	NA	NA	Genome Instability and Mutation	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135679	NA	378938	4193	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ACTFS|HDMX|hdm2	MALAT1 Activates the P53 Signaling Pathway by Regulating MDM2 to Promote Ischemic Stroke. Both MALAT1 and MDM2 were localized in the nuclei. Down regulation of MALAT1 and MDM2 enhanced cell proliferation ability and reduced apoptosis, resulting in decreased infarct size in MCAO/R brains. These results indicate that MALAT1/MDM2/p53 signaling pathway axis may provide more effective clinical therapeutic strategy for patients with ischemic stroke.	30419554	RID00886	expression association
Hepatocellular carcinoma	HOXA-AS2	GPC3	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-520c-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000147257	NA	285943	2719	HOXA3as	DGSX|GTR2-2|MXR7|OCI-5|SDYS|SGB|SGBS|SGBS1	HOXA-AS2 Promotes Proliferation and Induces Epithelial-Mesenchymal Transition via the miR-520c-3p/GPC3 Axis in Hepatocellular Carcinoma. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. By bioinformatic analysis and dual-luciferase reporter assay, we found that miR-223-3p directly targeted the 3'-untranslated region (UTR) of Glypican-3 (GPC3), one of the key players in HCC.	30415263	RID00887	ceRNA or sponge
Papillary thyroid carcinoma	HOXA-AS2	S100A4	positively-E	western blot;luciferase reporter assay;RIP;IHC	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-520c-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000196154	NA	285943	6275	HOXA3as	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	Long Noncoding RNA HOXA-AS2 Promotes Papillary Thyroid Cancer Progression by Regulating miR-520c-3p/S100A4 Pathway. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOXA-AS2 and miR-520c-3p in PTC.MiR-520c-3p was down-regulated in PTC tissues, and S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay.	30384358	RID00888	ceRNA or sponge
Cardiomyopathy	KCNQ1OT1	miR-214-3p	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell death(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	miRNA	ENSG00000269821	GRCh38_11:2608328-2699994	NA	NA	10984	NA	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	NA	LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1.	30355944	RID00889	expression association
Cardiomyopathy	KCNQ1OT1	CASP1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell death(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000137752	NA	10984	834	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	ICE|IL1BC|P45	LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1.	30355944	RID00890	expression association
Malignant glioma	H19	SOX4	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR;sequencing	TCGA;GSE16011;GSE4290	GBM.zip;GSE16011.zip;GSE4290.zip	epithelial to mesenchymal transition(+)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000124766	NA	283120	6659	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	EVI16	H19 Functions as a Competing Endogenous RNA to Regulate EMT by Sponging miR-130a-3p in Glioma. H19 and SOX4 are both direct target of miR-130a-3p. H19 could compete with SOX4 via sponging miR-130a-3p.	30282068	RID00891	ceRNA or sponge
Colorectal adenocarcinoma	H19	miR-194-5p	negatively-F	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma. H19 modified miR-194-5p expression through directly targeting at it. LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.	30278464	RID00892	ceRNA or sponge
Colorectal adenocarcinoma	H19	FOXM1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111206	NA	283120	2305	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma. H19 modified miR-194-5p expression through directly targeting at it. LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.	30278464	RID00893	expression association
Hepatocellular carcinoma	MALAT1	VIM	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-30a-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma. Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion.	30278452	RID00894	ceRNA or sponge
Non-small cell lung cancer	AFAP1-AS1	IRF7	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000185507	NA	84740	3665	AFAP1-AS|AFAP1AS	IMD39|IRF-7|IRF-7H|IRF7A|IRF7B|IRF7C|IRF7H	lncRNA AFAP1-AS1 promotes migration and invasion of non-small cell lung cancer via up-regulating IRF7 and the RIG-I-like receptor signaling pathway.	30278439	RID00895	expression association
Cervical cancer	DLG1-AS1	ZHX1	positively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-107)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000227375	GRCh38_3:197298252-197303755	ENSG00000165156	NA	100507086	11244	NA	NA	lncRNA DLG1-AS1 Promotes Cell proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer.	30231238	RID00896	ceRNA or sponge
Lung cancer	HOTAIR	EZH2	interact	RIP;RNAi	upregulation	qRT-PCR	NA	NA	chemosensitivity(+)	interact with protein	binding/interaction	RNA-protein	ATL-1;erlotinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Repression of PDK1- and LncRNA HOTAIR-Mediated EZH2 Gene Expression Contributes to the Enhancement of Atractylenolide 1 and Erlotinib in the Inhibition of Human Lung Cancer Cells. While silencing HOTAIR inhibited the expressions of PDK1 and EZH2, overexpression of HOTAIR reduced the ATL-1-reduced PDK1 and EZH2 protein expressions and EZH2 promoter activity. In addition, ATL-1 reduced the HOTAIR binding to the EZH2 protein. Thus, targeting the PDK1- and HOTAIR-mediated downstream molecule EZH2 by the combination of ATL-1 and erlotinib potentially facilitates the development of an additional novel strategy to combat lung cancer. major bioactive compound of Atractylodes macrocephula Koidz atractylenolide 1 (ATL-1)	30223276	RID00897	interact with protein
Hepatocellular carcinoma	PVT1	HILPDA	positively-E	western blot;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-150)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000135245	NA	5820	29923	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Non-Coding RNA PVT1/miR-150/ HIG2 Axis Regulates the Proliferation, Invasion and the Balance of Iron Metabolism of Hepatocellular Carcinoma. PVT1 could directly bind to microRNA (miR)-150 and down-regulate miR-150 expression. miR-150 directly targets 3-UTR of HIG2 to regulate its expression	30205391	RID00898	ceRNA or sponge
Ovarian cancer	HOTAIR	CCND1	positively-E	western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer.HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.	30205383	RID00899	ceRNA or sponge
Ovarian cancer	HOTAIR	CCND2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000118971	NA	100124700	894	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	KIAK0002|MPPH3	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer.	30205383	RID00900	ceRNA or sponge
Atherosclerosis	GAS5	PDCD4	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150593	NA	60674	27250	NCRNA00030|SNHG2	H731	Association Between the Deletion Allele of Ins/Del Polymorphism (Rs145204276) in the Promoter Region of GAS5 with the Risk of Atherosclerosis. GAS5 directly targets miR-21 and functions as a competing endogenous RNA to suppress miR-21 expression.GAS5 positively regulated PDCD4 expression via inhibiting miR-21 expression. In summary, rs145204276 was associated with the risk of atherosclerosis by affecting the proliferation and apoptosis of endothelial cells via regulating the GAS5/miR-21/PDCD4 signaling pathway.	30205366	RID00901	ceRNA or sponge
Breast cancer	KCNQ1OT1	CCNE2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000175305	NA	10984	9134	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CYCE2	The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells. KKCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2.	30157476	RID00902	ceRNA or sponge
Colorectal cancer	SNHG6	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE14333;GSE37892;GSE20916;GSE18105;TCGA	GSE14333.zip;GSE37892.zip;GSE20916.zip;GSE18105.zip;COAD.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells.	30157475	RID00903	epigenetic regulation
Gastric cancer	EGFR-AS1	EGFR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000146648	NA	100507500	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer. And the expression of EGFR-AS1 positively correlated with EGFR in tissues	30138934	RID00904	expression association
Multiple myeloma	MEG3	HOXA11	positively-E	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE5900;GSE2658	GSE5900.zip;GSE2658.zip	cancer progression(-)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000005073	NA	55384	3207	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HOX1|HOX1I|RUSAT1	Long Non-Coding RNA MEG3 Functions as a Competing Endogenous RNA to Regulate HOXA11 Expression by Sponging miR-181a in Multiple Myeloma. Importantly, several mechanism experiments revealed that MEG3, acting as an endogenous competitive RNA, could contend with miR-181a to inhibit tumor progression. Our present work supplies the first discovery of a MEG3/miR-181a/HOXA11 regulatory network in MM and highlights that MEG3 may serve as a promising target for MM therapy in the future.	30134227	RID00905	ceRNA or sponge
Multiple myeloma	LINC00515	ATG14	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell autophagy(+)	ceRNA(miR-140-5p)	regulation	NA	melphalan	NA	Evading Apoptosis	Cancer	Myeloma	lncRNA	PCG	ENSG00000260583	GRCh38_21:25582775-25583224	ENSG00000126775	NA	282566	22863	NA	ATG14L|BARKOR|KIAA0831	Linc00515 enhanced autophagy and chemoresistance of melphalan-resistant myeloma by directly inhibiting miR-140-5p, which elevated ATG14 level. Results were shown by the dual-luciferase reporter gene assay that linc00515 directly targeted miR-140-5p, which directly bound to ATG14	30121664	RID00906	ceRNA or sponge
Colorectal cancer	BCYRN1	NPR3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000113389	NA	618	4883	BC200|BC200a|LINC00004|NCRNA00004	ANP-C|ANPR-C|ANPRC|C5orf23|GUCY2B|NPR-C|NPRC	Long Noncoding RNA BCYRN1 Promotes the proliferation of Colorectal Cancer Cells via Up-Regulating NPR3 Expression	30114690	RID00907	expression association
Hepatocellular carcinoma	TUG1	ZEB1	positively-E	luciferase reporter assay;RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-142-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148516	NA	55000	6935	LINC00080|NCRNA00080|TI-227H	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1. miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulation ZEB1 was via direct binding to miR-142-3p. ZEB1 was identified as a target of miR-142-3p.	30092578	RID00908	ceRNA or sponge
Spinal cord glioma	LINC01260	CARD11	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);NF-kB signaling pathway(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000283440	GRCh38_20:44656451-44663498	ENSG00000198286	NA	79015	84433	NA	BENTA|BIMP3|CARMA1|IMD11|IMD11A|PPBL	Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-kB Signaling Pathway.CARD11 was confirmed to be a target gene of LINC01260 and was found to be involved in regulating the NF-kB pathway. A dual-luciferase reporter assay was conducted to verify the target relationship between LINC01260 and CARD11. Our findings demonstrate that overexpression of LINC01260 inhibits spinal cord glioma cell proliferation, migration and invasion by targeting CARD11 via NF-kB signaling suppression	30071522	RID00909	transcriptional regulation
Pituitary cancer	SNHG1	TGFBR2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-302;miR-372;miR-373;miR-520)	regulation	NA	NA	NA	NA	Cancer	Pituitary cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000163513	NA	23642	7048	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AAT3|FAA3|LDS1B|LDS2|LDS2B|MFS2|RIIC|TAAD2|TBR-ii|TBRII|TGFR-2|TGFbeta-RII	Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/beta-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.	30048990	RID00910	ceRNA or sponge
Pituitary cancer	SNHG1	RAB11A	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-302;miR-372;miR-373;miR-520)	regulation	NA	NA	NA	NA	Cancer	Pituitary cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000103769	NA	23642	8766	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	YL8	Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/beta-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.	30048990	RID00911	ceRNA or sponge
Breast cancer	LOC101930370	SHH	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	ceRNA(miR-1471)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245213	GRCh38_4:173131933-173169652	ENSG00000164690	NA	101930370	6469	NA	HHG1|HLP3|HPE3|MCOPCB5|SMMCI|ShhNC|TPT|TPTPS	LOC101930370/MiR-1471 Axis Modulates the Hedgehog Signaling Pathway in Breast Cancer. LOC101930370 positively regulates the expression of SHH by sponging miR-1471	30041193	RID00912	ceRNA or sponge
Clear cell renal cell carcinoma	MIAT	LOXL2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-29c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000134013	NA	440823	4017	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	LOR|LOR2|WS9-14	Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma.Our data indicated that MIAT might be an oncogenic lncRNA that promoted proliferation and metastasis of ccRCC, and could be a potential therapeutic target in human ccRCC.	30041179	RID00913	ceRNA or sponge
Lung adenocarcinoma	NEAT1	USF1	positively-E	luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE7670;GSE10072;GSE19188;GSE31210;GSE27262;GSE4376;TCGA	GSE7670.zip;GSE10072.zip;GSE19188.zip;GSE31210.zip;GSE27262.zip;GSE4376.zip;COAD.zip	tumorigenesis(+);cancer progression(+)	ceRNA(miR-193a-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000158773	NA	283131	7391	LINC00084|NCRNA00084|TncRNA|VINC	FCHL|FCHL1|HYPLIP1|MLTF|MLTFI|UEF|bHLHb11	The LncRNA NEAT1 Accelerates Lung Adenocarcinoma Deterioration and Binds to Mir-193a-3p as a Competitive Endogenous RNA. The dual-luciferase reporter assay demonstrated that miR-193a-3p directly targeted NEAT1 at its 3'-UTR. NEAT1 may function as a ceRNA to sponge miR-193a-3p and abrogate the inhibitory effect of miR-193a-3p on USF1. Our findings indicate that NEAT1 plays important roles in the occurrence and progression of LUAD. It may exert its role by acting as a ceRNA to regulate miR-193a-3p.	30036873	RID00914	ceRNA or sponge
Clear cell renal cell carcinoma	LUCAT1	AKT1	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	KIRC.zip	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000142208	NA	100505994	207	SCAL1|SCAT5	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long Non-Coding RNA LUCAT1 Promotes Proliferation and Invasion in Clear Cell Renal Cell Carcinoma Through AKT/GSK-3beta Signaling Pathway. Mechanistic investigations showed that LUCAT1 induced cell cycle G1 arrest by regulating the expression of cyclin D1, cyclin-dependent kinase 4, and phosphorylated retinoblastoma transcriptional corepressor 1. Moreover, LUCAT1 promoted proliferation and invasion in ccRCC cells partly through inducing the phosphorylation of AKT and suppressing the phosphorylation of GSK-3beta	30032137	RID00915	expression association
Clear cell renal cell carcinoma	LUCAT1	GSK3B	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	KIRC.zip	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000082701	NA	100505994	2932	SCAL1|SCAT5	NA	Long Non-Coding RNA LUCAT1 Promotes Proliferation and Invasion in Clear Cell Renal Cell Carcinoma Through AKT/GSK-3beta Signaling Pathway.Moreover, LUCAT1 promoted proliferation and invasion in ccRCC cells partly through inducing the phosphorylation of AKT and suppressing the phosphorylation of GSK-3beta	30032137	RID00916	expression association
Ovarian cancer	MALAT1	ATG7	positively-E	luciferase reporter assay;western blot	Upregulation	qPCR	NA	NA	cell autophagy(+);cell invasion(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000197548	NA	378938	10533	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG7-LIKE|APG7L|GSA7	Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer.MARCH7 interacted with MALAT1 by miR-200a (microRNA-200a). MARCH7 may function as a competing endogenous RNA (ceRNA) to regulate the expression of ATG7 by competing with miR-200a.	29794480	RID00917	expression association
Urinary bladder cancer	CDR1-AS	miR-135a	negatively-F	RIP;RNA pull-down assay;RNA-FISH	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	circRNA	miRNA	NA	NA	NA	NA	103611090	NA	CDR1NAT|CDR1as|ciRS-7	NA	CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a.	29694981	RID00918	ceRNA or sponge
Lupus nephritis	TUG1	miR-223	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell injury(-)	NA	regulation	NA	NA	NA	NA	Urinary system disease	Nephritis	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 protects renal tubular epithelial cells against injury induced by lipopolysaccharide via regulating microRNA-223. LPS administration inhibited HK-2 cell viability and proliferation, increased expression of pro-inflammatory factors, and promoted cell apoptosis. TUG1 overexpression protected HK-2 cells against LPS-induced injury via negatively regulating miR-223 expression.	29800915	RID00919	expression association
Osteoarthritis	ZFAS1	WNT3A	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000154342	NA	441951	89780	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Role of long noncoding RNA ZFAS1 in proliferation, apoptosis and migration of chondrocytes in osteoarthritis. overexpressed ZFAS1 significantly decreased Wnt3a factors.Our study demonstrates that ZFAS1 may promote chondrocyte proliferation, and migration, and decrease apoptosis and matrix synthesis in OA possible via targeting Wnt3a signaling.	29703568	RID00920	expression association
Breast cancer	HOTAIR	PTEN	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Downregulation of Long Noncoding RNA HOTAIR and EZH2 Induces Apoptosis and Inhibits Proliferation, Invasion, and Migration of Human Breast Cancer Cells. HOTAIR could bind specifically to EZH2 and PTEN, highlighting the capability of HOTAIR to inhibit the expression of PTEN by recruiting EZH2 in breast cancer.the downregulation of HOTAIR or silencing of EZH2 was revealed to repress the proliferation, invasion, and migration, while acting to promote the apoptosis of the breast cancer cells.	30048163	RID00921	epigenetic regulation
Endometrial cancer	LINC00261	FOXO1	positively-E	RIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000150907	NA	140828	2308	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	FKH1|FKHR|FOXO1A	Long noncoding RNA LINC00261 regulates endometrial carcinoma progression by modulating miRNA/FOXO1 expression. Overexpressed LINC00261 lowered these dissociative miRNAs, resulting in increase of FOXO1 protein levels.LINC00261 promotes FOXO1 expression through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion.	30019459	RID00922	ceRNA or sponge
Chronic myeloid leukemia	STAT3	MEG3	negatively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	JAK/STAT signaling pathway(+);cell proliferation(+);apoptosis process(-)	phosphorylated	binding/interaction	protein-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	TF	lncRNA	ENSG00000168610	NA	ENSG00000214548	GRCh38_14:100779410-100861031	6774	55384	ADMIO|ADMIO1|APRF|HIES	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00923	interact with protein
Chronic myeloid leukemia	MEG3	JAK2	negatively-E	RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	JAK/STAT signaling pathway(-);cell proliferation(-);apoptosis process(+)	mediate protein interactions	binding/interaction	protein-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000096968	NA	55384	3717	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	JTK10|THCYT3	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00924	interact with protein
Chronic myeloid leukemia	MEG3	miR-147	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	JAK/STAT signaling pathway(-);cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia. the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. A dual luciferase reporter assay was performed to verify the interaction between miR-147 and MEG3, MEG3 overexpression decreased the expressionof miR-147. MEG3 Overexpression Substantially Reduced the Phosphorylation of JAK2 and STATs. STAT3 Regulated the Expression of MEG3.LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.	30072211	RID00925	ceRNA or sponge
Esophageal cancer	FALEC	PDK1	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);AKT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000152256	NA	100874054	5163	FAL1|LINC00568|ncRNA-a1	NA	Long non-coding RNA FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in esophageal cancer cells. Overexpressed FAL1 activated Akt pathway via interacting with PDK1 in EC cell lines.FAL1 regulated cell proliferation through Akt pathway via targeting PDK1 in EC cells. These findings revealed that FAL1 exhibited oncogenic activity in EC, and inhibiting FAL1 might be useful for preventing the progression of EC.The interaction effect between FAL1 and 3-phosphoinositide-dependent protein kinase 1 (PDK1) was evaluated by chromatin immunoprecipitation (ChIP) assay.	30178844	RID00926	interact with protein
Malignant choroid melanoma	FOXCUT	MMP9	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Choroid cancer	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000100985	NA	101927703	4318	LINC01379|TCONS_00011636	CLG4B|GELB|MANDP2|MMP-9	Coordinated targeting of MMP-2/MMP-9 by miR-296-3p/FOXCUT exerts tumor-suppressing effects in choroidal malignant melanoma. Bioinformatics prediction and our experiments validated that MMP-2 and MMP-9 were simultaneously targeted by miR-296-3p and FOXC1 promoter upstream transcript (FOXCUT). Our data indicated that MMP-2/MMP-9 was coordinately targeted by two non-coding RNAs, miR-296-3p and FOXCUT, which were decreased, and tumor-suppressing factors in CMM.	29260433	RID00927	transcriptional regulation
Malignant choroid melanoma	FOXCUT	MMP2	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Choroid cancer	lncRNA	PCG	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000087245	NA	101927703	4313	LINC01379|TCONS_00011636	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Coordinated targeting of MMP-2/MMP-9 by miR-296-3p/FOXCUT exerts tumor-suppressing effects in choroidal malignant melanoma. Bioinformatics prediction and our experiments validated that MMP-2 and MMP-9 were simultaneously targeted by miR-296-3p and FOXC1 promoter upstream transcript (FOXCUT). Our data indicated that MMP-2/MMP-9 was coordinately targeted by two non-coding RNAs, miR-296-3p and FOXCUT, which were decreased, and tumor-suppressing factors in CMM.	29260433	RID00928	transcriptional regulation
Colon cancer	CASC15	LGR5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+)	ceRNA(miR-4310)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000272168	GRCh38_6:21664185-22654455	ENSG00000139292	NA	401237	8549	CANT|LINC00340|lnc-SOX4-1	FEX|GPR49|GPR67|GRP49|HG38	LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR-4310/LGR5/Wnt/beta-catenin signaling pathway. CASC15 was observed to act as a sponge to suppress microRNA (miR)-4310 that targeted LGR5. Through the inhibition of miR-4310, CASC15 promoted leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/beta-catenin signaling pathway. The results revealed that the inhibition of the Wnt/beta-catenin signaling pathway in CASC15-overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion.	29956772	RID00929	ceRNA or sponge
Osteosarcoma	AFAP1-AS1	TCF4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(-);cell invasion(-)	ceRNA(miR-4695-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196628	NA	84740	6925	AFAP1-AS|AFAP1AS	E2-2|FECD3|ITF-2|ITF2|PTHS|SEF-2|SEF2|SEF2-1|SEF2-1A|SEF2-1B|SEF2-1D|TCF-4|bHLHb19	Long noncoding RNA AFAP1-AS1 enhances cell proliferation and invasion in osteosarcoma through regulating miR-4695-5p/TCF4-beta-catenin signaling. AFAP1-AS1 served as a sponge to repress the level of microRNA (miR)-4695-5p, which targeted transcription factor (TCF)4, a pivot effector of Wnt/beta-catenin signaling pathway. It was demonstrated that overexpression of AFAP1-AS1 inhibited the expression of miR-4695-5p, while miR-4695-5p overexpression decreased TCF4 expression and reduced activation of Wnt/beta-catenin pathway.AFAP1-AS1 knockdown significantly inhibited the proliferation and invasion of OS cells in vitro.	29901121	RID00930	ceRNA or sponge
Colorectal cancer	PCBP2-OT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124762	NA	102157401	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	uc.338 targets p21 and cyclin D1 via PI3K/AKT pathway activation to promote cell proliferation in colorectal cancer. Further investigations in vivo and in vitro revealed that uc.338 could promote proliferation and cell cycle G1/S transition, and might target p21 downregulation and cyclin D1 upregulation via the PI3K/AKT pathway in CRC cells.	29901203	RID00931	expression association
Colorectal cancer	PCBP2-OT1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000110092	NA	102157401	595	NA	BCL1|D11S287E|PRAD1|U21B31	uc.338 targets p21 and cyclin D1 via PI3K/AKT pathway activation to promote cell proliferation in colorectal cancer. Further investigations in vivo and in vitro revealed that uc.338 could promote proliferation and cell cycle G1/S transition, and might target p21 downregulation and cyclin D1 upregulation via the PI3K/AKT pathway in CRC cells.	29901203	RID00932	expression association
Thyroid cancer	BANCR	MAP1LC3A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000101460	NA	100885775	84557	LINC00586	ATG8E|LC3|LC3A|MAP1ALC3|MAP1BLC3	Effects of serine/threonine-protein kinase B-Raf-activated long-chain non-coding RNA on apoptosis and autophagy in thyroid carcinoma cells. Inhibition of lncRNA-BANCR expression attenuated the proliferation and invasion ability of thyroid cancer cells; but the apoptosis was enhanced; the expression levels of autophagy protein LC3-I and LC3-II were also increased.Western blot was used to detect the changes of autophagy proteins LC3-I and LC3-II after the lncRNA-BANCR expression was suppressed.	30124210	RID00935	expression association
Thyroid cancer	BANCR	MAP1LC3B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000140941	NA	100885775	81631	LINC00586	ATG8F|LC3B|MAP1A/1BLC3|MAP1LC3B-a	Effects of serine/threonine-protein kinase B-Raf-activated long-chain non-coding RNA on apoptosis and autophagy in thyroid carcinoma cells. Inhibition of lncRNA-BANCR expression attenuated the proliferation and invasion ability of thyroid cancer cells; but the apoptosis was enhanced; the expression levels of autophagy protein LC3-I and LC3-II were also increased.Western blot was used to detect the changes of autophagy proteins LC3-I and LC3-II after the lncRNA-BANCR expression was suppressed.	30124210	RID00936	expression association
Esophagus squamous cell carcinoma	PART1	BCL2	positively-E	RIP;miRcode;Targetscan;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-129)	regulation	NA	gefitinib	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000152931	GRCh38_5:60487713-60548813	ENSG00000171791	NA	25859	596	NCRNA00206	Bcl-2|PPP1R50	Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA. Knockdown of lncRNA PART1 potently promoted the gefitinib-induced cell death, while elevated PART1 promoted gefitinib resistance by competitively binding to miR-129 to facilitate Bcl-2 expression in ESCC cells.	30049286	RID00937	ceRNA or sponge
Papillary thyroid carcinoma	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	Upregulation of lncRNA-ATB by Transforming Growth Factor beta1 (TGF-beta1) Promotes Migration and Invasion of Papillary Thyroid Carcinoma Cells. lncRNA-ATB overexpression promoted tumor cell migration and invasion, lncRNA-ATB overexpression showed no significant effects on TGF-beta1 expression, and TGF-beta1 treatment increased the expression level of lncRNA-ATB. Upregulation of lncRNA-ATB by TGF-b1 promotes migration and invasion of PTC cells.	30042377	RID00938	expression association
Endometrial cancer	PVT1	FGFR1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000077782	NA	5820	2260	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Long non-coding RNA PVT1 promotes malignancy in human endometrial carcinoma cells through negative regulation of miR-195-5p. We observed that PVT1 promotes malignant cell behavior by decreasing miR-195-5p expression. Binding of PVT1 and miR-195-5p was confirmed using luciferase assays.At the molecular level, either PVT1 knockdown or miR-195-5p overexpression resulted in a decrease of acidic fibroblast growth factor receptor (FGFR1)4 and basic fibroblast growth factor (FGF2).5 FGFR1 and FGF2 are targets of miR-195-5p that play a critical role in endometrial carcinoma by activating PI3K/AKT and MAPK/Erk pathways.	30031900	RID00939	ceRNA or sponge
Endometrial cancer	PVT1	FGF2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-195-5p)	regulation	NA	NA	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000138685	NA	5820	2247	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BFGF|FGF-2|FGFB|HBGF-2	Long non-coding RNA PVT1 promotes malignancy in human endometrial carcinoma cells through negative regulation of miR-195-5p. We observed that PVT1 promotes malignant cell behavior by decreasing miR-195-5p expression. Binding of PVT1 and miR-195-5p was confirmed using luciferase assays.At the molecular level, either PVT1 knockdown or miR-195-5p overexpression resulted in a decrease of acidic fibroblast growth factor receptor (FGFR1)4 and basic fibroblast growth factor (FGF2).5 FGFR1 and FGF2 are targets of miR-195-5p that play a critical role in endometrial carcinoma by activating PI3K/AKT and MAPK/Erk pathways.	30031900	RID00940	ceRNA or sponge
Alzheimer's disease	NEAT1	CDK5R1	negatively-E	RNAi	downregulation	qPCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000176749	NA	283131	8851	LINC00084|NCRNA00084|TncRNA|VINC	CDK5P35|CDK5R|NCK5A|p23|p25|p35|p35nck5a	Multiple Layers of CDK5R1 Regulation in Alzheimer's Disease Implicate Long Non-Coding RNAs. We demonstrated that NEAT1 and HOTAIR negatively regulate CDK5R1 mRNA levels, while MALAT1 has a positive effect. we observed a strong positive correlation between CDK5R1 and NEAT1 expression levels in brain tissues, suggesting a possible neuroprotective role of NEAT1 in AD to compensate for increased CDK5R1 levels. Overall, our work provides evidence of another level of CDK5R1 expression regulation mediated by lncRNAs and points to NEAT1 as a biomarker, as well as a potential pharmacological target for AD therapy.	29997370	RID00941	expression association
Colorectal cancer	SPINT1-AS1	SPINT1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000261183	GRCh38_15:40835808-40844387	ENSG00000166145	NA	102724362	6692	NA	HAI|HAI1|MANSC2	Increased expression of antisense lncRNA SPINT1-AS1 predicts a poor prognosis in colorectal cancer and is negatively correlated with its sense transcript. Compared with AN tissues, the expression of SPINT1-AS1 was increased in CRC tissues, while SPINT1 mRNA expression was decreased in CRC, and there was an obviously negative correlation between SPINT1-AS1 expression and its sense transcript.SPINT1-AS1 is upregulation in CRC tissues and plays an essential role in CRC progression and prognosis.	30022840	RID00942	expression association
Glioblastoma	CASC2c	F10	positively-E	RNAi	downregulation	qPCR	NA	NA	macrophage polarization(-)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046821-118210153	ENSG00000126218	NA	NA	2159	NA	NA	Coagulation Factor X Regulated by CASC2c Recruited Macrophages and Induced M2 Polarization in Glioblastoma Multiforme. although the lncRNA CASC2c has been verified to function as a miR-101 competing endogenous RNA (ceRNA) to promote miR-101 target genes in GBM cells, we first confirmed that CASC2c did not function as a miR-338-3p ceRNA to promote FX expression, and that FX was a target gene of miR-338-3p.CASC2c interacted with and reciprocally repressed miR-338-3p.we first found that FX was highly expressed and positively correlated with TAM density in human GBM. CASC2c repressed M2 subtype macrophage polarization. Our findings revealed a novel mechanism highlighting CASC2c and FX as potential therapeutic targets to improve GBM patients by altering the GBM microenvironment.	30034397	RID00943	expression association
Astrocytoma	CASC2c	CPEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Astrocytoma	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046821-118210153	ENSG00000214575	NA	NA	64506	NA	CPE-BP1|CPEB|CPEB-1|h-CPEB|hCPEB-1	Coagulation Factor X Regulated by CASC2c Recruited Macrophages and Induced M2 Polarization in Glioblastoma Multiforme. lncRNA CASC2c directly bound miR-101 and influenced miR-101 to mature, and CASC2c acted as a competing endogenous RNA (ceRNA) of miR-101 to competitively regulate CPEB1 and promote the malignant growth of astrocytoma	29458374;28252647	RID00944	ceRNA or sponge
Atherosclerosis	miR-103	lncWDR59	negatively-F	RNAi;RNAhybrid	upregulation	qPCR	NA	NA	cell proliferation(+);DNA damage(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Genome Instability and Mutation	Cardiovascular system disease	Atherosclerosis	miRNA	lncRNA	NA	NA	NA	GRCh38_8:111444252:111449827	NA	NA	NA	NA	miR-103 promotes endothelial maladaptation by targeting lncWDR59. Here we show that hyperlipidemia- and oxLDL-induced upregulation of miR-103 inhibits EC proliferation and promotes endothelial DNA damage through targeting of novel lncWDR59. these data indicate that miR-103 programs ECs toward a maladapted phenotype through targeting of lncWDR59, which may promote atherosclerosis.	29980665	RID00945	ceRNA or sponge
Spinal cord injury	MALAT1	miR-199b	negatively-E	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	inflammatory response(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Other	Injury	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKbeta/NF-kB signaling pathway. we confirmed that LPS-induced MALAT1 activated IKKbeta/NF-kB signaling pathway and promoted the production of proinflammatory cytokines TNF-alpha and IL-1beta through downregulating miR-199b.	29631367	RID00946	ceRNA or sponge
Pneumonia	CRNDE	FOXM1	positively-E	RNAi	upregulation	qPCR	NA	NA	inflammatory response(+)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Lung disease	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000111206	NA	NA	2305	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Knockdown CRNDE alleviates LPS-induced inflammation injury via FOXM1 in WI-38 cells. FOXM1 was up-regulated by CRNDE and FOXM1 silence blocked the effect of CRNDE overexpression in cell apoptosis, inflammation and activation of NF-kB and JAK/STAT signaling pathways.	29864958	RID00947	expression association
Lung adenocarcinoma	NORAD	TGFB1	positively-E	luciferase reporter assay	upregulation	qPCR;sequencing	GSE109296	GSE109296.zip	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000105329	NA	647979	7040	LINC00657	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long noncoding RNA NORAD regulates transforming growth factor-beta signaling and epithelial-to-mesenchymal transition-like phenotype. Here, we show that NORAD upregulates transforming growth factor-beta (TGF-beta) signaling and regulates TGF-beta-induced epithelial-to-mesenchymal transition (EMT)-like phenotype, which is a critical step in the progression of lung adenocarcinoma, A549 cells.	29722104	RID00948	expression association
Cataract	KCNQ1OT1	SMAD4	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Nervous system disease	Cataract	lncRNA	TF	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000141646	NA	10984	4089	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	DPC4|JIP|MADH4|MYHRS	Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial-mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells. In the present study, KCNQ1OT1 and mothers against decapentaplegic homolog (SMAD)4 expression levels were upregulation in human cataract lens posterior capsular samples	29749509	RID00949	expression association
Prostate cancer	PCGEM1	miR-148a	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	MEF2-activated long non-coding RNA PCGEM1 promotes cell proliferation in hormone-refractory prostate cancer through downregulation of miR-148a. Expression levels of PCGEM1 in PC3 cancer cells were demonstrated to be regulated by MEF2, as PCGME1 mRNA was increased by MEF2 overexpression but decreased by MEF2 silencing.the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR-148a that controls cell apoptosis. downregulation of PCGEM1 expression in PC3 cells increased expression of miR-148a. By contrast, overexpression of PCGEM1 decreased miR-148a expression. Finally, PCGME1 silencing by small interfering RNA significantly induced early cell apoptosis but this effect was reduced by a miR-148a inhibitor.	29749452	RID00950	expression association
Pre-eclampsia	PGK1P2	PGK1	positively-E	RNAi;Targetscan	downregulation	qPCR	NA	NA	angiogenesis(+);glucose metabolic process(+)	ceRNA(miR-330-5p)	regulation	NA	NA	NA	Sustained Angiogenesis;Reprogramming Energy Metabolism	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000213290	GRCh38_19:12559571-12561105	ENSG00000102144	NA	5233	5230	PGK2	HEL-S-68p|MIG10|PGKA	Dysfunction of pseudogene PGK1P2 is involved in preeclampsia by acting as a competing endogenous RNA of PGK1. We also found PGK1P2 acted as a competing endogenous RNA (ceRNA) to regulate PGK1 expression through miR-330-5p.The levels of PGK1 and PGK1P2 mRNA and PGK1 protein in severe preeclamptic decidua were lower than those in normal pregnant controls.We proved that PGK1 and PGK1P2 are a pair of ceRNAs against miR-330-5p and they play a vital role in human decidualization by regulating angiogenesis and glycolysis metabolism.	30177069	RID00951	ceRNA or sponge
Major depressive disorder	NONHSAG045500	SLC6A4	negatively-E	RNAi	downregulation	qPCR	NA	NA	antidepressant(+);serotonin transporter(+)	NA	association	NA	NA	NA	NA	Disease of mental health	Major depressive disorder	lncRNA	PCG	NA	GRCh38_6:143503458-143506147	ENSG00000108576	NA	NA	6532	NA	NA	Therapeutic Antidepressant Potential of NONHSAG045500 in Regulating Serotonin Transporter in Major Depressive Disorder. Only the overexpression of NONHSAG045500 could significantly inhibit the expression of SERT;	29955033	RID00952	expression association
Medulloblastoma	LOXL1-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	NA	NA	100287616	NA	NA	NA	LncRNA LOXL1-AS1 Promotes the proliferation and Metastasis of Medulloblastoma by Activating the PI3K/AKT Pathway. Western blot analysis further revealed that knockdown of LOXL1-AS1 decreased the phosphorylated levels of PI3K and AKT without affecting their total protein levels.	30050750	RID00953	expression association
Medulloblastoma	LOXL1-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000261801	GRCh38_15:73908071-73928248	ENSG00000142208	NA	100287616	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	LncRNA LOXL1-AS1 Promotes the proliferation and Metastasis of Medulloblastoma by Activating the PI3K/AKT Pathway. Western blot analysis further revealed that knockdown of LOXL1-AS1 decreased the phosphorylated levels of PI3K and AKT without affecting their total protein levels.	30050750	RID00954	expression association
Liver cancer	MALAT1	CHUK	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000213341	NA	378938	1147	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation. we found that MALAT1-knockdown HepG2 and Huh7 cells expressed lower p-NF-kB,p-IKKaandp-IkBain comparison to the MALAT1 scramble-transfected liver cancer cells.	29702091	RID00955	expression association
Liver cancer	MALAT1	PARP1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143799	NA	378938	142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation.	29702091	RID00956	expression association
Liver cancer	MALAT1	NFKB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);apoptosis process(+)	NA	regulation	NA	5-fluorouracil	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Inhibition of MALAT1 sensitizes liver cancer cells to 5-flurouracil by regulating apoptosis through IKKalpha/NF-kB pathway. In addition, MALAT1 knockdown triggered 5-FU induced apoptosis in HepG2 cells by inducing intrinsic apoptosis-related signals, including Cyto-c, Apaf-1, cleaved Caspase-9/-7/-3 and poly (ADP-ribose) polymerase (PARP). Furthermore, phosphorylated nuclear factor-kB (p-NF-kB) was also down-regulated by MALAT1 silence. Importantly, suppression of IKKalpha/NF-kB significantly elevated apoptosis and reduced liver cancer cell viability in MALAT1-knockdown cells with 5-FU incubation.	29702091	RID00957	expression association
Hepatocellular carcinoma	MIR22HG	HMGB1	negatively-E	luciferase reporter assay;RIP	downregulation	microarray	GSE14520;TCGA	GSE14520.zip;LIHC.zip	cell proliferation(-);cell invasion(-);cell metastasis(-)	ceRNA(miR-22-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000189403	NA	84981	3146	C17orf91	HMG-1|HMG1|HMG3|SBP-1	Identification and Functional Characterization of Long Non-coding RNA MIR22HG as a Tumor Suppressor for Hepatocellular Carcinoma. MIR22HG derived miR-22-3p to target high mobility group box 1 (HMGB1), thereby inactivating HMGB1 downstream pathways. miR-22-3p suppression, HuR or HMGB1 overexpression rescued the inhibitory effects caused by MIR22HG overexpression. Forced expression of MIR22HG in HCC cells significantly suppressed proliferation, invasion, and metastasis in vitro and in vivo.	30083257	RID00958	ceRNA or sponge
Osteoarthritis	DANCR	SPHK2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-577)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000063176	NA	57291	56848	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	SK 2|SK-2|SPK 2|SPK-2	Long non-protein coding RNA DANCR functions as a competing endogenous RNA to regulate osteoarthritis progression via miR-577/SphK2 axis. The study also showed that DANCR acted as a competitive endogenous RNA to sponge miR-577, which targeted the mRNA of SphK2 to regulate the survival of OA chondrocytes. the study revealed that lncRNA DANCR might promote the proliferation of OA chondrocytes and reduce apoptosis through the miR-577/SphK2 axis.	29678573	RID00959	ceRNA or sponge
Pneumonia	HAGLROS	miR-100	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(-);PI3K/AKT/NF-kB signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Respiratory system disease	Lung disease	lncRNA	miRNA	ENSG00000226363	GRCh38_2:176177717-176179008	NA	NA	102800310	NA	NA	NA	Long noncoding RNA HAGLROS regulates cell apoptosis and autophagy in lipopolysaccharides-induced WI-38 cells via modulating miR-100/NF-kB axis. there was a negative correlation between HAGLROS and miR-100, and the effects of HAGLROS downregulation on LPS-induced apoptosis and autophagy in WI-38 cells were by regulation of miR-100.Knockdown of HAGLROS inhibited the activation of PI3K/AKT/NF-kB pathway. Furthermore, NFkB3 was verified as a functional target of miR-100 and effects of miR-100 inhibition on LPS-induced WI-38 cell injury were alleviated by knockdown of NFkB3.	29673591	RID00960	expression association
Renal cell carcinoma	SNHG1	miR-137	positively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Long Noncoding RNA Small Nucleolar RNA Host Gene 1 (SNHG1) Promotes Renal Cell Carcinoma Progression and Metastasis by Negatively Regulating miR-137.High levels of SNHG1 were correlated with poor prognosis of RCC patients. Knockdown of SNHG1 suppressed the proliferation, invasion, and EMT capacity in RCC. Overexpression of SNHG1 participates in RCC tumorigenesis by regulating miR-137.	29874202	RID00961	expression association
Retinoblastoma	CYTOR	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000171791	NA	112597	596	C2orf59|LINC00152|NCRNA00152	Bcl-2|PPP1R50	Knockdown of LINC00152 significantly inhibited cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and caspase-3 and caspase-8 activities in vitro, as well as suppressing tumorigenesis in vivo. We identified several genes related to proliferation, apoptosis, and invasion including Ki-67, Bcl-2, and MMP-9 that were transcriptionally inactivated by LINC00152.	29922070	RID00962	expression association
Retinoblastoma	CYTOR	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000100985	NA	112597	4318	C2orf59|LINC00152|NCRNA00152	CLG4B|GELB|MANDP2|MMP-9	Knockdown of LINC00152 significantly inhibited cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and caspase-3 and caspase-8 activities in vitro, as well as suppressing tumorigenesis in vivo. We identified several genes related to proliferation, apoptosis, and invasion including Ki-67, Bcl-2, and MMP-9 that were transcriptionally inactivated by LINC00152.	29922070	RID00963	expression association
Idiopathic pulmonary fibrosis	H19	COL1A1	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	fibrotic(+)	ceRNA(miR-196a)	regulation	NA	NA	NA	NA	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000108821	NA	283120	1277	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	EDSARTH1|EDSC|OI1|OI2|OI3|OI4	The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis.We further demonstrated that H19 was a direct target of miR-196a and was associated with COL1A1 expression by sponging miR-196a. downregulation of H19 alleviated fibroblast activation and lung fibrosis, and this effect was blocked by a miR-196a inhibitor. Knockdown of H19 Inhibited COL1A1, a Target of miR-196a	29411215	RID00964	ceRNA or sponge
Cholangiocarcinoma	DUXAP9	MYCN	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+);cancer progression(+)	ceRNA(miR-5095)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000134323	NA	503638	4613	NA	MODED|N-myc|NMYC|ODED|bHLHe37	Long noncoding RNA LINC01296 promotes tumor growth and progression by sponging miR-5095 in human cholangiocarcinoma. LINC01296 was demonstrated to sponge microRNA-5095 (miR-5095), which targets MYCN proto-oncogene bHLH transcription factor (MYCN) mRNA in human CCA. By inhibition of miR-5095, LINC01296 overexpression upregulation the expression of MYCN and promoted cell viability, migration and invasion in CCA cells.	29620172	RID00965	ceRNA or sponge
Colorectal cancer	PVT1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000198793	NA	5820	2475	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00966	expression association
Colorectal cancer	PVT1	ABCC1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000103222	NA	5820	4363	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC29|ABCC|GS-X|MRP|MRP1	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00967	expression association
Colorectal cancer	PVT1	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000085563	NA	5820	5243	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00968	expression association
Colorectal cancer	PVT1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000171791	NA	5820	596	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Bcl-2|PPP1R50	Knockdown of long non-coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells. RT-qPCR and western blotting demonstrated that the overexpression of PVT1 increased the mRNA and protein expression levels of multidrug resistance-associated protein 1, P-glycoprotein, serine/threonine-protein kinase mTOR and apoptosis regulator Bcl2. These results suggested that the expression of PVT1 may be associated with the development of 5-FU resistance in human CRC. The results indicated that PVT1 upregulation the expression of MRP1, P-gp, mTOR and Bcl-2, supporting the hypothesis that PVT1 may promote the development of MDR in CRC.	29693171	RID00969	expression association
Pulmonary fibrosis	PCAT29	RASAL1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000111344	NA	104472713	8437	NA	RASAL	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00970	expression association
Pulmonary fibrosis	PCAT29	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000102882	NA	104472713	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00971	expression association
Pulmonary fibrosis	PCAT29	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000100030	NA	104472713	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00972	expression association
Pulmonary fibrosis	PCAT29	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	PCG	ENST00000560655	GRCh38_15:69592200-69695750	ENSG00000105329	NA	104472713	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00973	expression association
Pulmonary fibrosis	PCAT29	miR-221	positively-E	RNAi	downregulation	qPCR	NA	NA	inflammatory response(-);fibrotic(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Respiratory system disease	Fibrosis	lncRNA	miRNA	ENST00000560655	GRCh38_15:69592200-69695750	NA	NA	104472713	NA	NA	NA	lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signal pathway. The results of the present study demonstrated that lncRNAPCAT29 induced miRNA-221 upregulation and TGF-beta1 downregulation. These observations were associated with reduced inflammation and progression of silica-induced pulmonary fibrosis via the TGF-beta1-regulated RASAL1/ERK1/2 signaling pathway, which may serve as a potential target for the treatment of pulmonary fibrosis. Analysis of the potential mechanism underlying silica-induced pulmonary fibrosis revealed that the expression levels of RAS protein activator like 1 (RASAL1) and extracellular signal-regulated kinases 1/2 (ERK1/2) were suppressed due to lncRNAPCAT29 expression.	29620190	RID00974	expression association
Urinary bladder cancer	NORAD	PUM2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cancer progression(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000055917	NA	647979	23369	LINC00657	PUMH2|PUML2	High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer. MTT and colony formation assay demonstrated that knockdown of NORAD results in lower proliferation in TSSCUP cells, whereas PUM2 expression was upregulation and E2F3 downregulated.High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer.	29605462	RID00975	expression association
Urinary bladder cancer	NORAD	E2F3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cancer progression(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000260032	GRCh38_20:36045618-36051018	ENSG00000112242	NA	647979	1871	LINC00657	E2F-3	High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer. MTT and colony formation assay demonstrated that knockdown of NORAD results in lower proliferation in TSSCUP cells, whereas PUM2 expression was upregulation and E2F3 downregulated.High expression of long noncoding RNA NORAD indicates a poor prognosis and promotes clinical progression and metastasis in bladder cancer.	29605462	RID00976	expression association
Cervical cancer	BDNF-AS	BDNF	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000176697	NA	497258	627	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	ANON2|BULN2	Long noncoding RNA BDNF-AS is downregulated in cervical cancer and has anti-cancer functions by negatively associating with BDNF.BDNF-AS overexpression is anti-cancer by inhibiting proliferation and migration in vitro, and transplantation in vivo.BDNF-AS is downregulated in CC. Overexpressing BDNF-AS may inhibit CC, possibly through inverse regulation on BDNF.	29572178	RID00977	expression association
Neuroblastoma	PAUPAR	PAX6	positively-F	RNA pull-down assay;ChIP	upregulation	microarray	GSE110033	GSE110033.zip	neurogenesis(+)	epigenetic regulation	association	NA	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000281880	GRCh38_11:31812307-32002405	ENSG00000007372	NA	103157000	5080	NA	AN|AN2|ASGD5|D11S812E|FVH1|MGDA|WAGR	The long non-coding RNA Paupar promotes KAP1-dependent chromatin changes and regulates olfactory bulb neurogenesis. We show here that the Paupar lncRNA directly binds KAP1, an essential epigenetic regulatory protein, and thereby regulates the expression of shared target genes important for proliferation and neuronal differentiation.Paupar-KAP1 genome-wide co-occupancy reveals a fourfold enrichment of overlap between Paupar and KAP1 bound sequences, the majority of which also appear to associate with PAX6.	29661885	RID00978	epigenetic regulation
Pre-eclampsia	H19	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00979	expression association
Pre-eclampsia	H19	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000142208	NA	283120	207	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00980	expression association
Pre-eclampsia	H19	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell autophagy(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells. LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. phosphorylated levels of PI3K, AKT, mTOR and p70S6K were all increased by lncRNA-H19 overexpression	29522949	RID00981	expression association
Myocarditis	TUG1	miR-29b	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation	Cardiovascular system disease	Myocarditis	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR-29b. TUG1 negatively modulated the expression of miR-29b and miR-29b mimic blocked the effect of TUG1 overexpression on cell viability, apoptosis, inflammation and inactivation of NF-kB and JAK/STAT signaling pathways in LPS-stimulated H9c2 cells.	29518613	RID00982	expression association
Fatty liver disease	H19	SREBF1	positively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	steatosis(+);hepatic lipid homeostasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000072310	NA	283120	6720	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	SREBP1|bHLHd1	Long noncoding RNA H19 interacts with polypyrimidine tract-binding protein 1 to reprogram hepatic lipid homeostasis. H19 RNA interacts with PTBP1 to facilitate its association with sterol regulatory element-binding protein 1c mRNA and protein, leading to increased stability and nuclear transcriptional activity. Ectopic expression of H19 induces steatosis and pushes the liver into a pseudo-fed state in response to fasting by promoting sterol regulatory element-binding protein 1c protein cleavage and nuclear translocation.Our study unveils an H19/PTBP1/sterol regulatory element-binding protein 1 feedforward amplifying signaling pathway to exacerbate the development of fatty liver.	29140550	RID00983	interact with protein
Fatty liver disease	H19	PTBP1	interact	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	steatosis(+);hepatic lipid homeostasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000011304	NA	283120	5725	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HNRNP-I|HNRNPI|HNRPI|PTB|PTB-1|PTB-T|PTB2|PTB3|PTB4|pPTB	Long noncoding RNA H19 interacts with polypyrimidine tract-binding protein 1 to reprogram hepatic lipid homeostasis. H19 RNA interacts with PTBP1 to facilitate its association with sterol regulatory element-binding protein 1c mRNA and protein, leading to increased stability and nuclear transcriptional activity. Ectopic expression of H19 induces steatosis and pushes the liver into a pseudo-fed state in response to fasting by promoting sterol regulatory element-binding protein 1c protein cleavage and nuclear translocation.Our study unveils an H19/PTBP1/sterol regulatory element-binding protein 1 feedforward amplifying signaling pathway to exacerbate the development of fatty liver.	29140550	RID00984	interact with protein
Epithelial ovarian cancer	HOTAIR	SNAI1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);tumorigenesis(+);cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Effects of Targeting lncRNA HOTAIR on the Invasion and Nude Mouse Tumorigenicity of Epithelial Ovarian Cancer Cells The lncRNA HOTAIR low expression resulted in increasing E-cadherin and decreasing snail expression detected by qRT-PCR in the shHOTAIR transfected SKOV3 cells of xenograft tumor,compared with the scramble control (P<0.05).Targeting lncRNA HOTAIR expression in SKOV3 cells with RNA interference can decrease snail,increase E-cadherin and significantly reduce the invasion and tumorigenicity of epithelial ovarian cancer SKOV3 cells.	30014633;24662839	RID00985	expression association
Epithelial ovarian cancer	HOTAIR	CDH1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);tumorigenesis(+);cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Effects of Targeting lncRNA HOTAIR on the Invasion and Nude Mouse Tumorigenicity of Epithelial Ovarian Cancer Cells The lncRNA HOTAIR low expression resulted in increasing E-cadherin and decreasing snail expression detected by qRT-PCR in the shHOTAIR transfected SKOV3 cells of xenograft tumor,compared with the scramble control (P<0.05).Targeting lncRNA HOTAIR expression in SKOV3 cells with RNA interference can decrease snail,increase E-cadherin and significantly reduce the invasion and tumorigenicity of epithelial ovarian cancer SKOV3 cells.	30014633;24662839	RID00986	expression association
Alzheimer's disease	MALAT1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087088	NA	378938	581	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L4	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00987	expression association
Alzheimer's disease	MALAT1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164305	NA	378938	836	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CPP32|CPP32B|SCA-1	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00988	expression association
Alzheimer's disease	MALAT1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00989	expression association
Alzheimer's disease	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00990	expression association
Alzheimer's disease	MALAT1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198793	NA	378938	2475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00991	expression association
Alzheimer's disease	MALAT1	GSK3B	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000082701	NA	378938	2932	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Abeta25-35 via blocking PI3K/mTOR/GSK3beta pathway Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3beta.	30043735	RID00992	expression association
Fatty liver disease	LNCARSR	SREBF1	positively-E	RNAi	upregulation	qPCR	NA	NA	adipogenesis(+);steatosis(+)	NA	regulation	NA	NA	NA	NA	Disease of metabolism	Fatty liver disease	lncRNA	TF	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000072310	NA	112577459	6720	NA	SREBP1|bHLHd1	we identified that lncARSR regulated hepatic lipogenesis via upregulating SREBP-1c, the key regulatory molecule involved in lipogenesis.our data indicated that lncARSR potentially contributes to the hepatic steatosis in NAFLD, which may be a new therapeutic target against NAFLD.	29555473	RID00993	expression association
Skin squamous cell carcinoma	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00994	expression association
Skin squamous cell carcinoma	MALAT1	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00995	expression association
Skin squamous cell carcinoma	MALAT1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma. MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and beta-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells.	29735442	RID00996	expression association
Hepatocellular carcinoma	LINC01138	PRMT5	interact	RNAi;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000274020	GRCh38_1:148290889-148519604	ENSG00000100462	NA	388685	10419	LINC00875	HRMT1L5|HSL7|IBP72|JBP1|SKB1|SKB1Hs	The LINC01138 drives malignancies via activating arginine methyltransferase 5 in hepatocellular carcinoma. LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumorigenicity, tumour invasion and metastasis by physically interacting with arginine methyltransferase 5 (PRMT5) and enhancing its protein stability by blocking ubiquitin/proteasome-dependent degradation in HCC.	29679004	RID00997	interact with protein
Rheumatoid arthritis	GAPLINC	miR-382-5p	negatively-F	miRanda;PITA;RNAhybrid;RNAi;CLIP-seq	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540	NA	Long Non-Coding RNA GAPLINC Promotes Tumor-Like Biologic Behaviors of Fibroblast-Like Synoviocytes as MicroRNA Sponging in Rheumatoid Arthritis Patients. Further verification of this model demonstrated that silencing of GAPLINC increased miR-382-5p and miR-575 expression.The results of this study suggest that GAPLINC may function as a novel microRNAs sponging agent affecting the biological characteristics of RA-FLSs.GAPLINC may also promote RA-FLS tumor-like behaviors in a miR-382-5p-dependent and miR-575-dependent manner. GAPLINC suppression in RA-FLS cells revealed significant alterations in cell proliferation, invasion, migration, and proinflammatory cytokines production.	29692777	RID00998	ceRNA or sponge
Rheumatoid arthritis	GAPLINC	miR-575	negatively-F	miRanda;PITA;RNAhybrid;RNAi;CLIP-seq	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000266835	GRCh38_18:3466250-3478978	NA	NA	100505592	NA	LINC01540	NA	Further verification of this model demonstrated that silencing of GAPLINC increased miR-382-5p and miR-575 expression.The results of this study suggest that GAPLINC may function as a novel microRNAs sponging agent affecting the biological characteristics of RA-FLSs.GAPLINC may also promote RA-FLS tumor-like behaviors in a miR-382-5p-dependent and miR-575-dependent manner. GAPLINC suppression in RA-FLS cells revealed significant alterations in cell proliferation, invasion, migration, and proinflammatory cytokines production.	29692777	RID00999	ceRNA or sponge
Cervical cancer	HOTAIR	miR-17-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer Interacting With MicroRNA-17-5p. Pearson's correlation analysis indicated that miR-17-5p expression was negatively correlated to that of HOTAIR. Luciferase reporter assay revealed that miR-17-5p directly targeted HOTAIR 3'-UTR.our results reveal the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p.Loss-of-function experiments showed that HOTAIR knockdown inhibited the proliferation, migration, and invasion of cervical cells.In summary, our results reveal the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer.	28745272	RID01000	ceRNA or sponge
Polycystic ovary syndrome	NPTN-IT1	TIMP2	positively-E	western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-);apoptosis process(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis	Syndrome	Polycystic ovary syndrome	lncRNA	PCG	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000035862	NA	101241892	7077	lncRNA-LET	CSC-21K|DDC8	LncRNA-LET inhibits cell viability, migration and EMT while induces apoptosis by up-regulation of TIMP2 in human granulosa-like tumor cell line KGN. Overexpression of lncRNA-LET inhibits cell viability, migration and EMT process, and increases apoptosis in KGN cells by up-regulating the expression of TIMP2 and activating the Wnt/beta-catenin and notch signaling pathways.	29432996	RID01001	expression association
Papillary thyroid carcinoma	E2F1	RGMB-AS1	positively-E	qRT-PCR;RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000246763	GRCh38_5:98769618-98773469	1869	503569	E2F-1|RBAP1|RBBP3|RBP3	NA	LncRNA RGMB-AS1 is activated by E2F1 and promotes cell proliferation and invasion in papillary thyroid carcinoma.Results of CHIP assay showed that E2F1 bound to lncRNA RGMB-AS1 promoter region.	29687852	RID01002	transcriptional regulation
Pre-eclampsia	HK2P1	HK2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell differentiation(+)	ceRNA(miR-6887-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228612	GRCh38_X:80571871-80574607	ENSG00000159399	NA	642546	3099	HK2P	HKII|HXK2	Dysregulated Pseudogene HK2P1 May Contribute to Preeclampsia as a Competing Endogenous RNA for Hexokinase 2 by Impairing Decidualization. there was a significant positive correlation between the expression of HK2P1 and HK2, and HK2P1 regulated the HK2 expression via competition for the shared miR-6887-3p. Downregulated HK2P1 or HK2 inhibited human endometrial stromal cells proliferation and differentiation. By sequence alignment, we found miR-6887-3p had 4 potential binding sites in HK2P1 as well as in the 3'-UTR of HK2	29440331	RID01003	ceRNA or sponge
Atherosclerosis	ENST00113	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	NA	NA	NA	NA	NA	NA	LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis. we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID01004	expression association
Atherosclerosis	ENST00113	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID01005	expression association
Atherosclerosis	ENST00113	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell survival(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_21:27722379-27751233	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	we found that the protein expressions of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR), and bcl-2 in HUVECs cells transfected with si-00113-1 or si-00113-2 were dramatically decreased compared with si-NC-transfected cells and control cells.LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis.	29668625	RID01006	expression association
Cerebral ischemia-reperfusion injury	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Mechanism of MALAT1 preventing apoptosis of vascular endothelial cells induced by oxygen-glucose deficiency and reoxidation. After OGD-R, over-expression of MALAT1 lentivirus increased phosphatidylinositol 3-kinase (PI3K) activity.This study first proposed that lncRNA MALAT1 can protect human cerebrovascular endothelial cells from OGD-R-induced apoptosis through a PI3K-dependent mechanism.Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells. lentiviral knockdown of MALAT1 decreased PI3K activities and the activation of Akt phosphorylation.In conclusion, to the best of our knowledge, the present study was the first to suggest that lncRNA MALAT1 may protect human brain vascular endothelial cells from OGD-R-induced apoptosis via a PI3K-dependent mechanism.	29575939;28413461	RID01007	expression association
Lung adenocarcinoma	MALAT1	CDKN1A	negatively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells. Flow cytometry analysis revealed that MALAT1-depleted cells exhibited G1 cell cycle arrest. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.p21 and FAS, well-known p53 targets, were upregulation by MALAT1 knockdown in A549 human lung adenocarcinoma cells. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.	29632545	RID01008	expression association
Lung adenocarcinoma	MALAT1	FAS	negatively-E	RNAi;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026103	NA	378938	355	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells. Flow cytometry analysis revealed that MALAT1-depleted cells exhibited G1 cell cycle arrest. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.p21 and FAS, well-known p53 targets, were upregulation by MALAT1 knockdown in A549 human lung adenocarcinoma cells. These results suggest that MALAT1 affects the expression of p53 target genes through repressing p53 promoter activity, leading to influence the cell cycle progression.	29632545	RID01009	expression association
Multiple myeloma	PDIA3P1	G6PD	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	regulation	RNA-DNA	bortezomib	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000180867	GRCh38_1:147172744-147179622	ENSG00000160211	NA	171423	2539	NA	G6PD1	LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma. we revealed that PDIA3P interacts with c-Myc to enhance its transactivation activity and binding to G6PD promoter, stimulating G6PD expression and PPP flux. PDIA3P promotes cell proliferation and bortezomib resistance through G6PD and the pentose phosphate pathway LncRNA PDIA3P interacts with c-Myc to regulate cell proliferation via induction of pentose phosphate pathway in multiple myeloma.we found lncRNA Protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P) is highly expressed in MM.	29501744	RID01010	transcriptional regulation
Lung cancer	FENDRR	FOXF1	positively-E	luciferase reporter assay;RNAi;ChIP	downregulation	sequencing	TCGA	LUSC_LUAD.zip	tumorigenesis(-)	ceRNA(miR-424)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000103241	NA	400550	2294	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ACDMPV|FKHL5|FREAC1	FENDRR can upregulate FOXF1 by competitively binding to miR-424. FENDRR, a long intergenic non-coding RNA (lincRNA) that functions to inhibit lung cancer by affecting expressions of an abundant number of genes, including the tumor suppressor FOXF1.	29293945	RID01011	ceRNA or sponge
Chronic myeloid leukemia	MEG3	miR-184	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long Noncoding RNA MEG3 Inhibits Cell Proliferation and Metastasis in Chronic Myeloid Leukemia via Targeting miR-184. overexpression of MEG3 significantly decreased the expression of miR-184, and MEG3 knockdown markedly increased it. Furthermore, our results showed that MEG3 interacted with miR-184 and subsequently mitigated the proliferation and invasion of leukemia cells by downregulating related proteins.	28653609	RID01012	ceRNA or sponge
Gastric cancer	NEAT1	miR-335-5p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 regulates the proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis. In addition, lncRNA NEAT1 inhibited the expression of miR-335-5p, and miR-335-5p targeted ROCK1 in BGC-823 cells. miR-335-5p overexpression significantly inhibited cell proliferation, migration and invasion, which was counteracted by ROCK1 overexpression concurrently. Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.	29544562	RID01013	expression association
Gastric cancer	NEAT1	ROCK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|NCRNA00084|TncRNA|VINC	P160ROCK|ROCK-I	Long non-coding RNA NEAT1 regulates the proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis. In addition, lncRNA NEAT1 inhibited the expression of miR-335-5p, and miR-335-5p targeted ROCK1 in BGC-823 cells. miR-335-5p overexpression significantly inhibited cell proliferation, migration and invasion, which was counteracted by ROCK1 overexpression concurrently. Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.	29544562	RID01014	expression association
Hepatocellular carcinoma	miR-122	HOTTIP	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	Hepatitis C virus core impacts expression of miR122 and miR204 involved in carcinogenic progression via regulation of TGFBRAP1 and HOTTIP expression. Our data suggests that the pathways of miR204-HPCAL1-lncRNAHOTTIP and miR122-TGFBRAP1 were likely involved in the carcinogenic progress due to the presence of HCV core, and that overexpression of miR122 and miR204 might inhibit the HCC progress by down-regulation of TGFBRAP1 and HOTTIP expression.	29535540	RID01015	expression association
Hepatocellular carcinoma	miR-204	HOTTIP	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. These results elucidate that the miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis.Hepatitis C virus core impacts expression of miR122 and miR204 involved in carcinogenic progression via regulation of TGFBRAP1 and HOTTIP expression. Our data suggests that the pathways of miR204-HPCAL1-lncRNAHOTTIP and miR122-TGFBRAP1 were likely involved in the carcinogenic progress due to the presence of HCV core, and that overexpression of miR122 and miR204 might inhibit the HCC progress by down-regulation of TGFBRAP1 and HOTTIP expression.	26710269;29535540	RID01016	ceRNA or sponge
Nasopharynx carcinoma	TGFB1	MALAT1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(-);cell migration(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TGF-beta regulates the ERK/MAPK pathway independent of the SMAD pathway by repressing miRNA-124 to increase MALAT1 expression in nasopharyngeal carcinoma.constant TGF-beta stimulation repressed miR-124 expression, whereas miR-124 overexpression antagonized TGF-beta-promoted NPC cell growth and migration.	29710466	RID01017	expression association
Osteocarcinoma	LIN28A	MALAT1	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	RNA stability	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Osteocarcinoma	TF	lncRNA	ENSG00000131914	NA	ENSG00000251562	GRCh38_11:65497688-65506516	79727	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RNA binding protein Lin28A promotes osteocarcinoma cells progression by associating with the long noncoding RNA MALAT1. Lin28A was found to harbor binding sites on MALAT1 sequences and associated with MALAT1, and increased MALAT1 stability and expression.Lin28A knockdown inhibited OS cells proliferation, migration, invasion and promoted cell apoptosis;Expressions of Lin28A and long noncoding RNA MALAT1 were positively correlated.	29204769	RID01018	interact with mRNA
Alzheimer's disease	EBF3-AS	EBF3	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Nervous system disease	Alzheimer's disease	lncRNA	TF	NA	GRCh38_10:129837700-129842171	ENSG00000108001	NA	NA	253738	NA	COE3|EBF-3|HADDS|O/E-2|OE-2	Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease. These results revealed that lncRNA EBF3-AS promoted neuron apoptosis in AD, and involved in regulating EBF3 expression.The expression of EBF3 was downregulated in Abeta25-35- and OA-treated SH-SY5Y, which was reversed by EBF3-AS knockdown.	29298096	RID01019	expression association
Gorham's disease	MALAT1	VEGFA	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-22-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Gorham's disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MVCD1|VEGF|VPF	MALAT1 enhanced the proliferation of human osteoblasts treated with ultra-high molecular weight polyethylene by targeting VEGF via miR-22-5p. Knockdown of MALAT1 inhibited the growth of UHMWPE-treated hFOB 1.19 cells, and this effect was associated with the upregulation of OPG, and downregulation of RANKL and VEGF.	29328414	RID01020	ceRNA or sponge
Malignant glioma	SNHG16	E2F1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-20a-5p)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000101412	NA	100507246	1869	Nbla10727|Nbla12061|ncRAN	E2F-1|RBAP1|RBBP3|RBP3	Long non-coding RNA SNHG16 contributes to glioma malignancy by competitively binding miR-20a-5p with E2F1. We also found that SNHG16 may act as a ceRNA for miR-20a-5p, enhancing the expression of E2F1.miR-20a-5p mimic enhanced the inhibition of cell proliferation, invasion, migration, and EMT, and increase of apoptosis induced by SNHG16 knockdown. In conclusion, SNHG16 promotes glioma tumorigenesis by sponging miR-20a-5p, leading to the enhancement of its endogenous targets E2F1. The data provides a new clue for the role of SNHG16/miR-20a-5p/E2F1 in the development of glioma.	29685003	RID01021	ceRNA or sponge
Atherosclerosis	HOTTIP	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000110092	NA	100316868	595	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01022	expression association
Atherosclerosis	HOTTIP	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000132646	NA	100316868	5111	HOXA-AS6|HOXA13-AS1|NCRNA00213	ATLD2	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01023	expression association
Atherosclerosis	HOTTIP	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000168036	NA	100316868	1499	HOXA-AS6|HOXA13-AS1|NCRNA00213	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01024	expression association
Atherosclerosis	HOTTIP	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000136997	NA	100316868	4609	HOXA-AS6|HOXA13-AS1|NCRNA00213	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HOTTIP promotes endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway. Ectopic expression of HOTTIP promoted endothelial cell proliferation and also increased the expression of proliferating makers cyclin D1 and PCNA. Moreover, elevated expression of HOTTIP promoted endothelial cell migration. Downregulation expression of HOTTIP suppressed endothelial cell proliferation and migration.we determined that overexpression of HOTTIP induced beta-catenin expression and enhanced the downstream protein c-Myc expression in the endothelial cell. Ectopic expression of HOTTIP increased endothelial cell proliferation and migration via activation of the Wnt/beta-catenin pathway.	29058802	RID01025	expression association
Chronic myeloid leukemia	H19	BCR-ABL	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Hypomethylation-mediated H19 overexpression increases the risk of disease evolution through the association with BCR-ABL transcript in chronic myeloid leukemia. H19 overexpression, a frequent event in CML, was associated with higher BCR-ABL transcript involving in disease progression.Moreover, H19 DMR/ICR hypomethylation in CML may be one of the mechanisms mediating H19 overexpression.	28776669	RID01026	expression association
Atherosclerosis	MEG3	miR-223	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Melatonin prevents endothelial cell pyroptosis via regulation of long noncoding RNA MEG3/miR-223/NLRP3 axis. We found that lncRNA MEG3 enhanced pyroptosis in HAECs. Moreover, MEG3 acted as an endogenous sponge by sequence complementarity to suppress the function of miR-223 and to increase NLRP3 expression and enhance endothelial cell pyroptosis.	29024030	RID01027	ceRNA or sponge
Atherosclerosis	MEG3	NLRP3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000162711	NA	55384	114548	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AGTAVPRL|AII|AVP|C1orf7|CIAS1|CLR1.1|DFNA34|FCAS|FCAS1|FCU|KEFH|MWS|NALP3|PYPAF1	Melatonin prevents endothelial cell pyroptosis via regulation of long noncoding RNA MEG3/miR-223/NLRP3 axis. We found that lncRNA MEG3 enhanced pyroptosis in HAECs. Moreover, MEG3 acted as an endogenous sponge by sequence complementarity to suppress the function of miR-223 and to increase NLRP3 expression and enhance endothelial cell pyroptosis.	29024030	RID01028	expression association
Psoriasis	MSX2P1	S100A7	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-6731-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000229590	GRCh38_17:58157028-58157800	ENSG00000143556	NA	55545	6278	HPX5|HSHPX5|MSX2P	PSOR1|S100A7c	Up-regulated lncRNA-MSX2P1 promotes the growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7. Competitive endogenous RNAs (ceRNAs) regulate RNA transcripts by competing for shared miRNAs and play critical roles in disease development. Immunohistochemistry demonstrated significantly increased expression levels of S100A7 in psoriatic lesions, compared with normal skin tissue. We observed a positive correlation between lncRNA-MSX2P1 expression and S100A7 expression. In addition, miR-6731-5p suppressed proliferation, accelerated apoptosis in IL-22-stimulated keratinocytes, and decreased the expressions of S100A7, IL-12beta, IL-23, HLA-C,CCHCR1, TNF-alpha, and NF-kB proteins. Our data demonstrated that MSX2P1 facilitate the progression and growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7.	29339075	RID01029	ceRNA or sponge
Non-small cell lung cancer	GHET1	LATS1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000131023	NA	102723099	9113	lncRNA-GHET1	WARTS|wts	Knockdown of lncRNA GHET1 suppresses cell proliferation, invasion and LATS1/YAP pathway in non small cell lung cancer. Knockdown of lncRNA GHET1 suppressed cell proliferation and invasion capacity and Epithelial-Mesenchymal Transition (EMT) phenomenon of NSCLC cells. Moreover, we demonstrated that knockdown of lncRNA GHET1 suppresses LATS1/YAP pathway signaling pathway by downregulating YAP1 expression in NSCLC cells.	29286919	RID01030	expression association
Non-small cell lung cancer	GHET1	YAP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000137693	NA	102723099	10413	lncRNA-GHET1	COB1|YAP|YAP2|YAP65|YKI	Knockdown of lncRNA GHET1 suppresses cell proliferation, invasion and LATS1/YAP pathway in non small cell lung cancer. Knockdown of lncRNA GHET1 suppressed cell proliferation and invasion capacity and Epithelial-Mesenchymal Transition (EMT) phenomenon of NSCLC cells. Moreover, we demonstrated that knockdown of lncRNA GHET1 suppresses LATS1/YAP pathway signaling pathway by downregulating YAP1 expression in NSCLC cells.	29286919	RID01031	expression association
Urinary bladder cancer	GAS5	EZH2	negatively-E	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	apoptosis process(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000106462	NA	60674	2146	NCRNA00030|SNHG2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA GAS5 promotes bladder cancer cells apoptosis through inhibiting EZH2 transcription. GAS5 effectively repressed EZH2 transcription by directly interacting with E2F4 and recruiting E2F4 to EZH2 promoter. We previously reported that miR-101 induced the apoptosis of BC cells by inhibiting the expression of EZH2. Interestingly, the present study showed that downregulation of EZH2 by GAS5 resulted in overexpression of miR-101 in T24 and EJ cells.	29445179	RID01032	transcriptional regulation
Atherosclerosis	H19	WNT1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	ceRNA(miR-148b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000125084	NA	283120	7471	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BMND16|INT1|OI15	H19 knockdown suppresses proliferation and induces apoptosis by regulating miR-148b/WNT/beta-catenin in ox-LDL-stimulated vascular smooth muscle cells. H19 inhibited miR-148b expression by direct interaction. Further mechanical explorations showed that WNT1 was a target of miR-148b and H19 acted as a competing endogenous RNA (ceRNA) of miR-148b to enhance WNT1 expression.H19 facilitated proliferation and inhibited apoptosis through modulating WNT/beta-catenin signaling pathway via miR-148b in ox-LDL-stimulated HA-VSMCs, implicating the potential values of H19 in AS therapy.	29415742	RID01033	ceRNA or sponge
Osteoarthritis	SNHG5	SOX2	positively-E	luciferase reporter assay;RIP;RNAi	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000181449	NA	387066	6657	C6orf160|LINC00044|NCRNA00044|U50HG	ANOP3|MCOPS3	LncRNA SNHG5/miR-26a/SOX2 signal axis enhances proliferation of chondrocyte in osteoarthritis. The relationship between SNHG5 and miR-26a was confirmed by RIP and the luciferase reporter assays. SOX2 was identified as a target gene of miR-26a by the luciferase reporter assay. Rescue assay was applied to verify the relationship among SNHG5, miR-26a, and SOX2. Our current study demonstrated that SNHG5 is involved in the mechanism of OA through functioning as a ceRNA to competitively sponge miR-26a, therefore, regulating the expression of SOX2.	29409014	RID01034	ceRNA or sponge
Spinal cord ischemia-reperfusion injury	CASC7	miR-30c	positively-E	RNA pull-down assay;RIP	downregulation	qPCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	miRNA	ENSG00000259758	GRCh38_8:140520156-140529501	NA	NA	NA	NA	NA	NA	Hydrogen sulfide upregulation lncRNA CasC7 to reduce neuronal cell apoptosis in spinal cord ischemia-reperfusion injury rat.knockdown of CasC7 could upregulate miR-30c expression, promote cell apoptosis and downregulate miR-30c's target gene expression.	29571256	RID01035	ceRNA or sponge
Gastric cancer	ZEB1	HOTAIR	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000148516	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6935	100124700	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Knock-down of ZEB1 inhibits the proliferation, invasion and migration of gastric cancer cells. Conclusion Knock-down of ZEB1 expression by RNA interference can decease lncRNA HOTAIR expression and restrain cell proliferation, invasion and migration in gastric cancer BGC823 cells	28871949	RID01036	expression association
Urinary bladder cancer	HOTAIR	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Tetracycline-controllable artificial microRNA-HOTAIR + EZH2 suppressed the progression of bladder cancer cells. we also found that HOTAIR expression was positively correlated with EZH2 expression	28671703	RID01037	expression association
Thyroid cancer	LINC00312	miR-197-3p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p	28539331	RID01038	expression association
Pancreatic cancer	linc-DYNC2H1-4	MMP3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell stemness(+)	ceRNA(miR-145)	regulation	NA	NA	CSC	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	PCG	NA	GRCh38_11:102831703-102832102	ENSG00000149968	NA	NA	4314	NA	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Linc-DYNC2H1-4 promotes EMT and CSC phenotypes by acting as a sponge of miR-145 in pancreatic cancer cells. We proved that MMP3, the nearby gene of linc-DYNC2H1-4 in the sense strand, was also a target of miR-145. Downregulation of MMP3 by miR-145 was reverted by linc-DYNC2H1-4, indicating that competing with miR-145 is one of the mechanisms for linc-DYNC2H1-4 to regulate MMP3.	28703793	RID01039	ceRNA or sponge
Atherosclerosis	TSLP	HOTAIR	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Atherosclerosis	PCG	lncRNA	ENSG00000145777	NA	ENSG00000228630	GRCh38_12:53962308-53974956	85480	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis. TSLP activated HOTAIR transcription through PI3K/AKT-IRF1 pathway and then regulates the EC proliferation and migration. TSLP-HOTAIR axis also plays a protective role in low-density lipoprotein (ox-LDL)-induced EC injury. Taken together, TSLP-HOTAIR may be a potential therapy for EC dysfunction in atherosclerosis.	28615347	RID01040	transcriptional regulation
Hirschsprung's disease	MEG3	miR-770-5p	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung's disease. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay.To determine whether MEG3 functions via the miR-770-5p/SRGAP1 pathway, we firstly transfected 293T and SH-SY5Y cells with MEG3 siRNA, miR-770-5p expression was downregulated, whereas SRGAP1 was upregulation at the mRNA and protein levels. Secondly, infection of the two cell lines with MEG3-overexpression lentivirus resulted in increased MEG3 expression levels, whereas SRGAP1 expression was downregulated at the mRNA and protein levels	29050236	RID01041	expression association
Hirschsprung's disease	MEG3	SRGAP1	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000196935	NA	55384	57522	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ARHGAP13|NMTC2	Downregulation of lncRNA MEG3 and miR-770-5p inhibit cell migration and proliferation in Hirschsprung's disease. SRGAP1 mRNA and protein upregulation was inversely correlated with miR-770-5p expression in tissue samples and cell lines, which was confirmed to be a target gene of miR-770-5p by dual-luciferase reporter assay.To determine whether MEG3 functions via the miR-770-5p/SRGAP1 pathway, we firstly transfected 293T and SH-SY5Y cells with MEG3 siRNA, miR-770-5p expression was downregulated, whereas SRGAP1 was upregulation at the mRNA and protein levels. Secondly, infection of the two cell lines with MEG3-overexpression lentivirus resulted in increased MEG3 expression levels, whereas SRGAP1 expression was downregulated at the mRNA and protein levels	29050236	RID01042	expression association
Epithelial ovarian cancer	SLC7A11-AS1	SLC7A11	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-);cell migration(-)	NA	association	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000250033	GRCh38_4:138057464-138178177	ENSG00000151012	NA	641364	23657	NA	CCBR1|xCT	Antisense lncRNA As-SLC7A11 suppresses epithelial ovarian cancer progression mainly by targeting SLC7A11. We also demonstrated that overexpression of As-SLC7A11 could significantly suppress the expression of SLC7A11, indicating a negative correlation between As-SLC7A11 and SLC7A11 in ovarian cancer cells.	29441937	RID01043	expression association
Colorectal cancer	SNHG1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000136997	NA	23642	4609	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA SNHG1 promotes cell proliferation and tumorigenesis in colorectal cancer via Wnt/beta-catenin signaling. Moreover, SNHG1 can promote the expression of target genes, and SNHG1 expression is positively correlated with WNT expression. SNHG1 regulates colorectal cancer by the Wnt signaling pathway. Next, Pearson's correlation was conducted to compare the expression of SNHG1 and Myc. The results show that there was a positive correlation between SNHG1 and c-Myc expression (Fig. 5B), also with the correlation between SNHG1 and TCF7 expression as shown in Fig. 5C. siSNHG1 downregulates the gene expression of c-Myc/MMP-7/CyclinD1/TCF7/LEF in both mRNA and protein levels, while the oeSNHG1 has shown an opposite tendency.	29441936	RID01044	expression association
Colorectal cancer	SNHG1	TCF7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+);WNT/beta-catenin signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000081059	NA	23642	6932	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	TCF-1	Long non-coding RNA SNHG1 promotes cell proliferation and tumorigenesis in colorectal cancer via Wnt/beta-catenin signaling. Moreover, SNHG1 can promote the expression of target genes, and SNHG1 expression is positively correlated with WNT expression. SNHG1 regulates colorectal cancer by the Wnt signaling pathway. Next, Pearson's correlation was conducted to compare the expression of SNHG1 and Myc. The results show that there was a positive correlation between SNHG1 and c-Myc expression (Fig. 5B), also with the correlation between SNHG1 and TCF7 expression as shown in Fig. 5C. siSNHG1 downregulates the gene expression of c-Myc/MMP-7/CyclinD1/TCF7/LEF in both mRNA and protein levels, while the oeSNHG1 has shown an opposite tendency.	29441936	RID01045	expression association
Osteoarthritis	PVT1	miR-488-3p	negatively-F	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 Regulates Chondrocyte Apoptosis in Osteoarthritis by Acting as a Sponge for miR-488-3p	28520497	RID01046	ceRNA or sponge
Esophageal cancer	MALAT1	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA MALAT1 functions as a competing endogenous RNA to regulate the expressions of ZEB1 and ZEB2 by sponging miR-200a and promotes invasion and migration of esophageal cancer cells through inducing epithelial-mesenchymal transition	28635228	RID01047	ceRNA or sponge
Esophageal cancer	MALAT1	ZEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA MALAT1 functions as a competing endogenous RNA to regulate the expressions of ZEB1 and ZEB2 by sponging miR-200a and promotes invasion and migration of esophageal cancer cells through inducing epithelial-mesenchymal transition	28635228	RID01048	ceRNA or sponge
Non-small cell lung cancer	LINC00630	HDAC1	positively-F	mass spectrometry;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223546	GRCh38_X:102769158-102885406	ENSG00000116478	NA	100287765	3065	NA	GON-10|HD1|KDAC1|RPD3|RPD3L1	DDX23-Linc00630-HDAC1 axis activates the Notch pathway to promote metastasis. By RNA pull-down and mass spectrometry we identified Histone deacetylases 1 (HDAC1) and DEAD-box helicase 23 (DDX23) as the linc00630-binding protein that associated with mechanism of linc00630.DDX23 can specific bind with the promoter of Linc00630 to up-regulate the RNA level and high level of linc00630 strength the protein stability of HDAC1 to regulate the downstream pathway.	28473661	RID01049	interact with protein
Non-small cell lung cancer	LINC00630	DDX23	positively-F	mass spectrometry;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000223546	GRCh38_X:102769158-102885406	ENSG00000174243	NA	100287765	9416	NA	PRPF28|SNRNP100|U5-100K|U5-100KD|prp28	DDX23-Linc00630-HDAC1 axis activates the Notch pathway to promote metastasis. By RNA pull-down and mass spectrometry we identified Histone deacetylases 1 (HDAC1) and DEAD-box helicase 23 (DDX23) as the linc00630-binding protein that associated with mechanism of linc00630.DDX23 can specific bind with the promoter of Linc00630 to up-regulate the RNA level and high level of linc00630 strength the protein stability of HDAC1 to regulate the downstream pathway.	28473661	RID01050	interact with protein
Endometrial carcinoma	NEAT1	HMGA1	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-214-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000137309	NA	283131	3159	LINC00084|NCRNA00084|TncRNA|VINC	HMG-R|HMGA1A|HMGIY	NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/beta-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells	28447190	RID01051	ceRNA or sponge
Clear cell renal cell carcinoma	DLEU2	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-30a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000169554	NA	8847	9839	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The putative tumor suppressor microRNA-30a-5p modulates clear cell renal cell carcinoma aggressiveness through repression of ZEB2. In addition, miR-30a-5p may be downregulated by the long non-coding RNA DLEU2.Increasing evidence has shown that lncRNAs contain motifs with sequences complementary to miRNAs and can inhibit miRNAs expression and activity. To examine whether miR-30a-5p is regulated in such a manner in ccRCC cells, interactions between miR-30a-5p and lncRNAs were predicted using starBASE v2.0. The lncRNA DLEU2 was identified as containing a conserved target site in the miR-30a-5p seed region	28569782	RID01052	ceRNA or sponge
Gastric cancer	UCA1	CCND1	positively-E	RIP;luciferase reporter assay;ChIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000110092	NA	652995	595	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA UCA1 induced by SP1 promotes cell proliferation via recruiting EZH2 and activating AKT pathway in gastric cancer.This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.	28569779	RID01053	transcriptional regulation
Prostate cancer	lncRNA625	miR-432	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	NA	GRCh38_17:81709333-81712153	NA	NA	NA	NA	NA	NA	lncRNA625 could functionally inhibit PC3 cells proliferation and promote cells apoptosis through regulating the Wnt/beta-catenin pathway by targeting miR-432. miR-432 is a direct target of lncRNA625. Most importantly, we further found that miR-432 could deactivate Wnt/beta-catenin pathway via suppressing TRIM29 and PYGO2 directly.	28678327	RID01054	ceRNA or sponge
Hepatocellular carcinoma	miR-26a	MEG3	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MicroRNA-26a inhibits proliferation and metastasis of human hepatocellular carcinoma by regulating DNMT3B-MEG3 axis. we demonstrated that DNA methyltransferase 3b (DNMT3B) was a direct target gene of miR-26a.It verified again that DNMT3B could imitate the effect of 5-aza-CdR to down-regulate the expression of MEG3 in HCC cells.Together, the present study added miR-26a/DNMT3B/MEG3 axis to the complex mechanisms of HCC development.	28440439	RID01055	epigenetic regulation
Nasopharynx carcinoma	FOXCUT	FOXC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000054598	NA	101927703	2296	LINC01379|TCONS_00011636	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	The long noncoding RNA FOXCUT promotes proliferation and migration by targeting FOXC1 in nasopharyngeal carcinoma.FOXCUT expression was positively correlated with FOXC1 expression	28635400	RID01056	expression association
Hepatocellular carcinoma	AL163636.1	EGFR	positively-F	luciferase reporter assay;RNA pull-down assay;mass spectrometry;RIP	upregulation	qPCR	NA	NA	immune evasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Immune Detection	Cancer	Liver cancer	lncRNA	PCG	ENSG00000258451	GRCh38_14:20693480-20707120	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long noncoding RNA lnc-EGFR stimulates T-regulatory cells differentiation thus promoting hepatocellular carcinoma immune evasion. lnc-EGFR specifically binds to EGFR and blocks its interaction with and ubiquitination by c-CBL, stabilizing it and augmenting activation of itself and its downstream AP-1/NF-AT1 axis, which in turn elicits EGFR expression.	28541302	RID01057	interact with protein
Non-small cell lung cancer	LINC00673	HOXA5	negatively-E	RIP;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106004	NA	100499467	3202	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	HOX1|HOX1.3|HOX1C	Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5	28423732	RID01058	epigenetic regulation
T-cell acute lymphocytic leukemia	TLX3	MIR99AHG	positively-F	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000164438	NA	ENSG00000215386	GRCh38_21:15928296-16645467	30012	388815	HOX11L2|RNX	NA	Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia.Finally, we established that TLX3 directly regulates miR-125b production through binding and transactivation of LINC00478, a long noncoding RNA gene, which is the host of miR-99a/Let-7c/miR-125b. Altogether, our results reveal an original functional link between TLX3 and oncogenic miR-125b in T-ALL development.	29296717	RID01059	interact with protein
T-cell acute lymphocytic leukemia	MIR99AHG	miR-125b	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	host	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	miRNA	ENSG00000215386	GRCh38_21:15928296-16645467	NA	NA	388815	NA	NA	NA	Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia.Finally, we established that TLX3 directly regulates miR-125b production through binding and transactivation of LINC00478, a long noncoding RNA gene, which is the host of miR-99a/Let-7c/miR-125b. Altogether, our results reveal an original functional link between TLX3 and oncogenic miR-125b in T-ALL development.	29296717	RID01060	expression association
Breast cancer	UCA1	miR-18a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Urothelial carcinoma-associated 1 enhances tamoxifen resistance in breast cancer cells through competitively inhibiting miR-18a. UCA1 directly interacted with miR-18a and reduced its expression in ER positive breast cancer cells. UCA1 was significantly upregulation in tamoxifen resistant LCC2, LCC9, and BT474 cells than in tamoxifen sensitive MCF-7 cells.	28416841	RID01061	ceRNA or sponge
Parkinson's disease	HOTAIR	LRRK2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Nervous system disease	Parkinson's disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000188906	NA	100124700	120892	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AURA17|DARDARIN|PARK8|RIPK7|ROCO2	The long noncoding RNA HOTAIR promotes Parkinson's disease by upregulating LRRK2 expression. With the presence of HOTAIR overexpression in SH-SY5Y cells, the expression of LRRK2 was increased compared with that in the control.	28445933	RID01062	expression association
Cerebral ischemia-reperfusion injury	MALAT1	AKT1	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Ischemia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells. lentiviral knockdown of MALAT1 decreased PI3K activities and the activation of Akt phosphorylation.In conclusion, to the best of our knowledge, the present study was the first to suggest that lncRNA MALAT1 may protect human brain vascular endothelial cells from OGD-R-induced apoptosis via a PI3K-dependent mechanism	28413461	RID01063	expression association
Osteoarthritis	HOTAIR	ADAMTS5	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154736	NA	100124700	11096	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADAM-TS 11|ADAM-TS 5|ADAM-TS5|ADAMTS-11|ADAMTS-5|ADAMTS11|ADMP-2	Long non-coding RNA HOTAIR promotes expression of ADAMTS-5 in human osteoarthritic articular chondrocytes. Lentiviral overexpression and knockdown of HOTAIR markedly increased and decreased the expression of ADAMTS-5, respectively.In conclusion, this study provides the first evidence supporting that HOTAIR strongly promotes the expression of ADAMTS-5 by increasing its mRNA stability in human OA articular chondrocytes; this effect is enhanced by TNF-alpha. It adds new insights into the pathogenesis of OA and suggests that HOTAIR could be a new therapeutic target for ADAMTS-5 inhibition in human OA cartilage.	29441864	RID01064	expression association
Osteosarcoma	MEG3	NOTCH1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148400	NA	55384	4851	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AOS5|AOVD1|TAN1|hN1	MEG3 long non-coding RNA prevents cell growth and metastasis of osteosarcoma. In addition, MEG3 over-expression markedly inhibited Notch1, Hes1,TGF-beta and N-cadheren expression, and the expression level of E-cadheren was improved. These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-beta signaling pathway, thus providing a potential therapeutic target for OS treatment	29198132	RID01065	expression association
Osteosarcoma	MEG3	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105329	NA	55384	7040	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-beta signaling pathway, thus providing a potential therapeutic target for OS treatment	29198132	RID01066	expression association
Acute myocardial infarction	H19	SOX8	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell injury(-);PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-139)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cardiovascular system disease	Myocardial infarction	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000005513	NA	283120	30812	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139.H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139.These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.	29179202	RID01067	ceRNA or sponge
Type 2 diabetes mellitus	lncRNA-p3134	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	NA	NA	NA	NA	NA	NA	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01068	expression association
Type 2 diabetes mellitus	lncRNA-p3134	AKT2	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	ENSG00000105221	NA	NA	208	NA	NA	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01069	expression association
Type 2 diabetes mellitus	lncRNA-p3134	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);insulin synthesis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Disease of metabolism	Diabetes mellitus	circRNA	PCG	NA	NA	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet beta-Cell Function. a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. lncRNA-p3134 overexpression significantly elevated the mRNA level of insulin signaling pathway genes, including PI3K, Akt2, and mTOR both in vitro and vivo the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells.The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve beta-cell function.	29590649	RID01070	expression association
Osteoarthritis	GAS5	KLF2	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	apoptosis process(-);inflammatory response(-);NF-kB signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Tumor Promoting Inflammation;Sustained Angiogenesis	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000127528	NA	60674	10365	NCRNA00030|SNHG2	LKLF	LncRNA GAS5 Overexpression Reverses LPS-Induced Inflammatory Injury and Apoptosis Through Up-Regulating KLF2 Expression in ATDC5 Chondrocytes. KLF2 was predicted and verified as a target of GAS5, and GAS5 functioned through regulating expression of KLF2. Besides, aberrant expression of KLF2 regulated expressions of key kinases involved in the NF-kB and Notch pathways.	29448248	RID01071	expression association
Osteoarthritis	RP11-445H22.4	CXCR4	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell injury(+)	ceRNA(miR-301a)	regulation	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	NA	GRCh38_20:44694892-44746021	ENSG00000121966	NA	NA	7852	NA	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis. miR-301a directly bound to RP11-445H22.4, and suppression of miR-301a inversed the effects of RP11-445H22.4 inhibition. Furthermore, CXCR4 was a direct target of miR-301a, and CXCR4 silencing increased cell viability, decreased apoptosis and inflammatory cytokines secretions in LPS-treated ATDC5 cells. Besides, we found that CXCR4 silencing blocked LPS-activated NF-kB and MAPK/ERK pathways. The study indicated that lncRNA RP11-445H22.4-miR-301a-CXCR4 axis played an important role in cartilage ATDC5 cells and provided a theoretical basis of lncRNA RP11-445H22.4 in OA.	29414810	RID01072	ceRNA or sponge
Non-small cell lung cancer	CCAT1	let-7c	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	WNT signaling pathway(+);cell proliferation(+)	NA	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	CCAT1 stimulation of the symmetric division of NSCLC stem cells through activation of the Wnt signalling cascade. CCAT1 inhibition decreased the ratio of symmetric division of stem cells, and both Let-7c and Axitinib significantly abolished CCAT1 induction of symmetric division by inhibiting Wnt signalling. Restoration of Let-7c blocked the CCAT1 effects, forming the CCAT1/Let-7c/Wnt regulatory axis to control the division of lung cancer stem cells.CCAT1 stimulation of the symmetric division of NSCLC stem cells through activation of the Wnt signalling cascade.	29350683	RID01073	expression association
Hepatocellular carcinoma	TUG1	miR-455-3p	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(+);glucose metabolic process(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Taurine up-regulated gene 1 functions as a master regulator to coordinate glycolysis and metastasis in hepatocellular carcinoma. we showed that knockdown of taurine up-regulated gene 1 (TUG1) induces marked inhibition of cell migration, invasion, and glycolysis through suppression of microRNA (miR)-455-3p. knockdown of TUG1 enhanced binding of the co-repressor p21 to E2F1 when these transcriptional factors are occupying the miR-455 promoter. MiR-455-3p, which is transcriptionally repressed by p21, directly targets the 3' untranslated region of adenosine monophosphate-activated protein kinase subunit beta 2 (AMPKbeta2). The TUG1/miR-455-3p/AMPKbeta2 axis regulates cell growth, metastasis, and glycolysis through regulation of hexokinase 2 (HK2).TUG1 is clearly associated with HK2 overexpression and unfavorable prognosis in HCC patients.Our data collectively highlight that novel regulatory associations among TUG1, miR-455-3p, AMPKbeta2, and HK2 are an important determinant of glycolytic metabolism and metastasis in HCC cells and support the potential utility of targeting TUG1/HK2 as a therapeutic strategy for HCC.	28802060	RID01074	expression association
Hepatocellular carcinoma	TUG1	HK2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(+);glucose metabolic process(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Reprogramming Energy Metabolism	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000159399	NA	55000	3099	LINC00080|NCRNA00080|TI-227H	HKII|HXK2	Taurine up-regulated gene 1 functions as a master regulator to coordinate glycolysis and metastasis in hepatocellular carcinoma. we showed that knockdown of taurine up-regulated gene 1 (TUG1) induces marked inhibition of cell migration, invasion, and glycolysis through suppression of microRNA (miR)-455-3p. knockdown of TUG1 enhanced binding of the co-repressor p21 to E2F1 when these transcriptional factors are occupying the miR-455 promoter. MiR-455-3p, which is transcriptionally repressed by p21, directly targets the 3' untranslated region of adenosine monophosphate-activated protein kinase subunit beta 2 (AMPKbeta2). The TUG1/miR-455-3p/AMPKbeta2 axis regulates cell growth, metastasis, and glycolysis through regulation of hexokinase 2 (HK2).TUG1 is clearly associated with HK2 overexpression and unfavorable prognosis in HCC patients.Our data collectively highlight that novel regulatory associations among TUG1, miR-455-3p, AMPKbeta2, and HK2 are an important determinant of glycolytic metabolism and metastasis in HCC cells and support the potential utility of targeting TUG1/HK2 as a therapeutic strategy for HCC.	28802060	RID01075	expression association
Hepatocellular carcinoma	LINC00589	STAT3	positively-F	RIP;RNAi;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+);IL6/STAT3 signaling pathway(-)	phosphorylation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000251191	GRCh38_8:29673922-29748109	ENSG00000168610	NA	619351	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA TSLNC8 is a tumor suppressor that inactivates the interleukin-6/STAT3 signaling pathway. TSLNC8 significantly suppresses the proliferation and metastasis of HCC cells in vitro and in vivo. TSLNC8 exerts its tumor suppressive activity by competitively interacting with transketolase and signal transducer and activator of transcription 3 (STAT3) and modulating the STAT3-Tyr705 and STAT3-Ser727 phosphorylation levels and STAT3 transcriptional activity, thus resulting in inactivation of the interleukin-6-STAT3 signaling pathway in HCC cells.	28746790	RID01076	interact with protein
Rheumatoid arthritis	ZFAS1	miR-27a	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	LncRNA ZFAS1 promotes cell migration and invasion of fibroblast-like synoviocytes by suppression of miR-27a in rheumatoid arthritis. Further investigation demonstrated that ZFAS1 directly interacted with miR-27a and decreased miR-27a expression. ZFAS1 promotes RA-FLS migration and invasion in an miR-27a-dependent manner.	28721682	RID01077	ceRNA or sponge
Kidney injury	MALAT1	miR-146a	negatively-E	RIP;western blot	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Other	Injury	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Mechanism of long non-coding RNA MALAT1 in lipopolysaccharide-induced acute kidney injury is mediated by the miR-146a/NF-kB signaling pathway. The results revealed that the upregulation of MALAT1 reduced the expression of miR-146a, and there was a negative linear correlation between MALAT1 and miR-146a in a RNA-induced silencing complex-dependent manner.miR-146a was found to be transcriptionally induced by NF-kB, and miR-146a repressed the pro-inflammatory NF-kB pathway and downstream transcription factors. The expression levels of miR-146a were lower in the kidney injury specimens and NRK-52E cells, compared with those in the controls.	29115409	RID01078	expression association
Hepatic ischemia-reperfusion injury	MEG3	NFE2L2	negatively-E	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	hepatic function(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Ischemia	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000116044	NA	55384	4780	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HEBP1|IMDDHH|NRF2	The mechanism of long non-coding RNA MEG3 for hepatic ischemia-reperfusion: Mediated by miR-34a/Nrf2 signaling pathway.we demonstrated that MEG3 functioned as a competing endogenous RNA (ceRNA) for miR-34a, and there was reciprocal repression between MEG3 and miR-34a.MEG3 protected hepatocytes from HIR injury through down-regulating miR-34a expression, which could add our understanding of the molecular mechanisms in HIR injury.	28708282	RID01079	ceRNA or sponge
Osteosarcoma	MEG3	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);apoptosis process(-);JNK/WNT signaling pathway(+)	ceRNA(miR-127)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148516	NA	55384	6935	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Knockdown of lncRNA MEG3 inhibits viability, migration, and invasion and promotes apoptosis by sponging miR-127 in osteosarcoma cell. MEG3 acted as an endogenous sponge by binding to miR-127. More interestingly, MEG3 silence could not suppress OS-732 cells growth and metastasis when miR-127 was knocked down. ZEB1 was a target gene of miR-127, and miR-127 overexpression-induced impairments in cell growth and metastasis were attenuated when ZEB1 was overexpressed. Moreover,miR-127 suppression activated JNK and Wnt signaling pathways, while these activations were recovered by ZEB1 silence.	28636101	RID01080	ceRNA or sponge
Osteoarthritis	MALAT1	miR-127-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1/miR-127-5p Regulates Osteopontin (OPN)-Mediated Proliferation of Human Chondrocytes Through PI3K/Akt Pathway. MALAT1 could directly bind to miR-127-5p to inhibit its expression, so as to rescue OPN expression and promote chondrocyte proliferation through PI3K/Akt pathway.miR-127-5p inhibition could promote chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt;	28590075	RID01081	ceRNA or sponge
Acute liver failure	miR-19a	NBR2	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(-);AMPK/PPARalpha signaling pathway(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Other	Liver failure	miRNA	lncRNA	NA	NA	ENSG00000198496	GRCh38_17:43125551-43153671	NA	10230	NA	NCRNA00192	MiR-19a Affects Hepatocyte Autophagy via Regulating lncRNA NBR2 and AMPK/PPARalpha in D-GalN/Lipopolysaccharide-Stimulated Hepatocytes. Moreover, both NBR2 and PPARalpha were targeted regulated by miR-19a according to luciferase reporter assay. our data suggested that miR-19a negatively controlled the autophagy of hepatocytes attenuated in D-GalN/LPS-stimulated hepatocytes via regulating NBR2 and AMPK/PPARalpha signaling. In hepatic tissue of 20 ALF patients and D-GalN/LPS-stimulated hepatocytes, miR-19a was upregulation and NBR2 was downregulated.	28586153	RID01082	ceRNA or sponge
Hepatocellular carcinoma	DGCR5	KLF14	positively-E	RIP;RNA pull-down assay;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	ceRNA(miR-346)	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000237517	GRCh38_22:18970514-18994628	ENSG00000266265	NA	26220	136259	LINC00037|NCRNA00037	BTEB5	LncRNA DGCR5 represses the development of hepatocellular carcinoma by targeting the miR-346/KLF14 axis. MiR-346 was found to be increased in HCC cells and DGCR5 can act as a sponge of miR-346 to modulate the progression of HCC.Kruppel-like factor 14 (KLF14) was predicted as a downstream target of miR-346 and miR-346 can induce the development of HCC by inhibiting KLF14.DGCR5 overexpression could repress HCC cell growth, migration, and invasion considerably. Taken together, it was indicated in our study that DGCR5 can restrain the progression of HCC through sponging miR-346 and modulating KLF14 in vitro.	30216442	RID01083	ceRNA or sponge
Malignant glioma	GAS5	miR-18a-5p	negatively-F	starBase;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Long noncoding RNA GAS5 regulates the proliferation, migration, and invasion of glioma cells by negatively regulating miR-18a-5p. we identified one miR-18a-5p-binding site within exon 2 of GAS5 that is partially responsible for the tumor-suppressor functions of GAS5. Taken together, our findings suggest that GAS5 is a tumor suppressor in human gliomas that acts in part by repressing miR-18a-5p.	30078184	RID01084	ceRNA or sponge
Osteosarcoma	MALAT1	CDK9	positively-E	RIP;RNA pull-down assay;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136807	NA	378938	1025	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C-2k|CDC2L4|CTK1|PITALRE|TAK	MALAT1 induces osteosarcoma progression by targeting miR-206/CDK9 axis. MALAT1 can function as a competing endogenous RNA by sponging miR-206.CDK9 was predicted as a downstream gene of miR-206, and we observed that MALAT1 can regulate osteosarcoma progress by modulating CDK9 expression via sponging miR-206.It was found that miR-206 was decreased and CDK9 was elevated in human osteosarcoma cells.It was exhibited that knockdown of MALAT1 was able to inhibit osteosarcoma cell proliferation, which suggested that MALAT1 played an oncogenic role in osteosarcoma development.	30076726	RID01085	ceRNA or sponge
Acute-on-chronic liver failure	TNF	HIF1A-AS1	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Other	Liver failure	PCG	lncRNA	ENSG00000232810	NA	ENSG00000258777	GRCh38_14:61681041-61695823	7124	100750246	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	5'aHIF-1A|5'aHIF1alpha	Long noncoding RNA hypoxia-inducible factor 1 alpha-antisense RNA 1 promotes tumor necrosis factor-alpha-induced apoptosis through caspase 3 in Kupffer cells. we found that HIF1A-AS1 could be upregulation by TNF-alpha by lncRNA array analysis and knockdown of HIF1A-AS1 significantly rescued cell apoptosis induced by TNF-alpha.Moreover, inhibition of HIF1A-AS1 markedly reduced mRNA level of caspase 3 which can be significantly enhanced by TNF-alpha.	29369172	RID01086	expression association
Acute-on-chronic liver failure	HIF1A-AS1	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Other	Liver failure	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	we found that HIF1A-AS1 could be upregulation by TNF-alpha by lncRNA array analysis and knockdown of HIF1A-AS1 significantly rescued cell apoptosis induced by TNF-alpha.inhibition of HIF1A-AS1 markedly reduced mRNA level of caspase 3 which can be significantly enhanced by TNF-alpha.	29369172	RID01087	expression association
Hepatocellular carcinoma	HOTAIR	OGFR	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000060491	NA	100124700	11054	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Integrated Proteomic and Transcriptomic Analysis Reveals Long Noncoding RNA HOX Transcript Antisense Intergenic RNA (HOTAIR) Promotes Hepatocellular Carcinoma Cell Proliferation by Regulating Opioid Growth Factor Receptor (OGFr). Further functional studies of the opioid growth factor receptor (OGFr), a negative biological regulator of cell proliferation in HCC, revealed that HOTAIR exerts its effects on cell proliferation, at least in part, through the regulation of OGFr expression.	29079719	RID01088	expression association
Atherosclerosis	H19	miR-130b	negatively-F	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	inflammatory response(+);adipogenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Silencing of H19 inhibits the adipogenesis and inflammation response in ox-LDL-treated Raw264.7 cells by up-regulating miR-130b. the adding of LncRNA H19 abolished the facilitating effect of miR-130b inhibitor on adipogenesis and inflammation response by up-regulating the expression of miR-130b. The bioinformatic analysisshowed that there existed complementary site of miR-130b in H19 RNA.	29172088	RID01089	ceRNA or sponge
Lung adenocarcinoma	LINC00472	DEDD	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	ceRNA(miR-24-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233237	GRCh38_6:71343427-71420745	ENSG00000158796	NA	79940	9191	C6orf155|P53RRA	CASP8IP1|DEDD1|DEFT|FLDED1|KE05	Long Noncoding RNA LINC00472 Inhibits Proliferation and Promotes Apoptosis of Lung Adenocarcinoma Cells via Regulating miR-24-3p/ DEDD. Both LINC00472 and death effector domain-containing DNA-binding protein can bind to miR-24-3p. Long Noncoding RNA LINC00472 Inhibits Proliferation and Promotes Apoptosis of Lung Adenocarcinoma Cells via Regulating miR-24-3p/ DEDD.	30175664	RID01090	ceRNA or sponge
Coronary artery disease	GAS5	MTOR	negatively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Coronary artery disease	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000198793	NA	60674	2475	NCRNA00030|SNHG2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Plasma Long Non-Coding RNA (lncRNA) GAS5 is a New Biomarker for Coronary Artery Disease. GAS5 knockdown significantly increased the level of phospho-mTOR (p-mTOR), and GAS5 overexpression significantly decreased the level of p-mTOR.GAS5 plays a role as upstream regulator of the mTOR pathway to participate in the development of CAD.	29267258	RID01091	expression association
Head and neck squamous cell carcinoma	circPVT1	miR-497-5p	NA	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Head and neck cancer	circRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	The oncogenic role of circPVT1 in head and neck squamous cell carcinoma is mediated through the mutant p53/YAP/TEAD transcription-competent complex. circPVT1 acts as an oncogene modulating the expression of miR-497-5p and genes involved in the control of cell proliferation.	29262850	RID01092	ceRNA or sponge
Bronchopulmonary dysplasia	MALAT1	CDC6	positively-E	RNAi	upregulation	qPCR;microarray	GSE25286;GSE43830	GSE25286.zip;GSE43830.zip	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Other	Bronchopulmonary dysplasia	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000094804	NA	378938	990	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDC18L|HsCDC18|HsCDC6|MGORS5	Long non-coding RNA MALAT1 protects preterm infants with bronchopulmonary dysplasia by inhibiting cell apoptosis. Bioinformative data analysis of MALAT1 knockdown in WI-38 cells showed various differentially expressed genes were found enriched in apoptosis related pathway. Down-regulation of antiapoptopic gene, CDC6 expression was further verified by q-PCR result.we found that up-regulation of lncRNA MALAT1 could protect preterm infants with BPD by inhibiting cell apoptosis.	29237426	RID01094	expression association
Esophagus squamous cell carcinoma	LINC-ROR	SOX9	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);motility(+);chemoresistance(+);self-renewal(+)	ceRNA(miR-15b;miR-33a;miR-129;miR-145;miR-206)	regulation	NA	cisplatin	NA	Limitless Replicative Potential	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000125398	NA	100885779	6662	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CMD1|CMPD1|SRA1|SRXX2|SRXY10	Linc-ROR promotes esophageal squamous cell carcinoma progression through the derepression of SOX9. A positive correlation between linc-ROR and SOX9 expression was found in clinical ESCC specimens (r=0.562, P=0.036), cell lines, and tumorspheres.Silencing of linc-ROR significantly inhibited cell proliferation, motility, chemoresistance, and self-renewal capacity. Mechanistically, linc-ROR modulating the derepression of SOX9 by directly sponging multiple miRNAs including miR-15b, miR-33a, miR-129, miR-145, and miR-206. We foundthat linc-ROR repression resulted in the sensitization of EC9706 cells to cisplatin, which is one of the most fre-quently used chemotherapeutic drug for esophageal cancer. The observation that linc-ROR and SOX9 are coordinatelyexpressed in ESCC tissues led to the hypothesis that linc-ROR might promote stem cell-like properties and cancerprogression through the regulation of pluripotency tran-scription factor SOX9.	29237490	RID01095	ceRNA or sponge
Myocardial infarction	XIST	PDE4D	positively-E	luciferase reporter assay	upregulation	qPCR;microarray	GSE66360	GSE66360.zip	apoptosis process(+);cell proliferation(-)	ceRNA(miR-130a-3p)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000113448	NA	7503	5144	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ACRDYS2|DPDE3|HSPDE4D|PDE43|PDE4DN2|STRK1	LncRNA XIST regulates myocardial infarction by targeting miR-130a-3p. XIST and PDE4D were overexpressed in post-MI myocardial cells, while miR-130a-3p was underexpressed in post-MI myocardial cells. High-expressed XIST and PDE4D both promoted myocardial cell apoptosis. High-expressed XIST also inhibited myocardial cell proliferation. XIST down-regulated miR-130a-3p and PDE4D was a direct target of miR-130a-3p. LncRNA XIST promotes MI by targeting miR-130a-3p. MI induced by PDE4D can be reversed by miR-130a-3p.	29226319	RID01096	ceRNA or sponge
Ischemic stroke	HIF1A-AS2	HIF1A	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-153-3p)	regulation	NA	NA	NA	Sustained Angiogenesis	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000100644	NA	100750247	3091	3'aHIF-1A|aHIF	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	lncRNAs HIF1A-AS2 facilitates the up-regulation of HIF-1alpha by sponging to miR-153-3p, whereby promoting angiogenesis in HUVECs in hypoxia.HIF1A-AS2 serves as a 'sponge' to miR-153-3p, which decreased the post-transcriptional silencing of HIF-1alpha by miR-153-3p. This function of HIF1A-AS2 facilitated the activation of HIF-1alpha/VEGFA/Notch1 cascades, by which HUVECs viability, migration ability and tube formation were promoted.	28985553	RID01097	ceRNA or sponge
Hepatocellular carcinoma	LINC00941	SNAI1	positively-E	RNA pull-down assay;RIP	upregulation	microarray	GSE70880;TCGA	GSE70880.zip;LIHC.zip	epithelial to mesenchymal transition(+);WNT/beta-catenin signaling pathway(+)	ceRNA(miR-34a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000235884	GRCh38_12:30755167-30802602	ENSG00000124216	NA	100287314	6615	lncRNA-MUF	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Mesenchymal Stem Cells Promote Hepatocarcinogenesis via lncRNA-MUF Interaction with ANXA2 and miR-34a. We identified a novel lncRNA that we termed lncRNA-MUF (MSC-upregulation factor) that is highly expressed in HCC tissues and correlated with poor prognosis. Depleting lncRNA-MUF in HCC cells repressed EMT and inhibited their tumorigenic potential. Conversely, lncRNA-MUF overexpression accelerated EMT and malignant capacity. Mechanistic investigations showed that lncRNA-MUF bound Annexin A2 (ANXA2) and activated Wnt/beta-catenin signaling and EMT. Furthermore, lncRNA-MUF acted as a competing endogenous RNA for miR-34a, leading to Snail1 upregulation and EMT activation.	28947421	RID01098	ceRNA or sponge
Hepatocellular carcinoma	LINC00941	ANXA2	interact	RNA pull-down assay;RIP	upregulation	microarray	GSE70880;TCGA	GSE70880.zip;LIHC.zip	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000235884	GRCh38_12:30755167-30802602	ENSG00000182718	NA	100287314	302	lncRNA-MUF	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Mesenchymal Stem Cells Promote Hepatocarcinogenesis via lncRNA-MUF Interaction with ANXA2 and miR-34a. We identified a novel lncRNA that we termed lncRNA-MUF (MSC-upregulation factor) that is highly expressed in HCC tissues and correlated with poor prognosis. Depleting lncRNA-MUF in HCC cells repressed EMT and inhibited their tumorigenic potential. Conversely, lncRNA-MUF overexpression accelerated EMT and malignant capacity. Mechanistic investigations showed that lncRNA-MUF bound Annexin A2 (ANXA2) and activated Wnt/beta-catenin signaling and EMT. Furthermore, lncRNA-MUF acted as a competing endogenous RNA for miR-34a, leading to Snail1 upregulation and EMT activation.	28947421	RID01099	interact with protein
Intervertebral disc degeneration	RP11-296A18.3	HIF1A	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENST00000366181.2	GRCh38_1:51195095-51235096	ENSG00000100644	NA	NA	3091	NA	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA-RP11-296A18.3/miR-138/HIF1A Pathway Regulates the Proliferation ECM Synthesis of Human Nucleus Pulposus Cells (HNPCs). RP11-296A18.3 regulates HNPC proliferation and ECM synthesis through miR-138. As the target gene of miR-138, hypoxia-inducible factor 1-alpha (HIF1A) was closely associated with cell proliferation which was also regulated by RP11-296A18.3 via miR-138. RP11-296A18.3 was positively correlated to HIF1A.We revealed that RP11-296A18.3 promote HIF1A expression through sponging miR-138, thus to promote HNPC proliferation and ECM synthesis.	28543639	RID01100	ceRNA or sponge
Atherosclerosis	TP53COR1	OLR1	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000173391	NA	102800311	4973	TRP53COR1|linc-p21|lincRNA-p21	CLEC8A|LOX1|LOXIN|SCARE1|SLOX1	Long intergenic noncoding RNA p21 mediates oxidized LDL-induced apoptosis and expression of LOX-1 in human coronary artery endothelial cells. Lentiviral overexpression of lincRNA-p21 markedly increased oxLDL-induced apoptosis and the expression of LOX-1 in HCAECs.	28983628	RID01101	expression association
Non-small cell lung cancer	XIST	LARP1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-374a)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000155506	NA	7503	23367	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	LARP	LARP1 is regulated by the XIST/miR-374a axis and functions as an oncogene in non-small cell lung carcinoma. we found that XIST functioned as a competing endogenous RNA to suppress miR-374a, which regulated its downstream target LARP1. The expression of miR-374a was negatively correlated with the expression of LARP1 in NSCLC tissues. Knockdown of LARP1 inhibited cell proliferation, migration and invasion in NSCLC cells and tumourigenicity in H520 cells.	29039571	RID01102	ceRNA or sponge
Thyroid cancer	H19	IRS1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169047	NA	283120	3667	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HIRS-1	Long Noncoding RNA H19 Inhibits Cell Viability, Migration, and Invasion Via Downregulation of IRS-1 in Thyroid Cancer Cells. Furthermore, long noncoding RNA H19 negatively regulated the expression of insulin receptor substrate 1 and thus effect on cell proliferation and apoptosis. Insulin receptor substrate 1 regulated the activation of phosphatidyl inositide 3-kinases/AKT and nuclear factor kB signal pathways. In conclusion, long noncoding RNA H19 could suppress cell viability, migration, and invasion via downregulation of insulin receptor substrate 1 in SW579 and TPC-1 cells.	29332545	RID01103	expression association
Hepatitis	MALAT1	CXCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	inflammatory response(+);fibrotic(+)	NA	association	NA	NA	NA	Tumor Promoting Inflammation	Gastrointestinal system disease	Liver disease	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163735	NA	378938	6374	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENA-78|SCYB5	Altered expression of MALAT1 lncRNA in nonalcoholic steatohepatitis fibrosis regulates CXCL5 in hepatic stellate cells. Two potential target mRNAs, syndecan 4 (SDC4), and C-X-C motif chemokine ligand 5 (CXCL5) were identified for hepatocellular carcinoma upregulation lncRNA and MALAT1, respectively, but only CXCL5 showed differential expression among the different histologic classes. Knockdown of MALAT1 expression reduced CXCL5 transcript and protein levels by 50% and 30%, respectively, in HepG2 cells. The expression of MALAT1 and CXCL5 was upregulation in activated hepatic stellate (LX-2) cells compared to cells in the quiescent state, and MALAT1 expression was regulated by hyperglycemia and insulin in HepG2 cells, but only by insulin in LX-2 cells. Dysregulated lncRNA expression is associated with inflammation and fibrosis in NASH.	28993096	RID01104	expression association
Skin disease	H19	DSG1	negatively-E	western blot;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-130b-3p)	regulation	NA	NA	NA	NA	Integumentary system disease	Skin disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000134760	NA	283120	1828	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CDHF4|DG1|DSG|EPKHE|EPKHIA|PPKS1|SPPK1	H19 lncRNA regulates keratinocyte differentiation by targeting miR-130b-3p. we demonstrated that lncRNA-H19 act as an endogenous 'sponge', which binds directly to miR-130b-3p and therefore inhibits its activity on Dsg1. MiR-130b-3p was illustrated to inhibit keratinocyte differentiation by targeting Dsg1. H19 regulates Dsg1 expression and the consequent keratinocyte differentiation through miR-130b-3p.Aberrant differentiation of keratinocytes has been demonstrated to be associated with a number of skin diseases.	29192645	RID01105	ceRNA or sponge
Non-small cell lung cancer	uc.339	CCNE2	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cell growth(+);cell migration(+);tumorigenesis(+)	ceRNA(miR-339-3p;miR-663b-3p;miR-95-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_12:53677039-53677887	ENSG00000175305	NA	NA	9134	NA	CYCE2	Transcribed ultraconserved region 339 promotes carcinogenesis by modulating tumor suppressor microRNAs. To investigate the mechanism of action of uc.339, we hypothesized that the T-UCR might work as a decoy for complementary mature miRNAs. A structural analysis of the uc.339 transcript with the RNAhybrid algorithm14 revealed the presence of sequences complementary to three mature miRNAs (namely, miR-339-3p, -663b-3p, and -95-5p from now on referred to as miR-339, -663b, and -95, respectively) in the uc.339 RNA transcript. We find that transcribed uc.339 is upregulation in archival NSCLC samples, functioning as a decoy RNA for miR-339-3p,-663b-3p, and -95-5p. As a result, Cyclin E2, a direct target of all these microRNAs is upregulation, promoting cancer growth and migration.	29180617	RID01106	ceRNA or sponge
Breast cancer	YAP1	BCAR4	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+);glucose metabolic process(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Reprogramming Energy Metabolism	Cancer	Breast cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000262117	GRCh38_16:11819829-11828845	10413	400500	COB1|YAP|YAP2|YAP65|YKI	NA	LncRNA wires up Hippo and Hedgehog signaling to reprogramme glucose metabolism. The expression levels of BCAR4 and YAP are positively correlated in tissue samples from breast cancer patients, where high expression of both BCAR4 and YAP is associated with poor patient survival outcome.YAP promotes the expression of BCAR4, which subsequently coordinates the Hedgehog signaling to enhance the transcription of glycolysis activators HK2 and PFKFB3.	28963395	RID01107	transcriptional regulation
Prostate cancer	HOTAIR	miR-193a	negatively-E	ChIP;luciferase reporter assay;western blot	NA	NA	NA	NA	cancer progression(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691	RID01108	epigenetic regulation
Prostate cancer	miR-193a	HOTAIR	negatively-F	ChIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691	RID01109	ceRNA or sponge
Endometriosis	MALAT1	miR-200c	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Reproductive system disease	Endometriosis	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo. We demonstrated that expression of MALAT1 in ectopic endometrial specimens was negatively correlated with that of miR-200c and that MALAT1 knockdown increased the level of miR-200c in HESCs. Exogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). The MALAT1/miR-200c sponge may be a potential therapeutic target for endometriosis.	29116025	RID01110	ceRNA or sponge
Colon cancer	LINC01567	miR-93	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000224310	GRCh38_16:24661422-24671062	NA	NA	400511	NA	LOCCS	NA	Long intergenic non-protein-coding RNA 1567 (LINC01567) acts as a sponge against microRNA-93 in regulating the proliferation and tumorigenesis of human colon cancer stem cells.We also found an lncRNA, LOCCS, with obviously upregulation expression in colon CSCs. Knockdown of LOCCS reduced cell proliferation, invasion, migration, and generation of tumor xenografts. Furthermore, microRNA-93 (miR-93) and Musashi-1 mediated the tumor suppression of LOCCS knockdown. There was reciprocal repression between LOCCS and miR-93. Research on mechanisms suggested direct binding, as a predicted miR-93 binding site was identified in LOCCS.	29110645	RID01111	ceRNA or sponge
Breast cancer	HOTAIR	miR-34a	NA	NA	NA	NA	NA	NA	cell autophagy(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	The Long Noncoding RNA HOTAIR in Breast Cancer: Does Autophagy Play a Role. HOTAIR can regulate autophagy, important for breast cancer cells survival, through the interaction with miRNAs specific for autophagy genes and directly with these genes.Many studies point at miR-34a as a major component of HOTAIR-miRNAs-cancer cross-talk. The most important role of HOTAIR can be attributed to cancer progression as its overexpression stimulates invasion and metastasis. These studies point at miR-34a as an important element of HOTAIR regulation, which was suggested earlier. Similarly, HOTAIR was reported to indirectly regulate miR-34a expression.	29469819	RID01112	expression association
Estrogen-receptor negative breast cancer	WDR7-7	GPER1	negatively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(-)	NA	regulation	NA	calycosin	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	"ENSP00000409300.1,ENST00000449340.1"	GRCh38_1:111439890-111449308	ENSG00000164850	NA	NA	2852	NA	NA	Calycosin inhibits the in vitro and in vivo growth of breast cancer cells through WDR7-7-GPR30 Signaling. Here, we show that calycosin inhibited the proliferation of both ER- (MDA-MB-468 and SKBR3) and ER+ breast cancer cells (MCF-7 and T47D) and that these inhibitory effects were associated with the up-regulation of the long non-coding RNA (lncRNA) WDR7-7.  The target of WDR7-7, G-protein coupled estrogen receptor 30 (GPR30, formerly known as GPER), was present in both ER+ and ER- breast cancer cells, as confirmed by a luciferase reporter assay. we demonstrate that the expression of WDR7-7 is reduced in breast cancer cell lines and that the overexpression of WDR7-7 inhibits growth through a mechanism that involves G-protein coupled estrogen receptor 30 (GPR30).in all four GPR30-positive breast cancer lines, calycosin decreased the phosphorylation levels of SRC, EGFR, ERK1/2 and Akt, but the inhibition of WDR7-7 blocked these changes and increased proliferation. These results suggest the possibility that calycosin inhibited the proliferation of breast cancer cells, at least partially, through WDR7-7-GPR30 signaling, which may explain why calycosin can exert inhibitory effects on ER- breast cancer.	29096683	RID01113	expression association
Osteosarcoma	XIST	RSF1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);oncogenic role(+)	ceRNA(miR-193a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000048649	NA	7503	51773	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	HBXAP|RSF-1|XAP8|p325	RSF1 functions as an oncogene in osteosarcoma and is regulated by XIST/miR-193a-3p axis. RSF1 was identified as a direct target of miR-193a-3p.we found that miR-193a-3p was negatively correlated with RSF1 expression in OS tissues.our data showed that XIST could function as competing endogenous RNA to repress miR-193a-3p, which regulated its downstream target RSF1. RSF1 inhibition suppressed OS cell proliferation and invasion. In conclusion, our findings demonstrated that the XIST/miR-193a-3p/RSF1 axis might contribute to the progression and act as a therapeutic target of OS patients.	28843909	RID01114	ceRNA or sponge
Pancreatic ductal adenocarcinoma	YY1	SOX2-OT	negatively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	TF	lncRNA	ENSG00000100811	NA	ENSG00000242808	GRCh38_3:180989762-181836880	7528	347689	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	NCRNA00043|SOX2OT	Yin Yang-1 suppresses pancreatic ductal adenocarcinoma cell proliferation and tumor growth by regulating SOX2OT-SOX2 axis. Luciferase reporter, electrophoretic mobility shift (EMSA), and chromatin immunoprecipitation (ChIP) assays revealed binding of YY1 to the SOX2OT promoter. Moreover, YY1 suppressed PDAC cell proliferation through SOX2OT transcriptional inhibition and subsequent decreased SOX2 expression.	28867247	RID01115	transcriptional regulation
Non-small cell lung cancer	LINC00346	JAK2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255874	GRCh38_13:110863987-110870251	ENSG00000096968	NA	283487	3717	C13orf29|NCRNA00346	JTK10|THCYT3	The expressions of LINC00346 were relatively high in NSCLC tissues and cells. LINC00346 promotes the proliferation and inhibits the apoptosis of NSCLC cells through regulating the JAK-STAT3 signaling pathway.Western blotting showed that LINC00346 could exert its function through partially regulating the Janus kinase/signal transducer and activator of transcription 3 (JAK-STAT3) signaling pathway.	29228425	RID01116	expression association
Non-small cell lung cancer	LINC00346	STAT3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000255874	GRCh38_13:110863987-110870251	ENSG00000168610	NA	283487	6774	C13orf29|NCRNA00346	ADMIO|ADMIO1|APRF|HIES	The expressions of LINC00346 were relatively high in NSCLC tissues and cells. LINC00346 promotes the proliferation and inhibits the apoptosis of NSCLC cells through regulating the JAK-STAT3 signaling pathway.Western blotting showed that LINC00346 could exert its function through partially regulating the Janus kinase/signal transducer and activator of transcription 3 (JAK-STAT3) signaling pathway.	29228425	RID01117	expression association
Hepatocellular carcinoma	IATPR	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000148516	NA	101929447	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Knockdown of long noncoding RNA linc-ITGB1 suppresses migration, invasion of hepatocellular carcinoma via regulating ZEB1.Further study revealed that silenced linc-ITGB1 inhibited the expression of ZEB1 and then suppressed epithelial to mesenchymal transition (EMT), which was important during the metastasis of hepatocellular carcinoma.The results indicate that linc-ITGB1, a novel oncogene in tumorigenesis, could promote the metastasis and EMT via ZEB1, which may offer a possible therapeutic target in hepatocellular carcinoma.	29228420	RID01118	expression association
Osteosarcoma	TP73-AS1	miR-142	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000227372	GRCh38_1:3735511-3747373	NA	NA	57212	NA	KIAA0495|PDAM	NA	Knockdown of long non-coding RNA TP73-AS1 inhibits osteosarcoma cell proliferation and invasion through sponging miR-142.	29864904	RID01119	ceRNA or sponge
Urinary bladder cancer	FOXD2-AS1	ABCC3	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-143)	binding/interaction	RNA-RNA	gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000237424	GRCh38_1:47432133-47434641	ENSG00000108846	NA	84793	8714	NA	ABC31|EST90757|MLP2|MOAT-D|MRP3|cMOAT2	Long noncoding RNA FOXD2-AS1 accelerates the gemcitabine-resistance of bladdercancer by sponging miR-143.Bioinformatics program and validation experiments confirmed that FOXD2-AS1 positively regulated ABCC3 protein through targeting miR-143, acting as a competing endogenous RNA (ceRNA)	29674277	RID01120	ceRNA or sponge
Urinary bladder cancer	ZFAS1	miR-329	negatively-F	luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000177410	GRCh38_20:49278178-49299600	NA	NA	441951	NA	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	NA	Long noncoding RNA ZFAS1 facilitates bladder cancer tumorigenesis by sponging miR-329	29653362	RID01121	ceRNA or sponge
Non-small cell lung cancer	DANCR	miR-758-3p	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000226950	GRCh38_4:52712404-52720351	NA	NA	57291	NA	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	NA	The long non-coding RNA-DANCR exerts oncogenic functions in non-small cell lung cancer via miR-758-3p.we concluded that DANCR promotes NSCLC cell proliferation, migration and invasion by regulating the tumor suppressor miR-758-3p.	29635134	RID01122	expression association
Oral cavity cancer	CDKN2B-AS1	miR-125a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	The role of long non-coding RNA ANRIL in the carcinogenesis of oral cancer by targeting miR-125a.Furthermore, we found a negative correlation between ARNIL and miR-125a, and ARNIL acts as a miRNA-sponge by directly interacting with miR-125a.	29635126	RID01123	ceRNA or sponge
Colorectal cancer	HEIH	BCL2L1	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000171552	NA	100859930	598	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939 Mediated Transcriptional Repression of Bcl-xL. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor kB (NF-kB), increases the binding of NF-kB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL.	29081216	RID01124	expression association
Colorectal cancer	HEIH	miR-939	negatively-F	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939 Mediated Transcriptional Repression of Bcl-xL. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor kB (NF-kB), increases the binding of NF-kB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL.	29081216	RID01125	ceRNA or sponge
Ovarian cancer	NEAT1	ROCK1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-382-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067900	NA	283131	6093	LINC00084|NCRNA00084|TncRNA|VINC	P160ROCK|ROCK-I	Long non-coding RNA NEAT1 promoted ovarian cancer cells' metastasis through regulation of miR-382-3p/ROCK1 axial	29790629	RID01126	ceRNA or sponge
Ovarian cancer	GAS5	SPRY2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-21)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000136158	NA	60674	10253	NCRNA00030|SNHG2	IGAN3|hSPRY2	Long non-coding RNA GAS5 inhibits ovarian cancer cell proliferation via the control of microRNA-21 and SPRY2 expression.Luciferase assay data indicated that miR-21 was a direct target of GAS5 and that SPRY2 was a target gene of miR-21 in ovarian cancer-derived A2780 cells	29896229	RID01127	ceRNA or sponge
Non-small cell lung cancer	SNHG1	MTDH	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000147649	NA	23642	92140	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	3D3|AEG-1|AEG1|LYRIC|LYRIC/3D3	Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p	29466052	RID01128	ceRNA or sponge
Breast cancer	MAGI2-AS3	FAS	positively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000026103	NA	100505881	355	NA	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL).	29679339	RID01129	expression association
Breast cancer	MAGI2-AS3	FASLG	positively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234456	GRCh38_7:79452877-79471208	ENSG00000117560	NA	100505881	356	NA	ALPS1B|APT1LG1|APTL|CD178|CD95-L|CD95L|FASL|TNFSF6|TNLG1A	Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL).	29679339	RID01130	expression association
Colorectal cancer	HAGLR	miR-217	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000224189	GRCh38_2:176164051-176188958	NA	NA	401022	NA	HOXD-AS1|MIR7704HG|Mdgt	NA	HOXD-AS1 functionedas a competing endogenous RNA for miR-217	29749477	RID01131	ceRNA or sponge
Gastric cancer	MEG3	miR-21	negatively-E	western blot	downregulation	qPCR	NA	NA	cell motility(+);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer.The expression of miR-21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT. Co-transfection of lncRNA-MEG3 and miR-21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3, suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer.	29749532	RID01132	expression association
Breast cancer	ITGB2-AS1	ITGB2	positively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000227039	GRCh38_21:44921051-44929678	ENSG00000160255	NA	100505746	3689	NA	CD18|LAD|LCAMB|LFA-1|MAC-1|MF17|MFI7	LncRNA ITGB2-AS1 Could Promote the Migration and invasion of Breast Cancer Cells through Up regulating ITGB2	29941860	RID01133	expression association
Lung cancer	MIR22HG	YBX1	negatively-E	RNAi	downregulation	microarray;sequencing	GSE31210;GSE68465;TCGA	GSE31210.zip;GSE68465.zip;LUSC_LUAD.zip	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000065978	NA	84981	4904	C17orf91	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01134	expression association
Lung cancer	MIR22HG	MET	negatively-E	RNAi	downregulation	microarray;sequencing	NA	NA	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000105976	NA	84981	4233	C17orf91	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01135	expression association
Lung cancer	MIR22HG	CDKN1A	negatively-E	RNAi	downregulation	microarray;sequencing	NA	NA	cell survival(-);cell death(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000186594	GRCh38_17:1711493-1717174	ENSG00000124762	NA	84981	1026	C17orf91	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer	29669758	RID01136	expression association
Head and neck cancer	HOTAIRM1	DLGAP1	negatively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000170579	NA	100506311	9229	HOXA-AS1|HOXA1-AS1|NCRNA00179	DAP-1|DAP-1-ALPHA|DAP-1-BETA|DAP1|DLGAP1A|DLGAP1B|GKAP|SAPAP1	HOTAIRM1 competed endogenously with miR-148a to regulate DLGAP1 in head and neck tumor cells.HOTAIRM1 was confirmed as a tumor suppressor via sponging miR-148a and promote the expression of DLGAP1, which could be regarded as an important target for the prevention and treatment of HNT.	29905017	RID01137	ceRNA or sponge
Hepatocellular carcinoma	PVT1	STAT1	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-);immunotherapies(-)	histone modification	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000115415	NA	5820	6772	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	Long noncoding RNA PVT1 inhibits interferon-alpha mediated therapy for hepatocellular carcinoma cells by interacting with signal transducer and activator of transcription 1.Taken together, these results for the first time indicate that IFN-alpha treatment promotes oncogenic PVT1 expression in HCC cells, which interacts with STAT1 to inhibit IFN-alpha signaling, ultimately blocking IFN-alpha-induced cells apoptosis, suggesting that lncRNA PVT1 may be a potential target to improve IFN-alpha-mediated HCC immunotherapies.	29715456	RID01138	epigenetic regulation
Liver cancer	HULC	PTEN	negatively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT/mTOR signaling pathway(+)	ceRNA(miR-15a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000171862	NA	728655	5728	HCCAT1|LINC00078|NCRNA00078	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA HULC accelerates liver cancer by inhibiting PTEN via autophagy cooperation to miR15a.Of significance, our observations also revealed that HULC inhibited PTEN through ubiquitin-proteasome system mediated by autophagy-P62	29895332	RID01139	ceRNA or sponge
Liver cancer	HULC	SQSTM1	positively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-15a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000161011	NA	728655	8878	HCCAT1|LINC00078|NCRNA00078	A170|DMRV|FTDALS3|NADGP|OSIL|PDB3|ZIP3|p60|p62|p62B	Long noncoding RNA HULC accelerates liver cancer by inhibiting PTEN via autophagy cooperation to miR15a.Mechanistically, HULC increasesthe expression of P62 via decreasing mature miR15a.	29895332	RID01140	ceRNA or sponge
Colorectal cancer	UCA1	CDKN1B	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Up-regulation of UCA1/mTOR axis suppressed p27 and miR-143 while the expression of CCND1 and KRAS were significantly increased compared with control.CAF-CM induces the upregulation of UCA1 in sw480 cells and leading to upregulation of mTOR. UCA1 in cooperation with mTOR regulates downstream key effectors and induces CCND1 and suppresses p27 and miR-143, subsequently, directs the cell proliferation, EMT and metastasis of CRC cell	29948578	RID01141	expression association
Colorectal cancer	UCA1	MTOR	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000198793	NA	652995	2475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Taken together, these results highlight the vital role of cooperation between lncRNA UCA1 and mTOR in proliferation and metastasis.	29948578	RID01142	expression association
Colorectal cancer	UCA1	KRAS	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000133703	NA	652995	3845	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Up-regulation of UCA1/mTOR axis suppressed p27 and miR-143 while the expression of CCND1 and KRAS were significantly increased compared with control.CAF-CM induces the upregulation of UCA1 in sw480 cells and leading to upregulation of mTOR. UCA1 in cooperation with mTOR regulates downstream key effectors and induces CCND1 and suppresses p27 and miR-143, subsequently, directs the cell proliferation, EMT and metastasis of CRC cell	29948578	RID01143	expression association
Non-small cell lung cancer	HOTAIR	miR-613	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long Noncoding RNA (lncRNA) HOTAIR Affects Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer by Upregulating miR-613.The targeting relationship between HOTAIR and miR-613 was further confirmed through the luciferase report assay.	29187267	RID01144	ceRNA or sponge
Osteosarcoma	TUG1	miR-153	negatively-F	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Knockdown of Long Noncoding RNA TUG1 Inhibits the Proliferation and Cellular Invasion of Osteosarcoma Cells by Sponging miR-153	28411362	RID01145	ceRNA or sponge
Melanoma	PVT1	miR-26b	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Melanoma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long Noncoding RNA PVT1 Promotes Melanoma Progression via Endogenous Sponging miR-26b	28409552	RID01146	ceRNA or sponge
Triple-receptor negative breast cancer	LINC-ROR	MUC1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000185499	NA	100885779	4582	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ADMCKD|ADMCKD1|CA 15-3|CD227|EMA|H23AG|KL-6|MAM6|MCD|MCKD|MCKD1|MUC-1|MUC-1/SEC|MUC-1/X|MUC1/ZD|PEM|PEMT|PUM	LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1.Furthermore, lincRNA-ROR functions as a competing endogenous RNAs (ceRNA) which sponges miR-145 and therefore upregulate the expression of Mucin1 (MUC1).	29673594	RID01147	ceRNA or sponge
Endometrial carcinoma	HOTAIR	NPM1	negatively-E	RIP;western blot;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-646)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181163	NA	100124700	4869	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	B23|NPM	Long noncoding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via the miR-646/NPM1 axis.Taken together, our findings presented that HOTAIR could regulate NPM1 via interacting with miR-646, thereby governing the viability, migration, and invasion of EC cells.	29466670	RID01148	ceRNA or sponge
Cervical cancer	SNHG20	ADAM10	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);MEK/ERK signaling pathway(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000137845	NA	654434	102	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	AD10|AD18|CD156c|CDw156|HsT18717|MADM|RAK|kuz	LncRNA SNHG20 promotes cell proliferation and invasion via miR-140-5p-ADAM10 axis in cervical cancer.Our study demonstrated that SNHG20 could function as an oncogenic lncRNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.	29604594	RID01149	ceRNA or sponge
Malignant glioma	SNHG6	CDKN1A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000124762	NA	641638	1026	HBII-276HG|NCRNA00058|U87HG	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA SNHG6 acts as a prognostic factor to regulate cell proliferation in glioma through targeting p21	29579705	RID01150	expression association
Prostate cancer	SNHG7	CCND1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-503)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000110092	NA	84973	595	NCRNA00061	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503	29571017	RID01151	ceRNA or sponge
Breast cancer	lncRNA-CTD-2108O9.1	LIFR	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENST00000508986	GRCh38_5:38425036-38427376	ENSG00000113594	NA	NA	3977	NA	CD118|LIF-R|SJS2|STWS|SWS	Long non-coding RNA-CTD-2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor	29603493	RID01152	expression association
Glioblastoma	CYTOR	miR-107	negatively-F	starBase;RNAi	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	NA	LncRNA LINC00152 promoted glioblastoma progression through targeting the miR-107 expression	29671226	RID01153	ceRNA or sponge
Colorectal cancer	OIP5-AS1	DYRK1A	positively-E	western blot;luciferase reporter assay	downregulation	qPCR;microarray	GSE95606	GSE95606.zip	radioresistance(-)	ceRNA(miR-369-3p)	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000157540	NA	729082	1859	cyrano|linc-OIP5	DYRK|DYRK1|HP86|MNB|MNBH|MRD7	LncRNA OIP5-AS1 regulates radioresistance by targeting DYRK1A through miR-369-3p in colorectal cancer cells	29773344	RID01154	ceRNA or sponge
Esophagus squamous cell carcinoma	TP63	LINC01503	positively-E	ChIP;RIP;luciferase reporter assay;RNA pull-down assay;mass spectrometry	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	transcriptional regulation;super-enhancer	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000073282	NA	ENSG00000233901	GRCh38_9:129332300-129359541	8626	100506119	AIS|B(p51A)|B(p51B)|EEC3|KET|LMS|NBP|OFC8|RHS|SHFM4|TP53CP|TP53L|TP73L|p40|p51|p53CP|p63|p73H|p73L	NA	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients.	29454790	RID01155	transcriptional regulation
Non-small cell lung cancer	XIST	NOTCH1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-137)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000148400	NA	7503	4851	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AOS5|AOVD1|TAN1|hN1	Furthermore,XIST could act as an endogenous sponge by directly binding to miR-137,negatively regulating its expression. Notch-1 was identified as a direct target gene of miR-137, with the XIST-miR-137 axis regulating activation of the Notch-1 pathway. We identified a branch of the XIST/miR-137/Notch-1 pathway that regulates proliferation and TGF-beta1-induced EMT in NSCLC,which could be involved in NSCLC progression. Knockdown of XIST suppressed cell proliferation and TGF-b1-induced EMT in A549 and H1299 cells	29812958	RID01156	ceRNA or sponge
Malignant glioma	HAGLR	E2F8	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-130a)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000129173	NA	401022	79733	HOXD-AS1|MIR7704HG|Mdgt	E2F-8	HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8	29341117	RID01157	ceRNA or sponge
Urinary bladder cancer	AWPPH	SMAD4	negatively-E	RIP;ChIP	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell autophagy(+);cell migration(+);apoptosis process(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111195866-111495161	ENSG00000141646	NA	NA	4089	NA	DPC4|JIP|MADH4|MYHRS	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression.LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.Then, RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2.	29231261	RID01158	epigenetic regulation
Hepatocellular carcinoma	XIST	MAPK1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-194-5p)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000100030	NA	7503	5594	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	LncRNA XIST functions as a molecular sponge of miR-194-5p to regulate MAPK1 expression.In brief, the above results elucidate the important role of XIST in HCC tumorigenesis, suggesting that XIST might be a candidate prognostic biomarker and a novel therapeutic target for treating HCC.	29227532	RID01159	ceRNA or sponge
Lung cancer	H19	miR-484	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 promotes epithelial-mesenchymal transition (EMT) by targeting miR-484 in human lung cancer cells.	29219208	RID01160	ceRNA or sponge
Prostate cancer	MALAT1	AKAP12	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-145-5p)	regulation	NA	docetaxel	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131016	NA	378938	9590	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP250|SSeCKS	Long noncoding RNA MALAT1 enhances the docetaxel resistance of prostate cancer cells via miR-145-5p-mediated regulation of AKAP12	29633510	RID01161	ceRNA or sponge
Colorectal cancer	H19	GRN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	ceRNA(miR-29b-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000030582	NA	283120	2896	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling	29754471	RID01162	ceRNA or sponge
Hepatocellular carcinoma	LINC00554	MARCKSL1	positively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260738	GRCh38_13:99994899-99997909	ENSG00000175130	NA	100861542	65108	NA	F52|MACMARCKS|MLP|MLP1|MRP	The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating cells via the protein kinase C substrates MARCKS and MARCKSL1. In conclusion,lncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1.Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes.	29588366	RID01163	transcriptional regulation
Hepatocellular carcinoma	LINC00554	MARCKS	positively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260738	GRCh38_13:99994899-99997909	ENSG00000277443	NA	100861542	4082	NA	80K-L|MACS|PKCSL|PRKCSL	The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating cells via the protein kinase C substrates MARCKS and MARCKSL1. In conclusion,lncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1.Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes.	29588366	RID01164	transcriptional regulation
Endometrial carcinoma	ABHD11-AS1	CCND1	positively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000225969	GRCh38_7:73735038-73736158	ENSG00000110092	NA	171022	595	LINC00035|NCRNA00035|WBSCR26	BCL1|D11S287E|PRAD1|U21B31	LncRNA ABHD11-AS1 promotes the development of endometrial carcinoma by targeting cyclin D1.LncRNA ABHD11-AS1 functions as an oncogene to promote cell proliferation and invasion in endometrial carcinoma by positively targeting cyclin D1. RNA pull down demonstrated that lncRNA ABHD11-AS1 binds directly to cyclin D1.	29799152	RID01165	interact with protein
Non-small cell lung cancer	AFAP1-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000124762	NA	84740	1026	AFAP1-AS|AFAP1AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA AFAP1-AS1 predicts a poor prognosis and regulates non-small cell lung cancer cell proliferation by epigenetically repressing p21 expression	29793547	RID01166	epigenetic regulation
Papillary thyroid carcinoma	RP5-1024C24.1	MPPED2	positively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000254489	GRCh38_11:30584130-30630508	ENSG00000066382	NA	NA	744	NA	239FB|C11orf8	The Long Non-Coding RNA RP5-1024C24.1 and Its Associated-Gene MPPED2 Are Down-Regulated in Human Thyroid Neoplasias and Act as Tumour Suppressors	29783666	RID01167	expression association
Prostate cancer	LINC00599	miR-185-5p	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000253230	GRCh38_8:9899871-9906678	NA	NA	157627	NA	NA	NA	Long non-coding RNA RNCR3 promotes prostate cancer progression through targeting miR-185-5p	29887969	RID01168	ceRNA or sponge
Hepatocellular carcinoma	LINC00473	USP9X	positively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000124486	NA	90632	8239	C6orf176|LNC473|bA142J11.1	DFFRX|FAF|FAM|MRX99|MRXS99F	Long noncoding RNA LNC473 inhibits the ubiquitination of survivin via association with USP9X and enhances cell proliferation and invasion in hepatocellular carcinoma cells	29605299	RID01169	expression association
Urinary bladder cancer	ZFAS1	KLF2	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	BLCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000127528	NA	441951	10365	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	LKLF	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01170	expression association
Urinary bladder cancer	ZFAS1	NKD2	positively-E	RNAi	upregulation	qPCR;microarray	TCGA	BLCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000145506	NA	441951	85409	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	Naked2	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01171	expression association
Urinary bladder cancer	ZFAS1	ZEB2	negatively-E	RNAi	downregulation	qPCR;microarray	TCGA	BLCA.zip	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000169554	NA	441951	9839	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01172	expression association
Urinary bladder cancer	ZFAS1	ZEB1	negatively-E	RNAi	downregulation	qPCR;microarray	TCGA	BLCA.zip	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000148516	NA	441951	6935	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression	29678899	RID01173	expression association
Prostate cancer	PVT1	TWIST1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	PRAD.zip	epithelial to mesenchymal transition(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000122691	NA	5820	7291	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Long noncoding RNA PVT1 promotes EMT via mediating microRNA-186 targeting of Twist1 in prostate cancer.We then confirmed that PVT1 acts as a sponge for miRNA-186-5p and positively regulates Twist1 by a sponge effect.	29452232	RID01174	ceRNA or sponge
Hepatocellular carcinoma	NEAT1	PNPLA2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000177666	NA	283131	57104	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1-modulated abnormal lipolysis via ATGL drives hepatocellular carcinoma proliferation.NEAT1 regulated ATGL expression by binding miR-124-3p. Additionally, NEAT1 knockdown attenuated HCC cell growth through miR-124-3p/ATGL/DAG+FFA/PPARalpha signaling.	29764424	RID01175	ceRNA or sponge
Gastric cancer	GAPLINC	MAPK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-378)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000100030	NA	100505592	5594	LINC01540	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long noncoding RNA GAPLINC promotes gastric cancer cell proliferation by acting as a molecular sponge of miR-378 to modulate MAPK1 expression	29785127	RID01176	ceRNA or sponge
Cervical squamous cell carcinoma	PVT1	TGFB1	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cervix carcinoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000105329	NA	5820	7040	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	LncRNA PVT1 promotes the growth of HPV positive and negative cervical squamous cell carcinoma by inhibiting TGF-beta1	29760583	RID01177	expression association
Lung cancer	UCA1	miR-144	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Noncoding RNA Urothelial Carcinoma-Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144	28762326	RID01178	ceRNA or sponge
Breast cancer	CAMTA1-DT	miR-20b	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell motility(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000237436	GRCh38_1:6783892-6784843	NA	NA	110841581	NA	lncCAMTA1	NA	Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of the Human Breast Cancer Cell Line MDA-MB-231 via Targeting miR-20b. The results showed that lncCAMTA1 expression promoted cell viability and migration/invasion, while knockdown of lncCAMTA1 promoted cell apoptosis via binding with miR-20b. lncCAMTA1 negatively regulated miR-20b expression. VEGF was a target of miR-20b, leading to the modification of the phosphorylation levels of MAPK, ERK, JAK, STAT1, and STAT3. Our findings suggested that lncCAMTA1 might promote proliferation and mobility of human breast cancer cells via binding with miR-20b. VEGF was a direct target of miR-20b and regulated activation of the MAPK/ERK and JAK/STAT3 signaling pathways. Therefore lncCAMTA1 has potential as a novel cancer diagnostic marker and as a putative novel therapeutic target for breast cancer treatment.	28550685	RID01179	ceRNA or sponge
Acute promyelocytic leukemia	CEBPB	NEAT1	positively-E	ChIP;luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	cell differentiation(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	NA	Cancer	Leukemia	TF	lncRNA	ENSG00000172216	NA	ENSG00000245532	GRCh38_11:65422774-65445540	1051	283131	C/EBP-beta|IL6DBP|NF-IL6|TCF5	LINC00084|NCRNA00084|TncRNA|VINC	C/EBPbeta contributes to transcriptional activation of long non-coding RNA NEAT1 during APL cell differentiation.we performed chromatin immunoprecipitation and luciferase reporter assays to demonstrate that C/EBP family transcription factor C/EBPbeta bind to and transactivate the promoter of lncRNA NEAT1 through the C/EBPbeta binding sites both around -54 bp and -1453 bp upstream of the transcription start site.	29111326	RID01180	transcriptional regulation
Hepatocellular carcinoma	MIAT	miR-214	negatively-F	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000225783	GRCh38_22:26646411-26676475	NA	NA	440823	NA	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	NA	lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214	29097358	RID01181	ceRNA or sponge
Malignant glioma	PVT1	miR-190a-5p	negatively-F	ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p. In conclusion, PVT1-miR-190a-5p/miR-488-3p-MEF2C-JAGGED1 axis is involved in proliferation and progression of glioma. Thus, PVT1 may become a novel target in glioma therapy.	29501773	RID01182	ceRNA or sponge
Malignant glioma	PVT1	miR-488-3p	negatively-F	ChIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p	29501773	RID01183	ceRNA or sponge
Colorectal cancer	TMEM238L	miR-942	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-);WNT/beta-catenin signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000263429	GRCh38_17:10794913-10804099	NA	NA	100289255	NA	NA	NA	Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/beta-catenin signaling	29524886	RID01184	expression association
Hepatoblastoma	OIP5-AS1	ZEB1	positively-E	RIP;luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-186a-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000148516	NA	729082	6935	cyrano|linc-OIP5	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Kockdown of OIP5-AS1 expression inhibits proliferation, metastasis and EMT progress in hepatoblastoma cells through up-regulating miR-186a-5p and down-regulating ZEB1. OIP5-AS1 is a ceRNA in Hepatoblastoma cells through modulating miR-186a-5p/ZEB1	29475118	RID01185	ceRNA or sponge
Lung adenocarcinoma	MALAT1	SP1	positively-F	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185591	NA	378938	6667	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 promotes lung adenocarcinoma by directly interacting with specificity protein 1	29575609	RID01186	interact with protein
Ovarian cancer	RP11-552M11.4	BRCA2	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000243960	GRCh38_1:111438638-111441364	ENSG00000139618	NA	NA	675	NA	BRCC2|BROVCA2|FACD|FAD|FAD1|FANCD|FANCD1|GLM3|PNCA2|XRCC11	Long non-coding RNA RP11-552M11.4 promotes cells proliferation, migration and invasion by targeting BRCA2 in ovarian cancer.Rescue experiment and luciferase reporter assay showed that lncRNA RP11-552M11.4 regulated SKOV3 cells functions through binding BRCA2. Further experiments in A-2780 cells also validated that lncRNA RP11-552M11.4 induced A-2780 cell proliferation while repressing apoptosis by targeting BRCA2. LncRNA RP11-552M11.4 inhibits BRCA2 expression by interacting at binding site in SKOV3 cells.	29478268	RID01187	interact with mRNA
Breast cancer	lncRNA-PRLB	SIRT1	positively-E	luciferase reporter assay;RIP	downregulation	qPCR;microarray	TCGA	BRCA.zip	cell proliferation(+);cell metastasis(+);chemoresistance(+)	ceRNA(miR-4766-5p)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000253802	GRCh38_8:40333173-40343363	ENSG00000096717	NA	NA	23411	NA	SIR2|SIR2L1|SIR2alpha	A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer.our findings indicated that lncRNA could regulate the progression and chemoresistance of breast cancer via modulating the expression levels of miR-4766-5p and SIRT1. LncRNA-PRLB promotes proliferation, metastasis, and chemoresistance partly by regulating SIRT1 expression through protecting it from miR-4766-5p-mediated degradation.LncRNA-PRLB abundantly sponges miR-4766-5p and miR-4766-5p promotes cell proliferation, metastasis, and chemoresistance in breast cancer. miR-4766-5p targets SIRT1 and regulates its expression.	29752439	RID01188	ceRNA or sponge
Gastric cancer	MRUL	ABCB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	adriamycin;vincristine	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENST00000432937	GRCh38_7:87152361-87196337	ENSG00000085563	NA	NA	5243	NA	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Long noncoding RNA MRUL promotes ABCB1 expression in multidrug-resistant gastric cancer cell sublines;Heterologous luciferase reporter assays demonstrated that MRUL might positively affect ABCB1 expression in an orientation- and position-independent manner.Furthermore, the relative expression levels of MRUL in GC tissues were negatively correlated with in vitro growth inhibition rates of GC specimens treated with chemotherapeutic drugs and indicated a poor prognosis for GC patients. MRUL knockdown in SGC7901/ADR and SGC7901/VCR cells led to increased rates of apoptosis, increased accumulation, and reduced doxorubicin (Adriamycin [ADR]) release in the presence of ADR or vincristine.	24958102	RID01189	expression association
Urinary bladder cancer	UCA1	SMARCA4	negatively-F	RNA pull-down assay;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000127616	NA	652995	6597	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA urothelial carcinoma associated 1 induces cell replication by inhibiting BRG1 in 5637 cells; we identified BRG1 as a UCA1 binding partner using an in vitro RNA pull-down assay, and RNA-binding protein immunoprecipitation assay confirmed UCA1-BRG binding in bladder cancer cells in vivo. UCA1 impairs both binding of BRG1 to the p21 promoter and chromatin remodeling activity of BRG1.Collectively, these results demonstrate that UCA1 promotes bladder cancer cell proliferation by inhibiting BRG1.	24993775	RID01190	interact with protein
Urinary bladder cancer	UCA1	CDKN1A	negatively-E	RNA pull-down assay;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA urothelial carcinoma associated 1 induces cell replication by inhibiting BRG1 in 5637 cells; we identified BRG1 as a UCA1 binding partner using an in vitro RNA pull-down assay, and RNA-binding protein immunoprecipitation assay confirmed UCA1-BRG binding in bladder cancer cells in vivo. UCA1 impairs both binding of BRG1 to the p21 promoter and chromatin remodeling activity of BRG1.Collectively, these results demonstrate that UCA1 promotes bladder cancer cell proliferation by inhibiting BRG1.	24993775	RID01191	epigenetic regulation
Pancreatic cancer	H19	HMGA2	negatively-E	luciferase reporter assay;RNAi;qRT-PCR	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(let-7)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	H19 promotes pancreatic cancer metastasis by derepressing let-7's suppression on its target HMGA2-mediated EMT;We further demonstrated that H19 promoted PDAC cell invasion and migration at least partially by increasing HMGA2-mediated epithelial-mesenchymal transition (EMT) through antagonizing let-7.H19 was reported as a sponge to antagonizing let-7.	24055342;17437991;24920070	RID01192	ceRNA or sponge
Colorectal cancer	MALAT1	PTBP2	positively-F	RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117569	NA	378938	58155	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	PTBLP|brPTB|nPTB	Long non-coding RNA MALAT1 promotes tumour growth and metastasis in colorectal cancer through binding to SFPQ and releasing oncogene PTBP2 from SFPQ/PTBP2 complex; MALAT1 could bind to SFPQ, thus releasing PTBP2 from the SFPQ/PTBP2 complex. In turn, the increased SFPQ-detached PTBP2 promoted cell proliferation and migration;MALAT1 and PTBP2 were overexpressed, both of which were associated closely with the invasion and metastasis of CRC	25025966	RID01193	interact with protein
Prostate cancer	H19	miR-675	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI;we found that the expression level of either H19 or miR-675 in P69 cells was negatively associated with the expression of transforming growth factor beta induced protein (TGFBI);Dual luciferase reporter assays showed that miR-675 directly bound with 3'UTR of TGFBI mRNA to repress its translation	24988946	RID01194	expression association
Prostate cancer	H19	TGFBI	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000120708	NA	283120	7045	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BIGH3|CDB1|CDG2|CDGG1|CSD|CSD1|CSD2|CSD3|EBMD|LCD1	lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI;we found that the expression level of either H19 or miR-675 in P69 cells was negatively associated with the expression of transforming growth factor beta induced protein (TGFBI);Dual luciferase reporter assays showed that miR-675 directly bound with 3'UTR of TGFBI mRNA to repress its translation	24988946	RID01195	expression association
Lung cancer	SOX2-OT	EZH2	positively-E	RIP;RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000106462	NA	347689	2146	NCRNA00043|SOX2OT	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival;knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions	24927902	RID01196	interact with protein
Lung cancer	SOX2-OT	CCNB1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000134057	NA	347689	891	NCRNA00043|SOX2OT	CCNB	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival.Sox2 overlapping transcript (Sox2ot) is a long noncoding RNA (lncRNA), localized on human chromosome 3q26.33, which is frequently amplified in lung squamous cell carcinomas (SCCs). In this study, we found that Sox2ot was up-regulated over two folds in 53.01% of human primary lung cancers (44/83). Importantly, knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions. Altogether, our data suggested that Sox2ot plays an important role in regulating lung cancer cell proliferation, and may represent a novel prognostic indicator for the disease.	24927902	RID01197	expression association
Lung cancer	SOX2-OT	CDK1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000242808	GRCh38_3:180989762-181836880	ENSG00000170312	NA	347689	983	NCRNA00043|SOX2OT	CDC2|CDC28A|P34CDC2	A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival.Sox2 overlapping transcript (Sox2ot) is a long noncoding RNA (lncRNA), localized on human chromosome 3q26.33, which is frequently amplified in lung squamous cell carcinomas (SCCs). In this study, we found that Sox2ot was up-regulated over two folds in 53.01% of human primary lung cancers (44/83). Importantly, knocking down Sox2ot decreased EZH2 expression and reintroduction of EZH2 allowed Sox2ot knockdown cells progressed through G2/M phase, which correlates with the restoration of Cyclin B1 and Cdc2 expressions. Altogether, our data suggested that Sox2ot plays an important role in regulating lung cancer cell proliferation, and may represent a novel prognostic indicator for the disease.	24927902	RID01198	expression association
Colon cancer	HOTAIR	CDH1	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01199	expression association
Colon cancer	HOTAIR	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000026025	NA	100124700	7431	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01200	expression association
Colon cancer	HOTAIR	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer.Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT)	24840737	RID01201	expression association
Breast cancer	LINC-ROR	ZEB2	positively-E	RNA pull-down assay;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-205)	regulation	NA	tamoxifen	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000169554	NA	100885779	9839	ROR|lincRNA-RoR|lincRNA-ST8SIA3	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.our data revealed that linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205;linc-ROR prevented the degradation of mir-205 target genes, including the EMT inducer ZEB2; Thus our results indicate that linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs. Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205.down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	24922071;28063065	RID01202	ceRNA or sponge
Gastric cancer	H19	RUNX1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	host(miR-675)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000159216	NA	283120	861	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells.Subsequently, the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in AGS cells, and knockdown of H19 or miR-675 enhanced RUNX1 expression.To our knowledge, this is the time to demonstrate that RUNX1 serves as a link between H19/miR-675 axis and Akt/mTOR signaling and is a pivotal mediator in gastric cancer progression induced by H19/miR-675. The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1;we found that miR-675 was positively expressed with H19 and was a pivotal mediator in H19-induced gastric cancer cell growth promotion;the tumor suppressor Runt Domain Transcription Factor1 (RUNX1) was confirmed to be a direct target of miR-675 using a luciferase reporter assay and Western blotting analyses;our study demonstrated that the novel pathway H19/miR-675/RUNX1 regulates gastric cancer development	26931432;24388988	RID01203	expression association
Oesophageal adenocarcinoma	HNF1A-AS1	H19	positively-E	RNAi;western blot	upregulation	qPCR;sequencing	GSE48240	GSE48240.zip	tumorigenesis(+)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	lncRNA	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000130600	GRCh38_11:1995176-2001470	283460	283120	C12orf27|HAS1|NCRNA00262	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Long non-coding RNA HNF1A-AS1 regulates proliferation and migration in oesophageal adenocarcinoma cells.The well known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs;Our findings suggest that dysregulation of HNF1A-AS1 participates in oesophageal tumorigenesis, and that this participation may be mediated, at least in part, by modulation of chromatin and nucleosome assembly as well as by H19 induction	24000294	RID01204	expression association
Cervical cancer	TUSC8	MYC	negatively-F	RNAi;western blot	downregulation	qPCR	NA	NA	prognosis(+);cell proliferation(-)	interact with protein	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	TF	ENSG00000237361	GRCh38_13:44400250-44405984	ENSG00000136997	NA	400128	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Low expression of long noncoding XLOC_010588 indicates a poor prognosis and promotes proliferation through upregulation of c-Myc in cervical cancer;Western blot assays confirmed that XLOC_010588 physically associates with c-Myc, consequently decreasing the expression of c-Myc	24667250	RID01205	interact with mRNA
Gastric cancer	H19	ISM1	positively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101230	NA	283120	140862	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	C20orf82|ISM|Isthmin|bA149I18.1|dJ1077I2.1	Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer;An H19 co-expression network identified ISM1 as a binding protein of H19, and its expression was positively correlated with that of H19; Our results suggest that the effect of H19 in GC is mediated by the direct upregulation of ISM1 and the indirect suppression of CALN1 expression via miR-675.	24810858	RID01206	interact with protein
Gastric cancer	H19	CALN1	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000183166	NA	283120	83698	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CABP8	Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer;CALN1 was identified as a target gene of miR-675 and its expression was negatively correlated with that of miR-675;H19 RNA actively binds to ISM1 and miR-675 targets CALN1;Our results suggest that the effect of H19 in GC is mediated by the direct upregulation of ISM1 and the indirect suppression of CALN1 expression via miR-675	24810858	RID01207	interact with protein
Gastric cancer	HOTAIR	ERBB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-);cancer progression(+)	ceRNA(miR-331-3p)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141736	NA	100124700	2064	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer;HOTAIR may act as a ceRNA, effectively becoming a sink for miR-331-3p, thereby modulating the derepression of HER2 and imposing an additional level of post-transcriptional regulation;HOTAIR overexpression represents a biomarker of poor prognosis in gastric cancer, and may confer malignant phenotype to tumor cells.Finally, the positive HOTAIR/HER2 correlation was significantly associated with advanced gastric cancers.	24775712	RID01208	ceRNA or sponge
Urinary bladder cancer	UCA1	WNT6	positively-E	luciferase reporter assay;RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);WNT signaling pathway(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000115596	NA	652995	7475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 increases chemoresistance of bladder cancer cells by regulating Wnt signaling.we showed that UCA1 positively regulates expression of wingless-type MMTV integration site family member 6 (Wnt6) in human bladder cancer cell lines. UCA1 and Wnt6 expression is also positively correlated in vivo. Up-regulation of UCA1 activates Wnt signaling in a Wnt6-dependent manner;We finally demonstrate that UCA1 increases the cisplatin resistance of bladder cancer cells by enhancing the expression of Wnt6	24495014	RID01209	expression association
Non-small cell lung cancer	BANCR	CDH1	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000039068	NA	100885775	999	LINC00586	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01210	expression association
Non-small cell lung cancer	BANCR	CDH2	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000170558	NA	100885775	1000	LINC00586	CD325|CDHN|CDw325|NCAD	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01211	expression association
Non-small cell lung cancer	BANCR	VIM	negatively-E	fluorescent immunohistochemistry;western blot	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000026025	NA	100885775	7431	LINC00586	NA	Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression	24655544	RID01212	expression association
Urinary bladder cancer	MALAT1	SUZ12	positively-F	RIP;RNA pull-down assay;ChIP;western blot;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178691	NA	378938	23512	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CHET9|JJAZ1	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;malat1 is associated with suppressor of zeste 12 (suz12), and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression. We performed RIP with antibodies against ezh2 or suz12 from nuclear extracts of T24 and RT4 cells. We observed a significant enrichment of malat1 with the suz12 antibody compared with the nonspecific immunoglobulin G (IgG) antibody control.	24449823	RID01213	interact with protein
Urinary bladder cancer	TGFB1	MALAT1	positively-E	RNA pull-down assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;TGF-beta induces malat1 expression and EMT in bladder cancer cells;malat1 knockdown inhibits TGF-beta-induced EMT;targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGF-beta;These data suggest that malat1 is an important mediator of TGF-beta-induced EMT	24449823	RID01214	expression association
Hepatocellular carcinoma	HOTAIR	RBM38	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132819	NA	100124700	55544	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HSRNASEB|RNPC1|SEB4B|SEB4D|dJ800J21.2	Long non-coding RNA HOTAIR promotes cell migration and invasion via down-regulation of RNA binding motif protein 38 in hepatocellular carcinoma cells;HOTAIR could promote migration and invasion of HCC cells by inhibiting RBM38, which indicated critical roles of HOTAIR and RBM38 in HCC progression	24663081	RID01215	expression association
Gastric cancer	miR-148a	MEG3	positively-E	MS-PCR;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MiR-148a regulates MEG3 in gastric cancer by targeting DNA methyltransferase 1;The positive correlation of MEG3 and miR-148a was further confirmed in SGC-7901 and BGC-823 gastric cancer cell lines; transfection of MEG3 siRNA into gastric cancer cells diminished the suppression of proliferation induced by overexpression of miR-148a;Our results suggest that the suppression of miR-148a may contribute to the down-regulation of MEG3 in gastric cancer by modulation of DNMT-1	24515776	RID01216	epigenetic regulation
Breast cancer	UCA1	CDKN1B	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes breast tumor growth by suppression of p27(Kip1);although hnRNP I enhances the translation of p27 (Kip1) through interaction with the 5'-untranslated region (5'-UTR) of p27 mRNAs, the interaction of UCA1 with hnRNP I suppresses the p27 protein level by competitive inhibition;we show a negative correlation between p27 and UCA in the breast tumor cancer tissue microarray	24457952	RID01217	interact with protein
Malignant glioma	H19	miR-675	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	host	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675;we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression;introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells	24466011	RID01218	expression association
Esophagus squamous cell carcinoma	HOTAIR	WIF1	negatively-E	RNAi;ChIP;western blot	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156076	NA	100124700	11197	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	WIF-1	HOTAIR, a prognostic factor in esophageal squamous cell carcinoma, inhibits WIF-1 expression and activates Wnt pathway;inverse correlation between HOTAIR and WIF-1 expression was demonstrated both in ESCC cells and tissues;HOTAIR directly decreased WIF-1 expression by promoting its histone H3K27 methylation in the promoter region and then activated the Wnt/beta-catenin signaling pathway;This newly identified HOTAIR/WIF-1 axis clarified the molecular mechanism of ESCC cell metastasis	24118380	RID01219	epigenetic regulation
Urinary bladder cancer	miR-125b	MALAT1	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Hsa-miR-125b suppresses bladder cancer development by down-regulating oncogene SIRT7 and oncogenic long non-coding RNA MALAT1;we report that hsa-miR-125b and oncogene SIRT7/oncogenic long non-coding RNA MALAT1 were inversely expressed in bladder cancer;Binding sites were confirmed between hsa-miR-125b and SIRT7/MALAT1;Up-regulation of hsa-miR-125b or down-regulation of SIRT7 inhibited proliferation, motility and increased apoptosis. The effects of up-regulation of hsa-miR-125b were similar to that of silencing MALAT1 in bladder cancer as we had previously described	24396870	RID01220	ceRNA or sponge
Lung adenocarcinoma	HOTAIR	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	The long noncoding RNA HOTAIR contributes to cisplatin resistance of human lung adenocarcinoma cells via downregualtion of p21(WAF1/CIP1) expression;HOTAIR was observed to be significantly downregulated in cisplatin-responding LAD tissues, and its expression was inversely correlated with p21 mRNA expression;siRNA/p21 or pcDNA/p21 could partially rescue the effects of siRNA/HOTAIR1 or pcDNA/HOTAIR on both p21 expression and cisplatin sensitivity in LAD cells;our findings suggest that upregulation of HOTAIR contributes to the cisplatin resistance of LAD cells, at least in part, through the regulation of p21 expression	24155936	RID01221	expression association
Non-small cell lung cancer	HOTAIR	HOXA5	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106004	NA	100124700	3202	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX1|HOX1.3|HOX1C	The long non-coding RNA HOTAIR indicates a poor prognosis and promotes metastasis in non-small cell lung cancer. Our findings indicate that HOTAIR is significantly up-regulated in NSCLC tissues, and regulates NSCLC cell invasion and metastasis, partially via the down-regulation of HOXA5	24103700	RID01222	expression association
Non-small cell lung cancer	MEG3	TP53	positively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA MEG3 inhibits NSCLC cells proliferation and induces apoptosis by affecting p53 expression;Our findings indicate that MEG3 is significantly down-regulated in NSCLC tissues that could be affected by DNA methylation, and regulates NSCLC cell proliferation and apoptosis, partially via the activition of p53	24098911	RID01223	expression association
Urinary bladder cancer	BLACAT1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);cell survival(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000178691	NA	101669762	23512	LINC00912|linc-UBC1|onco-lncRNA-30	CHET9|JJAZ1	linc-UBC1 physically associates with polycomb repressive complex 2 (PRC2) and acts as a negative prognostic factor for lymph node metastasis and survival in bladder cancer;RIP and ChIP assay confirmed that linc-UBC1 physically associates with PRC2 complex and regulates histone modification status of target genes.RNA immunoprecipitation (RIP) was performed to confirm that linc-UBC1 physically associates with EZH2 and SUZ12, core components of polycomb repressive complex 2 (PRC2).	23688781	RID01224	interact with protein
Urinary bladder cancer	BLACAT1	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);cell survival(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000106462	NA	101669762	2146	LINC00912|linc-UBC1|onco-lncRNA-30	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	linc-UBC1 physically associates with polycomb repressive complex 2 (PRC2) and acts as a negative prognostic factor for lymph node metastasis and survival in bladder cancer;RIP and ChIP assay confirmed that linc-UBC1 physically associates with PRC2 complex and regulates histone modification status of target genes.RNA immunoprecipitation (RIP) was performed to confirm that linc-UBC1 physically associates with EZH2 and SUZ12, core components of polycomb repressive complex 2 (PRC2).	23688781	RID01225	interact with protein
Acute promyelocytic leukemia	HOXA-AS2	TNFSF10	negatively-E	western blot	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000121858	NA	285943	8743	HOXA3as	APO2L|Apo-2L|CD253|TL2|TNLG6A|TRAIL	HOX antisense lincRNA HOXA-AS2 is an apoptosis repressor in all trans retinoic acid treated NB4 promyelocytic leukemia cells; The increase in death of HOXA-AS2 knockdown cells was accompanied by an elevated TNF-related apoptosis-inducing ligand (TRAIL) levels, but ATRA-induced NB4 cells treated with TRAIL did show an increase in HOXA-AS2 expression;These results demonstrate that all trans retinoic acid (ATRA) induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway	23649634	RID01226	expression association
Prostate cancer	CBR3-AS1	AR	positively-E	RIP;western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);apoptosis process(-);cell proliferation(+)	ceRNA(miR-34c;miR-297)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000169083	NA	100506428	367	PlncRNA-1|PlncRNA1	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa.The prostate cancer-up-regulated long noncoding RNA PlncRNA-1 modulates apoptosis and proliferation through reciprocal regulation of androgen receptor;PlncRNA-1 suppression by siRNA resulted in a decrease of androgen receptor (AR) mRNA, protein and AR downstream target	26808578;22264502	RID01227	ceRNA or sponge
Hepatocellular carcinoma	H19	miR-200	positively-E	RNA pull-down assay;ChIP;RIP;western blot	downregulation	qPCR	NA	NA	cell metastasis(-);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma;H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation. The results demonstrate that H19 can alter the miR-200 pathway, thus contributing to mesenchymal-to-epithelial transition and to the suppression of tumor metastasis	23222811	RID01228	epigenetic regulation
Urinary bladder cancer	UCA1	CREB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118260	NA	652995	1385	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CREB|CREB-1	Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells;UCA1 alteration paralleled to the expression and phosphorylation of CREB, and UCA1 obviously influenced AKT expression and activity;cell cycle progression was greatly reduced after PI3-K pathway was blocked by LY294002, indicating that UCA1 affected cell cycle progression through CREB	22285928	RID01229	expression association
Hepatocellular carcinoma	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. In vitro assays in the HCC cell line Bel7402 demonstrated that knockdown of HOTAIR lincRNA reduced cell proliferation and was associated with reductions in levels of matrix metalloproteinase-9 and vascular endothelial growth factor protein, which are important for cell motility and metastasis	22289527	RID01230	expression association
Hepatocellular carcinoma	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. In vitro assays in the HCC cell line Bel7402 demonstrated that knockdown of HOTAIR lincRNA reduced cell proliferation and was associated with reductions in levels of matrix metalloproteinase-9 and vascular endothelial growth factor protein, which are important for cell motility and metastasis	22289527	RID01231	expression association
Osteosarcoma	HOTAIR	CDKN2A	negatively-E	ChIP	upregulation	qPCR	NA	NA	chemosensitivity(+);cell viability(+);apoptosis process(-)	DNA methylation	regulation	NA	DNMT1 inhibitor	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000147889	NA	100124700	1029	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	A novel interplay between HOTAIR and DNA methylation in osteosarcoma cells indicates a new therapeutic strategy.A series of experiments show that HOTAIR represses the expression of CDKN2A through inhibiting the promoter activity of CDKN2A by DNA hypermethylation. Functionally, HOTAIR depletion increases the sensibility of OS cells to DNMT1 inhibitor through regulating the viability and apoptosis of OS cells via HOTAIR-miR126-DNMT1-CDKN2A axis.	28730284	RID01232	epigenetic regulation
Osteosarcoma	HOTAIR	DNMT1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(+);cell viability(+);apoptosis process(-)	NA	regulation	NA	DNMT1 inhibitor	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	A novel interplay between HOTAIR and DNA methylation in osteosarcoma cells indicates a new therapeutic strategy. Further evidence shows that HOTAIR activates the expression of DNMT1 through repressing miR-126, which is the negative regulator of DNMT1; Functionally, HOTAIR depletion increases the sensibility of OS cells to DNMT1 inhibitor through regulating the viability and apoptosis of OS cells via HOTAIR-miR126-DNMT1-CDKN2A axis.	28730284	RID01233	expression association
Osteoarthritis	NEAT1	SPP1	positively-E	luciferase reporter assay;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-181c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000118785	NA	283131	6696	LINC00084|NCRNA00084|TncRNA|VINC	NA	NEAT1/miR-181c Regulates Osteopontin (OPN)-Mediated Synoviocyte Proliferation in Osteoarthritis;among which NEAT1 showed to inversely regulate miR-181c;By performing Luciferase assays, we revealed that NEAT1 competed with OPN for miR-181c binding;OPN mRNA, and NEAT1 expression was upregulation, whereas miR-181c expression was downregulated, indicating that targeting NEAT1 to rescue miR-181c expression so as to inhibit OPN expression and synoviocyte proliferation might be an efficient strategy for OA treatment	28379604	RID01234	ceRNA or sponge
Liver fibrosis	NEAT1	KLF6	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	fibrotic(+)	ceRNA(miR-122)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000067082	NA	283131	1316	LINC00084|NCRNA00084|TncRNA|VINC	BCD1|CBA1|COPEB|CPBP|GBF|PAC1|ST12|ZF9	NEAT1 accelerates the progression of liver fibrosis via regulation of microRNA-122 and Kruppel-like factor 6;both NEAT1 and KLF6 are targets of miR-122;Pull-down assay confirmed a direct interaction between miR-122 and NEAT1; KLF6 and miR-122 were required for the effects of NEAT1 on HSC activation. NEAT1 contributes to HSC activation via competitively binding miR-122	28864835	RID01235	ceRNA or sponge
Osteosarcoma	ZBTB7A	LINC00473	negatively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	binding/interaction	protein-DNA	cisplatin	NA	NA	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000178951	NA	ENSG00000112541	GRCh38_6:165924048-165988039	51341	90632	FBI-1|FBI1|LRF|TIP21|ZBTB7|ZNF857A|pokemon	C6orf176|LNC473|bA142J11.1	ZBTB7A Enhances Osteosarcoma Chemoresistance by Transcriptionally Repressing lncRNA LINC00473-IL24 Activity;we found that ZBTB7A is increased in cisplatin-resistant osteosarcoma cells and that elevated ZBTB7A inhibits cisplatin-induced apoptosis by repressing LINC00473 expression;ZBTB7A directly binds to the promoter and suppresses the transcription of LINC00473	28942243	RID01236	transcriptional regulation
Osteosarcoma	LINC00473	IL24	negatively-E	western blot;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+)	transcriptional regulation	binding/interaction	RNA-DNA	cisplatin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000162892	NA	90632	11009	C6orf176|LNC473|bA142J11.1	C49A|FISP|IL10B|MDA7|MOB5|ST16	ZBTB7A Enhances Osteosarcoma Chemoresistance by Transcriptionally Repressing lncRNA LINC00473-IL24 Activity;Additionally, our data indicate that LINC00473 interacts with the transcript factor C/EBPbeta, facilitating its binding to the promoter of IL24, leading to decrease chemoresistance.	28942243	RID01237	transcriptional regulation
Osteosarcoma	NEAT1	miR-194	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression;Luciferase reporter assay validated that NEAT1 could interact with miR-194 and negatively modulated its expression;inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells	29047232	RID01238	ceRNA or sponge
Esophagus squamous cell carcinoma	GHET1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000039068	NA	102723099	999	lncRNA-GHET1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01239	expression association
Esophagus squamous cell carcinoma	GHET1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000170558	NA	102723099	1000	lncRNA-GHET1	CD325|CDHN|CDw325|NCAD	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01240	expression association
Esophagus squamous cell carcinoma	GHET1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000026025	NA	102723099	7431	lncRNA-GHET1	NA	LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT;western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin	28983895	RID01241	expression association
Esophagus squamous cell carcinoma	AC132217.4	IGF2	positively-F	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);epithelial to mesenchymal transition(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_11:2129121-2129964	ENSG00000167244	NA	NA	3481	NA	C11orf43|GRDF|IGF-II|PP9974	LncRNAAC132217.4, a KLF8-regulated long non-coding RNA, facilitates oral squamous cell carcinoma metastasis by upregulating IGF2 expression;One of the lncRNAs, termed AC132217.4, was remarkably upregulation and promoted cell migration and epithelial-mesenchymal transition (EMT) by upregulating IGF2 expression; AC132217.4 interacted with the 3'UTR of IGF2 mRNA and increased its stability, leading to increased IGF2 levels	28823965	RID01242	interact with mRNA
Esophagus squamous cell carcinoma	KLF8	AC132217.4	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	TF	lncRNA	ENSG00000102349	NA	NA	GRCh38_11:2129121-2129964	11279	NA	BKLF3|ZNF741	NA	LncRNAAC132217.4, a KLF8-regulated long non-coding RNA, facilitates oral squamous cell carcinoma metastasis by upregulating IGF2 expression. we found that KLF8 binds to the upstream sequence of AC132217.4, activating its expression at the transcriptional level, which accelerated OSCC metastasis via the AC132217.4-IGF2 axis both in vitro and in vivo	28823965	RID01243	transcriptional regulation
Malignant glioma	MALAT1	STMN1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117632	NA	378938	3925	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C1orf215|LAP18|Lag|OP18|PP17|PP19|PR22|SMN	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01244	ceRNA or sponge
Malignant glioma	MALAT1	RAB5A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000144566	NA	378938	5868	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RAB5	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01245	ceRNA or sponge
Malignant glioma	MALAT1	ATG4D	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell autophagy(+);cell proliferation(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000130734	NA	378938	84971	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	APG4-D|APG4D|AUTL4	Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma;We found that Malat1 served as an endogenous sponge to reduce miR-101 expression by directly binding to miR-101;Malat1 abolished the suppression effects of miR-101 on glioma cell autophagy and proliferation, which involved in upregulating the expression of miR-101 targets STMN1, RAB5A and ATG4D	28834690	RID01246	ceRNA or sponge
Recurrent miscarriage	YY1	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Other	Recurrent miscarriage	TF	lncRNA	ENSG00000100811	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7528	100124700	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The YY1-HOTAIR-MMP2 Signaling Axis Controls Trophoblast Invasion at the Maternal-Fetal Interface.Bioinformatics analysis identified two YY1-binding sites in the HOTAIR promoter region, and chromatin immunoprecipitation (ChIP) analysis verified that YY1 binds directly to its promoter region.HOTAIR overexpression effectively elevated matrix metalloproteinase 2 (MMP2) expression via the PI3K-AKT signaling pathway, enhancing trophoblast migration and invasion.	28750739	RID01247	transcriptional regulation
Recurrent miscarriage	HOTAIR	MMP2	positively-E	western blot	upregulation	qPCR	NA	NA	cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Other	Recurrent miscarriage	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087245	NA	100124700	4313	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	The YY1-HOTAIR-MMP2 Signaling Axis Controls Trophoblast Invasion at the Maternal-Fetal Interface.Bioinformatics analysis identified two YY1-binding sites in the HOTAIR promoter region, and chromatin immunoprecipitation (ChIP) analysis verified that YY1 binds directly to its promoter region.HOTAIR overexpression effectively elevated matrix metalloproteinase 2 (MMP2) expression via the PI3K-AKT signaling pathway, enhancing trophoblast migration and invasion.	28750739	RID01248	expression association
Myasthenia gravis	IFNG-AS1	HLA-DRB1	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	immune response(-)	NA	regulation	NA	NA	NA	Evading Immune Detection	Immune system disease	Autoimmune disease of the nervous system	lncRNA	PCG	ENSG00000255733	GRCh38_12:67989445-68234686	ENSG00000196126	NA	NA	3123	NA	DRB1|HLA-DR1B|HLA-DRB|SS1	IFNA-AS1 regulates CD4+ T cell activation in myasthenia gravis though HLA-DRB1;IFNG-AS1 could reduce the expression of HLA-DRB and HLA-DOB and they had a negative correlation in MG;Furthermore IFNG-AS1 influenced the expression levels of CD40L and CD4+ T cells activation in MG patient partly depend on effecting the HLA-DRB1 expression. It suggests that IFNG-AS1 may be involved in CD4+T cell-mediated immune responses in MG	28822831	RID01249	expression association
Liver fibrosis	H19	EPCAM	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	fibrotic(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000119888	NA	283120	4072	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	H19 promotes cholestatic liver fibrosis by preventing ZEB1-mediated inhibition of epithelial cell adhesion molecule; H19RNA impeded ZEB1's inhibitory action by interacting with ZEB1 protein to prevent its binding to the EpCAM promoter;Hepatic overexpression of ZEB1 or knockdown of EpCAM diminished H19-induced fibrosis;The up-regulation of H19RNA and EpCAM correlated positively with the down-regulation of ZEB1 in primary sclerosing cholangitis and primary biliary cirrhosis liver specimens	28407375	RID01250	transcriptional regulation
Osteosarcoma	TUG1	EZH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-144-3p)	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	TUG1 promotes osteosarcoma tumorigenesis by upregulating EZH2 expression via miR-144-3p;TUG1 regulated miR-144-3p expression through direct binding;EZH2, a verified target of miR-144-3p was upregulation in osteosarcoma tissues and negatively correlated with miR-144-3p;EZH2 was negatively regulated by miR-144-3p and positively regulated by TUG1;EZH2, a verified target of miR-144-3p was upregulation in osteosarcoma tissues and negatively correlated with miR-144-3p. EZH2 was negatively regulated by miR-144-3p and positively regulated by TUG1	28902349	RID01251	ceRNA or sponge
Aortic valve disease	MALAT1	SMAD4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell differentiation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141646	NA	378938	4089	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DPC4|JIP|MADH4|MYHRS	LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4;MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers;we identified Smad4 as a direct target of miR-204;MALAT1 positively regulated the expression of Smad4 through sponging miR-204, and promoted osteogenic differentiation of VICs	28522163	RID01252	ceRNA or sponge
Pulmonary fibrosis	MALAT1	PIK3R1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);fibrotic(+)	ceRNA(miR-503)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Respiratory system disease	Fibrosis	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000145675	NA	378938	5295	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MiR-503 modulates epithelial-mesenchymal transition in silica-induced pulmonary fibrosis by targeting PI3K p85 and is sponged by lncRNA MALAT1; overexpressed miR-503 inhibited silica-induced pulmonary fibrosis by attenuating the severity and the distribution of lesions in vivo and limiting the process of epithelial-mesenchymal transition (EMT) in vitro;the up-regulated lncRNA Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), acted as a competing endogenous RNA (ceRNA), can directly bound to miR-503, which indicated that lncRNA MALAT1 may modulate the expression of miR-503 thus triggering the activation of downstream fibrotic signaling pathways;Taken together, our data suggested that MALAT1-miR-503-PI3K/Akt/mTOR/Snail pathway plays critical roles in silica-induced pulmonary fibrosis. PI3K p85, also named PIK3R1, is a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), and it also consists of a catalytic subunit, p110	28900284	RID01253	ceRNA or sponge
Colorectal cancer	PURPL	TP53	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000250337	GRCh38_5:27217714-27496994	ENSG00000141510	NA	643401	7157	LINC01021	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer;Targeted depletion of PURPL in colorectal cancer cells results in elevated basal p53 levels and induces growth defects in cell culture and in mouse xenografts	28877474	RID01254	expression association
Hirschsprung's disease	AFAP1-AS1	RAP1B	positively-E	RIP;western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+);cancer progression(+)	ceRNA(miR-181a)	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hirschsprung's disease	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000127314	NA	84740	5908	AFAP1-AS|AFAP1AS	K-REV|RAL1B	LncRNA AFAP1-AS Functions as a Competing Endogenous RNA to Regulate RAP1B Expression by sponging miR-181a in the HSCR; Knockdown of AFAP1-AS in 293T and SH-SY5Y cells suppressed cell proliferation, migration, and induced the loss of cell stress filament integrity, possibly due to AFAP1-AS sequestering miR-181a in HSCR cells;Furthermore, AFAP1-AS could down-regulate RAP1B via its competing endogenous RNA (ceRNA) activity on miR-181a.These findings suggest that aberrant expression of lncRNA AFAP1-AS, a ceRNA of miR-181a, may involve in the onset and progression of HSCR by augmenting the miR-181a target gene, RAP1B.	28924375	RID01255	ceRNA or sponge
Non-small cell lung cancer	miR-101-3p	MALAT1	negatively-F	western blot;luciferase reporter assay;RNA pull-down assay	downregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);PI3K/AKT signaling pathway(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MiR-101-3p inhibits the growth and metastasis of non-small cell lung cancer through blocking PI3K/AKT signal pathway by targeting MALAT-1;overexpression of miR-101-3p could significantly inhibit the proliferation, migration and invasion of NSCLC cells in vitro, as well as MALAT-1 expression;miR-101-3p could specifically repress MALAT-1 expression through direct binding;MALAT-1 overexpression completely reversed the miR-101-3p-induced suppression on the viability, migration and invasion of NSCLC cellsand MALAT-1 expression;we confirmed that miR-101-3p could block the MALAT-1-induced activation of PI3K/AKT signal pathway and resulted in the inhibition on the growth and metastasis of NSCLC cells in vivo	28738500	RID01256	ceRNA or sponge
Breast cancer	NEAT1	SIN3A	interact	RIP;ChIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell migration(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000169375	NA	283131	25942	LINC00084|NCRNA00084|TncRNA|VINC	WITKOS	The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer;the FOXN3-NEAT1-SIN3A complex represses genes including GATA3 that are critically involved in epithelial-to-mesenchymal transition (EMT);We demonstrated that the FOXN3-NEAT1-SIN3A complex promotes EMT and invasion of breast cancer cells in vitro as well as dissemination and metastasis of breast cancer in vivo;Elevation of both FOXN3 and NEAT1 expression during breast cancer progression corresponded to diminished GATA3 expression, and high levels of FOXN3 and NEAT1 strongly correlated with higher histological grades and poor prognosis;Our experiments uncovered that NEAT1 is a facultative component of the SIN3A complex, shedding light on the mechanistic actions of NEAT1 and the SIN3A complex	28805661	RID01257	interact with protein
Breast cancer	NEAT1	GATA3	negatively-E	RIP;ChIP;RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cancer progression(+);cell metastasis(+)	transcriptional regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000107485	NA	283131	2625	LINC00084|NCRNA00084|TncRNA|VINC	HDR|HDRS	The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer;the FOXN3-NEAT1-SIN3A complex represses genes including GATA3 that are critically involved in epithelial-to-mesenchymal transition (EMT);We demonstrated that the FOXN3-NEAT1-SIN3A complex promotes EMT and invasion of breast cancer cells in vitro as well as dissemination and metastasis of breast cancer in vivo;Elevation of both FOXN3 and NEAT1 expression during breast cancer progression corresponded to diminished GATA3 expression, and high levels of FOXN3 and NEAT1 strongly correlated with higher histological grades and poor prognosis;Our experiments uncovered that NEAT1 is a facultative component of the SIN3A complex, shedding light on the mechanistic actions of NEAT1 and the SIN3A complex	28805661	RID01258	transcriptional regulation
Malignant glioma	MIR155HG	miR-155	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	epithelial to mesenchymal transition(+)	host	regulation	NA	NSC141562	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234883	GRCh38_21:25561909-25575168	NA	NA	114614	NA	BIC|MIRHG2|NCRNA00172	NA	Blocking MIR155HG/miR-155 axis inhibits mesenchymal transition in glioma;MIR155HG reduction by small interfering RNA inhibited cell proliferation, migration, invasion, and orthotopic glioma growth by repressing the generation of its derivatives miR-155-5p and miR-155-3p;High-throughput screening indicated that the MIR155HG/miR-155 axis inhibitor NSC141562 may be a useful candidate anti-glioma drug	28371892	RID01259	expression association
Malignant glioma	LINC01139	LDHA	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000215808	GRCh38_1:238476542-238486060	ENSG00000134333	NA	339535	3939	NA	GSD11|HEL-S-133P|LDHM|PIG19	Long non-coding RNA LINK-A promotes glioma cell growth and invasion via lactate dehydrogenase A; we found that lactate dehydrogenase A (LDH-A) was regulated by LINK-A, and enforced expression of LDH-A promoted glycolysis and proliferation in glioma cells	28714007	RID01260	expression association
Multiple myeloma	OIP5-AS1	KLF10	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PTEN/PI3K/AKT signaling pathway(-);cell proliferation(-);apoptosis process(+)	ceRNA(miR-410)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Myeloma	lncRNA	TF	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000155090	NA	729082	7071	cyrano|linc-OIP5	EGR-alpha|EGRA|TIEG|TIEG1	LncRNA OIP5-AS1 loss-induced microRNA-410 accumulation regulates cell proliferation and apoptosis by targeting KLF10 via activating PTEN/PI3K/AKT pathway in multiple myeloma;downregulated expression of lncRNA OIP5-AS1 was inversely correlated with miR-410 expression in MM tissues;LncRNA OIP5-AS1 could modulate the miR-410 expression and regulate its target KLF10/PTEN/AKT-mediated cellular behaviors.we predicted a target by Starbase 2.0 and found lncRNA OIP5-AS1 is a molecular sponge that modulates miR-410.	28796257	RID01261	ceRNA or sponge
Osteoarthritis	UCA1	miR-204-5p	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell survival(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA-UCA1 enhances MMP-13 expression by inhibiting miR-204-5p in human chondrocytes;These results suggested that UCA1 played as an important regulator of survival and matrix synthesis of chondrocytes partly through suppressing the miR-204-5p expression	29207643	RID01262	expression association
Hepatocellular carcinoma	lncSHRG	HES6	positively-E	western blot;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_2:91636683-91659949	ENSG00000144485	NA	NA	55502	NA	C-HAIRY1|HES-6|bHLHb41|bHLHc23	LncSHRG promotes hepatocellular carcinoma progression by activating HES6;Here we identified that a long noncoding RNA, lncSHRG, was greatly upregulation in human hepatocellular carcinoma samples. lncSHRG recruits SATB1 to bind to HES6 promoter and initiates HES6 expression	29050307	RID01263	transcriptional regulation
Type 2 diabetes mellitus	IGF2-AS	IGF2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	angiogenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	ENSG00000167244	NA	51214	3481	IGF2-AS1|IGF2AS|PEG8	C11orf43|GRDF|IGF-II|PP9974	Inhibition of long noncoding RNA IGF2AS promotes angiogenesis in type 2 diabetes. IGF2AS inhibition has angiogenic effect in diabetic GK mMVE cells. The functions of IGF2AS in type 2 diabetes are very likely through the inverse regulation of IGF2, but independent of IGF1.	28570978	RID01264	expression association
Lung cancer	XIST	PPP1R13L	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-140)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000104881	NA	7503	10848	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	IASPP|NKIP1|RAI|RAI4	lncRNA XIST interacts with miR-140 to modulate lung cancer growth by targeting iASPP.lncRNA-XIST was specifically upregulation in lung cancer cell lines and promoted lung cancer cell growth through targeting miR-140	28656261	RID01265	ceRNA or sponge
Breast cancer	LINC00313	SOX2	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+);epithelial to mesenchymal transition(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000185186	GRCh38_21:43461960-43479534	ENSG00000181449	NA	114038	6657	C21orf84|CH507-42P11.5|NCRNA00313	ANOP3|MCOPS3	Long noncoding RNA linc00617 exhibits oncogenic activity in breast cancer. We demonstrated that linc00617 upregulation the expression of stemness factor Sox2 in breast cancer cells, which was shown to promote the oncogenic activity of breast cancer cells by stimulating epithelial-to-mesenchymal transition and enhancing the tumor-initiating capacity. Thus, our data indicate that linc00617 functions as an important regulator of EMT and promotes breast cancer progression and metastasis via activating the transcription of Sox2	26207516	RID01266	transcriptional regulation
Pancreatic ductal adenocarcinoma	MIR31HG	miR-193b	negatively-F	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE28735	GSE28735.zip	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000171889	GRCh38_9:21410969-21559900	NA	NA	554202	NA	LncHIFCAR|hsa-lnc-31	NA	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b. Inhibition of miR-193b expression significantly upregulation the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	26549028	RID01267	ceRNA or sponge
Hepatocellular carcinoma	lnc-DILC	IL6	negatively-E	RIP	downregulation	qPCR;microarray	NA	NA	cell growth(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000198176	GRCh38_13:113584721-113641470	ENSG00000136244	NA	NA	3569	NA	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis. Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. The putative binding locus of lnc-DILC within IL-6 promoter was confirmed by pull down assay. Consistently, the oligoribonucleotide mimics and an oligodeoxynucleotide decoy of lnc-DILC abrogated the effects on IL-6 transcription, STAT3 activation and LCSC expansion triggered by lnc-DILC depletion and lnc-DILC overexpression.	26812074	RID01268	transcriptional regulation
Hepatocellular carcinoma	lnc-DILC	STAT3	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000198176	GRCh38_13:113584721-113641470	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis. Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. The putative binding locus of lnc-DILC within IL-6 promoter was confirmed by pull down assay. Consistently, the oligoribonucleotide mimics and an oligodeoxynucleotide decoy of lnc-DILC abrogated the effects on IL-6 transcription, STAT3 activation and LCSC expansion triggered by lnc-DILC depletion and lnc-DILC overexpression.	26812074	RID01269	expression association
Melanoma	SPRY4-IT1	DPP4	negatively-E	RNAi	upregulation	qPCR;microarray;sequencing	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000197635	NA	100642175	1803	SPRIGHTLY	NA	The Long Noncoding RNA SPRIGHTLY Regulates Cell Proliferation in Primary Human Melanocytes.Because down-regulation of DPPIV is known to be associated with malignant transformation in melanocytes, SPRIGHTLY-mediated DPPIV down-regulation may play an important role in melanoma pathobiology.	26829028	RID01270	expression association
Cervical cancer	OIP5-AS1	ELAVL1	negatively-E	RIP;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-424)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000066044	NA	729082	1994	cyrano|linc-OIP5	ELAV1|HUR|Hua|MelG	LncRNA OIP5-AS1/cyrano sponges RNA-binding protein HuR.Tagging OIP5-AS1 with MS2 hairpins to identify associated microRNAs revealed that miR-424 interacted with OIP5-AS1 and competed with HuR for binding to OIP5-AS1.We propose that OIP5-AS1 serves as a sponge or a competing endogenous (ce)RNA for HuR, restricting its availability to HuR target mRNAs and thereby repressing HuR-elicited proliferative phenotypes.	26819413	RID01271	ceRNA or sponge
Laryngeal squamous cell carcinoma	H19	DNMT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-148a-3p)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000130816	NA	283120	1786	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis.In this study, we reported that the lncRNA H19 was upregulated in LSCC. We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown. In summary, our study demonstrated that the lncRNA H19 promoted LSCC progression via miR-148a-3p and DNMT1.	26872375	RID01272	ceRNA or sponge
Pancreatic cancer	MALAT1	CDH1	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. RIP and ChIP assays suggest that EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression.	26848980	RID01273	epigenetic regulation
Metabolic syndrome	MEG3	HDAC7	positively-E	RNAi;luciferase reporter assay	downregulation	qPCR	NA	NA	cell protection(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	NA	Syndrome	Metabolic syndrome	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000061273	NA	55384	51564	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HD7|HD7A|HDAC7A	Pioglitazone up-regulates long non-coding RNA MEG3 to protect endothelial progenitor cells via increasing HDAC7 expression in metabolic syndrome.Overexpression of MEG3 resulted in the down-regulation of miR-140-5p. The luciferase reporter assay and RIP assay showed that MEG3 targeted miR-140-5p. In addition, the HDAC7 expression levels were regulated by miR-140-5p and MEG3. HDAC7 is a target gene of miR-140-5p.	26898430	RID01274	ceRNA or sponge
Nasopharynx carcinoma	MALAT1	SNAI2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	radioresistance(+)	ceRNA(miR-1)	regulation	NA	NA	CSC	NA	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000019549	NA	378938	6591	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma. Interestingly, we found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients.	26482776	RID01275	ceRNA or sponge
Non-small cell lung cancer	MEG3	SKP2	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	ceRNA(miR-3163)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000145604	NA	55384	6502	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	FBL1|FBXL1|FLB1|p45	Skp2 regulates non-small cell lung cancer cell growth by Meg3 and miR-3163. These data suggest that the Skp2 may be regulated by Meg3 at post-transcriptional level. Bioinformatics analyses showed that miR-3163 bound to 3'-UTR of Skp2 mRNA in NSCLC cells to inhibit its translation, which was supported by luciferase reporter assay. Meg3 augmented the effects of miR-3163 on Skp2 mRNA, possibly through binding-induced function enhancement, which was supported by the double fluorescent in situ hybridization showing co-localized intracellular Meg3 and miR-3163 signals in NSCLC cells. Thus, our data suggest that Meg3 and miR-3163 may coordinate suppression of translation of Skp2 mRNA in NSCLC cells to inhibit NSCLC cell growth.	26482610	RID01276	ceRNA or sponge
Cancer	FOXD3	OLA1P2	positively-E	ChIP	upregulation	qPCR;microarray	GSE76583	GSE76583.zip	tumor-suppressive function(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Cancer	TF	lncRNA	ENSG00000187140	NA	ENSG00000213671	GRCh38_17:20775642-20776905	27022	106479059	AIS1|Genesis|HFH2|VAMAS2	NA	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene. Subsequently, upregulation FOXD3 protein transcriptionally activates lncRNA OLA1P2 expression. OLA1P2 upregulation markedly affects STAT3 signaling pathway activity by inhibiting the nuclear import of phosphorylated STAT3.	26898989	RID01277	transcriptional regulation
Cancer	OLA1P2	STAT3	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR;microarray	GSE76583	GSE76583.zip	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Cancer	lncRNA	TF	ENSG00000213671	GRCh38_17:20775642-20776905	ENSG00000168610	NA	106479059	6774	NA	ADMIO|ADMIO1|APRF|HIES	The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation.Aspirin induces demethylation of the FOXD3 promoter and promotes expression of the FOXD3 gene. Subsequently, upregulation FOXD3 protein transcriptionally activates lncRNA OLA1P2 expression. OLA1P2 upregulation markedly affects STAT3 signaling pathway activity by inhibiting the nuclear import of phosphorylated STAT3. OLA1P2 interacts directly with STAT3 due to OLA1P2 sharing the same conservative STAT3 transcription response element as STAT3 targets.	26898989	RID01278	interact with protein
Malignant glioma	MALAT1	miR-140	negatively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	blood-tumor barrier(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140.	26619802	RID01279	expression association
Hepatocellular carcinoma	UHRF1	MEG3	negatively-E	RNAi;Bisulfite Sequencing	downregulation	qPCR	NA	NA	cell proliferation(-);prognosis(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000276043	NA	ENSG00000214548	GRCh38_14:100779410-100861031	29128	55384	ICBP90|Np95|RNF106|TDRD22|hNP95|hUHRF1|huNp95	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.	25641194	RID01280	epigenetic regulation
Hepatocellular carcinoma	MEG3	TP53	interact	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);cell proliferation(-);apoptosis process(+);cell growth(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long Noncoding RNA MEG3 Interacts with p53 Protein and Regulates Partial p53 Target Genes in Hepatoma Cells.In conclusion, our data demonstrates that MEG3 functions as a tumor suppressor in hepatoma cells through interacting with p53 protein to activate p53-mediated transcriptional activity and influence the expression of partial p53 target genes.Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26444285;27432655;25641194;26992211	RID01281	interact with protein
Cervical cancer	MALAT1	miR-145	negatively-F	RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 modulates radiosensitivity of HR-HPV+ cervical cancer via sponging miR-145. By performing RNA-binding protein immunoprecipitation (RIP) assay and RNA pull-down assay, we confirmed that miR-145 and MALAT1 were in the same Ago2 complex and there was a reciprocal repression between them.	26311052	RID01282	ceRNA or sponge
Pancreatic cancer	LINC-ROR	NANOG	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);tumorigenesis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000111704	NA	100885779	79923	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer. In conclusions, we demonstrated that decreased ROR expression could inhibit cell proliferation, invasion, and tumourigenicity by modulating Nanog.	26636540	RID01283	ceRNA or sponge
Colorectal cancer	ZFAS1	CDK1	positively-E	RIP;RNA pull-down assay	upregulation	qPCR;sequencing	NA	NA	cell cycle(+);apoptosis process(+)	ceRNA(miR-590-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000170312	NA	441951	983	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	CDC2|CDC28A|P34CDC2	Long non-coding RNA ZFAS1 interacts with CDK1 and is involved in p53-dependent cell cycle control and apoptosis in colorectal cancer. We identified Cyclin-dependent kinase 1 (CDK1) as interacting partner of ZFAS1 by pull-down experiment and RNA immunoprecipitation. Further, we have predicted by bioinformatics approach ZFAS1 to sponge miR-590-3p, which was proved to target CDK1.	26506418	RID01284	ceRNA or sponge
Hepatocellular carcinoma	miR-203	HULC	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC. Furthermore, we identified that miR-203 modulated ADAM9 and HULC in a novel post-transcriptional regulatory mechanism. Over-expression of HULC partly rescued the miR-203-mediated antitumor effects.	26179263	RID01285	ceRNA or sponge
Cervical cancer	MEG3	miR-21-5p	negatively-E	RNAi;western blot	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Long noncoding RNA MEG3 is downregulated in cervical cancer and affects cell proliferation and apoptosis by regulating miR-21.Furthermore, we focused on the function and molecular mechanism of MEG3, finding that overexpression of MEG3 reduced the level of miR-21-5p expression, causing inhibition of proliferation and increased apoptosis in cervical cancer cells.	26574780	RID01286	expression association
Urinary bladder cancer	UCA1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000148516	NA	652995	6935	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01287	expression association
Urinary bladder cancer	UCA1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000169554	NA	652995	9839	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01288	expression association
Urinary bladder cancer	UCA1	FSCN1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000075618	NA	652995	6624	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FAN1|HSN|SNL|p55	Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway.Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncRNA-UCA1 contributed to the reciprocal negative regulation of lncRNA-UCA1 and hsa-miR-145. Taken together, our results identified that lncRNA-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway.	26544536	RID01289	ceRNA or sponge
Coronary artery disease	CDKN2B-AS1	YY1	interact	RIP	upregulation	qPCR	NA	NA	inflammatory response(+)	interact with protein	binding/interaction	RNA-RNA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Coronary artery disease	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000100811	NA	100048912	7528	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	DELTA|GADEVS|INO80S|NF-E1|UCRBP|YIN-YANG-1	Long non-coding RNA ANRIL regulates inflammatory responses as a novel component of NF-kB pathway.For the first time, we establish the connection between ANRIL and NF-kB pathway and show that ANRIL regulates inflammatory responses through binding with YY1. The newly identified TNF-alpha-NF-kB-ANRIL/YY1-IL6/8 pathway enhances understanding of the etiology of CAD and provides potential therapeutic target for treatment of CAD.	26618242	RID01290	interact with protein
Cervical cancer	MALAT1	GRB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000177885	NA	378938	2885	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASH|EGFRBP-GRB2|Grb3-3|MST084|MSTP084|NCKAP2	MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells.MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis.	26242259	RID01291	ceRNA or sponge
Hepatocellular carcinoma	miR-192	HOTTIP	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. These results elucidate that the miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis.	26710269	RID01292	ceRNA or sponge
Prostate cancer	MALAT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 enhances oncogenic activities of EZH2 in castration-resistant prostate cancer.Using EZH2 antibody-based RNA immunoprecipitation-coupled high throughput sequencing (RIP-seq), we demonstrated that EZH2 binds to MALAT1, a long non-coding RNA (lncRNA) that is overexpressed during PCa progression. GST pull-down and RIP assays demonstrated that the 3' end of MALAT1 interacts with the N-terminal of EZH2. Together, these data indicate that MALAT1 may be a crucial RNA cofactor of EZH2 and that the EZH2-MALAT1 association may provide a new avenue for development new strategies for treatment of CRPC.	26516927	RID01293	interact with protein
Liver cancer	UCA1	TERT	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000164362	NA	652995	7015	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	CUDR promotes liver cancer stem cell growth through upregulating TERT and C-Myc.Therefore, CUDR-CCND1 complex loads onto the long noncoding RNA H19 promoter region that may lead to reduce the DNA methylation on H19 promoter region and then to enhance the H19 expression. Strikingly, the overexpression of H19 increases the binding of TERT to TERC and reduces the interplay between TERT with TERRA, thus enhancing the cell telomerase activity and extending the telomere length. On the other hand, insulator CTCF recruits the CUDR-CCND1 complx to form the composite CUDR-CCND1-insulator CTCF complex which occupancied on the C-myc gene promoter region, increasing the outcome of oncogene C-myc. Ultimately, excessive TERT and C-myc lead to liver cancer stem cell and hepatocyte-like stem cell malignant proliferation.	26513297	RID01294	expression association
Liver cancer	UCA1	MYC	positively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000136997	NA	652995	4609	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MRTL|MYCC|bHLHe39|c-Myc	CUDR promotes liver cancer stem cell growth through upregulating TERT and C-Myc.Therefore, CUDR-CCND1 complex loads onto the long noncoding RNA H19 promoter region that may lead to reduce the DNA methylation on H19 promoter region and then to enhance the H19 expression. Strikingly, the overexpression of H19 increases the binding of TERT to TERC and reduces the interplay between TERT with TERRA, thus enhancing the cell telomerase activity and extending the telomere length. On the other hand, insulator CTCF recruits the CUDR-CCND1 complx to form the composite CUDR-CCND1-insulator CTCF complex which occupancied on the C-myc gene promoter region, increasing the outcome of oncogene C-myc. Ultimately, excessive TERT and C-myc lead to liver cancer stem cell and hepatocyte-like stem cell malignant proliferation.	26513297	RID01295	transcriptional regulation
Liver fibrosis	GAS5	CDKN1B	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-222)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000111276	NA	60674	1027	NCRNA00030|SNHG2	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA.We identified GAS5 as a target of microRNA-222 (miR-222) and showed that miR-222 could inhibit the expression of GAS5. Interestingly, GAS5 could also repress miR-222 expression. A pulldown assay further validated that GAS5 could directly bind to miR-222. As a competing endogenous RNAs, GAS5 had no effect on primary miR-222 expression. In addition, GAS5 was mainly localized in the cytoplasm. Quantitative RT-PCR further demonstrated that the copy numbers of GAS5 per cell are higher than those of miR-222. GAS5 increased the level of p27 protein by functioning as a competing endogenous RNA for miR-222, thereby inhibiting the activation and proliferation of HSCs.	26446789	RID01296	ceRNA or sponge
Gastric cancer	TINCR	KLF2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000127528	NA	257000	10365	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	LKLF	SP1-induced upregulation of the long noncoding RNA TINCR regulates cell proliferation and apoptosis by affecting KLF2 mRNA stability in gastric cancer.Mechanistic analyses indicated that TINCR could bind to STAU1 (staufen1) protein, and influence KLF2 mRNA stability and expression, then KLF2 regulated cyclin-dependent kinase genes CDKN1A/P21 and CDKN2B/P15 transcription and expression, thereby affecting the proliferation and apoptosis of GC cells.	25728677	RID01297	expression association
Gastric cancer	MEG3	E2F3	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-141)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000112242	NA	55384	1871	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	E2F-3	MiR-141 Inhibits Gastric Cancer Proliferation by Interacting with Long Noncoding RNA MEG3 and Down-Regulating E2F3 Expression.These findings together suggested that miR-141 could be interacting with MEG3 and targeting E2F3, and these factors may play important anti-tumor effects in GC pathogenesis and provide therapeutic targets in the clinics.	26233544	RID01298	ceRNA or sponge
Breast cancer	miR-1	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1.MiR-1 functioned as a tumor suppressor by targeting K-RAS and MALAT1.	26275461	RID01299	ceRNA or sponge
Chronic heart failure	LSINCT5	CASP1	positively-E	RNAi;qRT-PCR;western blot	upregulation	qPCR;microarray	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000137752	NA	101234261	834	NA	ICE|IL1BC|P45	Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1beta signaling pathway.The results of the present study indicated that LSINCT5 silencing by small interfering RNA inhibits caspase-1/IL-1beta signaling, and suppresses apoptosis in BNP-treated HCM cells. Therefore, high expression levels of BNP promote the apoptosis of myocardial cells through the lncRNA LSINCT5 mediator, which activates the caspase-1/IL-1beta signaling pathway.	26323562	RID01300	expression association
Chronic heart failure	LSINCT5	IL1B	positively-E	RNAi;qRT-PCR;western blot	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Heart failure	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000125538	NA	101234261	3553	NA	IL-1|IL1-BETA|IL1F2	Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1beta signaling pathway.The results of the present study indicated that LSINCT5 silencing by small interfering RNA inhibits caspase-1/IL-1beta signaling, and suppresses apoptosis in BNP-treated HCM cells. Therefore, high expression levels of BNP promote the apoptosis of myocardial cells through the lncRNA LSINCT5 mediator, which activates the caspase-1/IL-1beta signaling pathway.	26323562	RID01301	expression association
Hepatocellular carcinoma	SIRT1-AS	SIRT1	interact	RNA stability assay;ribonuclease protection assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with mRNA;mutation(622U>C)	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_10:67916698-67918946	ENSG00000096717	NA	106633813	23411	NA	SIR2|SIR2L1|SIR2alpha	A novel mutation in SIRT1-AS leading to a decreased risk of HCC. SIRT1-AS overexpression promoted the proliferation of the human HCC cell lines by upregulating the SIRT1 protein level. The mechanism was that SIRT1-AS bound to SIRT1 mRNA at 3'UTR, masked the miR-29c binding site and stabilized SIRT1 mRNA. A single-nucleotide mutation (622U>C) in the SIRT1-AS sequence was found when we used gene sequencing as an assistant approach for HCC diagnosis. Bioinformatics and the RNase protection assay revealed that the mutation led to a marked alteration in the secondary structure of SIRT1-AS and caused its inability to bind with SIRT1 mRNA. The results of the present study suggest that the 622C mutant of SIRT1 antisense transcript suppresses HCC cell line proliferation, decreases the risk of HCC and is a potential target for gene therapy.	26324025	RID01302	interact with mRNA
Urinary bladder cancer	HOTAIR	CCNJ	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);mitosis progression(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000107443	NA	100124700	54619	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	bA690P14.1	Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer.Moreover, we have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter.	26469956	RID01303	expression association
Urinary bladder cancer	HOTAIR	miR-205	negatively-E	luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer.Moreover, we have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter.This study elucidates an important role that miR-205 had in the regulation of proliferation, migration and invasion of bladder cancer cells, suggesting a potential therapeutic target for combating bladder cancer.	26469956	RID01304	epigenetic regulation
Urinary bladder cancer	TUG1	ZEB2	positively-E	luciferase reporter assay;RIP;RNAi	upregulation	qPCR;microarray	NA	NA	radioresistance(+);epithelial to mesenchymal transition(+);cell invasion(+);cell metastasis(+)	ceRNA(miR-145)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000169554	NA	55000	9839	LINC00080|NCRNA00080|TI-227H	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Double-negative feedback loop between long non-coding RNA TUG1 and miR-145 promotes epithelial to mesenchymal transition and radioresistance in human bladder cancer cells.Interestingly, TUG1 decreased the expression of miR-145 and there was a reciprocal repression between TUG1 and miR-145 in an Argonaute2-dependent manner. ZEB2 was identified as a down-stream target of miR-145 and TUG1 exerted its function through the miR-145/ZEB2 axis.	26318860	RID01305	ceRNA or sponge
Colon cancer	FER1L4	miR-106a-5p	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-);tumor-suppressive function(+);prognosis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000088340	GRCh38_20:35558737-35607562	NA	NA	80307	NA	C20orf124	NA	Long non-coding RNA Fer-1-like protein 4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer.In addition, significant negative correlation between FER1L4 and miR-106a-5p expression levels was observed. Among the colon cancer cell lines, FER1L4 levels were relatively lower, with concurrent high levels of miR-106a-5p. Our findings indicated that FER1L4 could exert a tumor suppressive impact on colon cancer, which at least, in part, through suppressing miR-106a-5p expression, and depletion of FER1L4, alone or combined with overexpression of miR-106a-5p, is predictive of poor prognosis in colon cancer and may play a crucial role in cancer prevention and treatment.	26224446	RID01306	expression association
Liver cancer	HOTAIR	SETD2	negatively-E	RIP;ChIP;RT-PCR;western plot;luciferase reporter assay	upregulation	RT-PCR	NA	NA	DNA repair(-);cell growth(+);cell proliferation(+)	transcriptional regulation	regulation	NA	NA	CSC	Genome Instability and Mutation;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181555	NA	100124700	29072	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HBP231|HIF-1|HIP-1|HSPC069|HYPB|KMT3A|LLS|SET2|p231HBP	LncRNA HOTAIR promotes human liver cancer stem cell malignant growth through downregulation of SETD2.Long non-coding RNA HOTAIR predicts negative tumor prognosis and exhibits oncogenic activity. Herein, we demonstrate HOTAIR promotes human liver cancer stem cell malignant growth through downregulation of SETD2. Mechanistically, HOTAIR reduces the recuritment of the CREB, P300, RNA polII onto the SETD2 promoter region that inhibits SETD2 expression and its phosphorylation.	26172293	RID01307	transcriptional regulation
Hepatocellular carcinoma	TUG1	KLF2	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000127528	NA	55000	10365	LINC00080|NCRNA00080|TI-227H	LKLF	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.	26336870	RID01308	epigenetic regulation
Breast cancer	UCA1	miR-143	negatively-F	luciferase reporter assay;RIP;RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143.There are direct interactions between miR-143 and the miRNA recognition sites of UCA1. UCA1 is present in Ago2-containing RNA-induced silencing complex (RISC), through association with miR-143. Through downregulating miR-143, UCA1 can modulate breast cancer cell growth and apoptosis.	26439035	RID01309	ceRNA or sponge
Gastric cancer	MEG3	BCL2	positively-E	luciferase reporter assay;RIP	downregulation	qRT-PCR	NA	NA	cancer progression(-);cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-181)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Bcl-2|PPP1R50	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate gastric cancer progression.MEG3 is decreased in GC patients and cell lines, and its expression was associated with metastatic GC. Furthermore, MEG3 could up-regulated Bcl-2 via its competing endogenous RNA (ceRNA) activity on miR-181a.	26253106	RID01310	ceRNA or sponge
Prostate cancer	PCA3	PRUNE2	interact	RNase-resistant assay;RNA-FISH	NA	NA	NA	NA	tumor-suppressive function(+);RNA editing(+)	RNA editing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000106772	NA	50652	158471	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	BMCC1|BNIPXL|C9orf65|KIAA0367	PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing.	26080435	RID01311	interact with mRNA
Cervical cancer	HOTAIR	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	radioresistance(+);cell proliferation(+);cell apoptosis(-);cell migration(+);cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HOTAIR enhanced aggressive biological behaviors and induced radioresistance via inhibiting p21 in cervical cancer.Moreover, a high level of HOTAIR was notably associated with radioresistance and downregulation of p21 in the primary cultured cervical cancer cells. Further, we demonstrated that elevated HOTAIR could induce radio-resistance via inhibiting p21 in HeLa cells, while knockdown of HOTAIR upregulated p21 and consequentially increased the radiosensitivity of C33A cells.	25547435	RID01312	expression association
Hepatocellular carcinoma	WSPAR	TCF7	positively-E	RNA pull-down assay;mass spectrometry;ChIP	upregulation	qPCR;microarray;northern blot	GSE66515;GSE66529	GSE66515.zip;GSE66529.zip	self-renewal(+);WNT signaling pathway(+)	epigenetic regulation	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000081059	NA	105664404	6932	LncTCF7|TCONS_00009511	TCF-1	The long noncoding RNA lncTCF7 promotes self-renewal of human liver cancer stem cells through activation of Wnt signaling. Mechanistically, lncTCF7 recruits the SWI/SNF complex to the promoter of TCF7 to regulate its expression, leading to activation of Wnt signaling. Our data suggest that lncTCF7-mediated Wnt signaling primes liver CSC self-renewal and tumor propagation.	25842979	RID01313	epigenetic regulation
Chronic myeloid leukemia	BGLT3	PTEN	positively-E	luciferase reporter assay	NA	NA	NA	NA	tumor-suppressive function(+)	ceRNA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000260629	GRCh38_11:5244554-5245546	ENSG00000171862	NA	103344929	5728	BGL3|LINC01083|lncRNA-BGL3	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	A long noncoding RNA critically regulates Bcr-Abl-mediated cellular transformation by acting as a competitive endogenous RNA.Further experiments demonstrated that lncRNA-BGL3 functioned as a competitive endogenous RNA for binding these microRNAs to cross-regulate PTEN expression. Taken together, these results reveal that Bcr-Abl-mediated cellular transformation critically requires silence of tumor-suppressor lncRNA-BGL3 and suggest a potential strategy for the treatment of Bcr-Abl-positive leukemia.	24837367	RID01314	ceRNA or sponge
Glioblastoma	XIST	miR-152	negatively-F	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell apoptosis(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152.Further, there was reciprocal repression between XIST and miR-152. Mechanistic investigations defined the direct binding ability of the predicted miR-152 binding site on the XIST. In addition, XIST and miR-152 are probably in the same RNA induced silencing complex (RISC). Finally, miR-152 mediated the tumor-suppressive effects that knockdown of XIST exerted.	25578780	RID01315	ceRNA or sponge
Renal cell carcinoma	MALAT1	EZH2	interact	RIP;western blot;qPCR	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell apoptosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2 and Interacts with miR-205.We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas beta-catenin expression was decreased through Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	25600645	RID01316	interact with protein
Renal cell carcinoma	MALAT1	miR-205	negatively-F	luciferase reporter assay;RIP;ChIP	upregulation	RT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell apoptosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2 and Interacts with miR-205.We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas beta-catenin expression was decreased through Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	25600645	RID01317	ceRNA or sponge
Non-small cell lung cancer	PANDAR	BCL2	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+);cell proliferation(-);prognosis(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000171791	NA	101154753	596	PANDA	Bcl-2|PPP1R50	Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2.We also showed that PANDAR-mediated growth regulation is in part due to the transcriptional modulation of Bcl-2 by interacting with NF-YA, thus affecting NSCLC cell apoptosis. The p53/PANDAR/NF-YA/Bcl-2 interaction might serve as targets for NSCLC diagnosis and therapy.	25719249	RID01318	expression association
Atherosclerosis	RP5-833A20.1	miR-382-5p	positively-E	RNAi	upregulation	microarray	NA	NA	cholesterol homeostasis(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	miRNA	ENSG00000237853	GRCh38_1:61248945-61253510	NA	NA	NA	NA	NA	NA	RP5-833A20.1/miR-382-5p/NFIA-dependent signal transduction pathway contributes to the regulation of cholesterol homeostasis and inflammatory reaction. Moreover, we showed that long noncoding RNA RP5-833A20.1 may decreases NFIA expression by inducing hsa-miR-382-5p expression in vitro.	25265644	RID01319	expression association
Atherosclerosis	RP5-833A20.1	NFIA	negatively-E	RNAi	upregulation	microarray	NA	NA	cholesterol homeostasis(-);inflammatory response(-)	NA	regulation	NA	NA	NA	Tumor Promoting Inflammation	Cardiovascular system disease	Atherosclerosis	lncRNA	TF	ENSG00000237853	GRCh38_1:61248945-61253510	ENSG00000162599	NA	NA	4774	NA	BRMUTD|CTF|NF-I/A|NF1-A|NFI-A|NFI-L	RP5-833A20.1/miR-382-5p/NFIA-dependent signal transduction pathway contributes to the regulation of cholesterol homeostasis and inflammatory reaction. Moreover, we showed that long noncoding RNA RP5-833A20.1 may decreases NFIA expression by inducing hsa-miR-382-5p expression in vitro.	25265644	RID01320	expression association
Osteoarthritis	MEG3	VEGFA	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	angiogenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000112715	NA	55384	7422	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MVCD1|VEGF|VPF	The Long Noncoding RNA MEG3 Is Downregulated and Inversely Associated with VEGF Levels in Osteoarthritis.The results show that human MEG3 is significantly downregulated in OA patients compared to normal cartilage samples. However, higher levels of VEGF mRNA and protein are found in OA compared to the control. Moreover, MEG3 levels are inversely associated with VEGF levels, suggesting that MEG3 may be involved in OA development through the regulation of angiogenesis.	26090403	RID01321	expression association
Tongue squamous cell carcinoma	miR-26a	MEG3	negatively-E	RNAi;Methylation-specific PCR	downregulation	microarray	GSE51829;GSE51700	GSE51829.zip;GSE51700.zip	cell proliferation(-);cell cycle(-);apoptosis process(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Oral cavity cancer	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma.Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR-26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue.Considering the poor prognostic outcomes associated with reduced miR-26a and MEG3, our findings imply that these factors likely play important antitumor effects in TSCC pathogenesis.Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma. We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR-26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue. Furthermore, the overexpression of miR-26a or MEG3 in SCC-15 and CAL27 cells inhibited cell proliferation and cell cycle progression, and promoted cell apoptosis.It could therefore be of interest to investigate a possible link between miR-148a and MEG3 expression in ovarian cancer. In addition, miR-26a and MEG3 expression were correlated in TSCC (Tongue Squamous Cell Carcinoma) cells and it has been postulated that this relationship depends on the ability of miR-26a to target DNMT3B in this model and thus prevent meg3 promoter methylation	25537514;24343426	RID01322	epigenetic regulation
Liver fibrosis	MEG3	TP53	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell apoptosis(+);cell growth(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Gastrointestinal system disease	Fibrosis	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Inhibitory effects of long noncoding RNA MEG3 on hepatic stellate cells activation and liver fibrogenesis. Enforced expression of MEG3 in LX-2 cells inhibited TGF-beta1-induced cell proliferation, while promoting cell apoptosis. More importantly, overexpression of MEG3 could activate p53 and mediate cytochrome c release, subsequently leading to caspase-3-dependent apoptosis in TGF-beta1-treated LX-2 cells.	25201080	RID01323	expression association
Hepatocellular carcinoma	VLDLR-AS1	ABCG2	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell viability(+);cell cycle(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000236404	GRCh38_9:2421597-2643359	ENSG00000118777	NA	401491	9429	linc-VLDLR|lincRNA-VLDLR	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	Involvement of extracellular vesicle long noncoding RNA (linc-VLDLR) in tumor cell responses to chemotherapy.RNAi-mediated knockdown of linc-VLDLR decreased cell viability and abrogated cell-cycle progression. Moreover, knockdown of linc-VLDLR reduced expression of ABCG2 (ATP-binding cassette, subfamily G member 2), whereas overexpression of this protein reduced the effects of VLDLR knockdown on sorafenib-induced cell death.	24874432	RID01324	expression association
Prostate cancer	PCGEM1	miR-145	negatively-F	luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells.To test this hypothesis, the interaction between PCGEM1 and miR-145 was examined using a luciferase reporter assay.We demonstrate a reciprocal negative control relationship between PCGEM1 and miR-145 that regulates both LNCaP cell proliferation and nu/nu PCa tumor growth.	25200485	RID01325	ceRNA or sponge
Non-small cell lung cancer	MALAT1	BCL2	positively-E	RNAi	downregulation	microarray	NA	NA	prognosis(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171791	NA	378938	596	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Bcl-2|PPP1R50	Prognostic impact of Bcl-2 depends on tumor histology and expression of MALAT-1 lncRNA in non-small-cell lung cancer.Among the tested apoptotic markers only Bcl-2 demonstrated prognostic impact (hazard ratio = 0.64, p = 0.012). Besides tumor histology, prognostic impact of Bcl-2 was also found to depend on MALAT-1 lncRNA expression. Gene expression analysis of A549 adenocarcinoma cells with differential MALAT-1 lncRNA expression demonstrated an influence on the expression of Bcl-2 and its interacting proteins. We found Bcl-2 expression to depend on MALAT-1 expression status in a positively related manner. i.e., strong MALAT-1 expression results in elevated Bcl-2 expression values (log-fold change = 0.46), confirming the hypothesis of Guo et al.Best transfection rates and strongest downregulation of MALAT-1 lncRNA was achieved in A549 lung cancer cell line.	25036876	RID01326	expression association
Malignant glioma	OIP5-AS1	YAP1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000247556	GRCh38_15:41283990-41309737	ENSG00000137693	NA	729082	10413	cyrano|linc-OIP5	COB1|YAP|YAP2|YAP65|YKI	Knockdown of linc-OIP5 inhibits proliferation and migration of glioma cells through down-regulation of YAP-NOTCH signaling pathway.Further mechanistic studies revealed the effect of linc-OIP5 knockdown on glioma cell phenotype at least partially through down-regulation of YAP and inhibition of Notch signaling pathway activity.	28189759	RID01327	expression association
Gastric cancer	HOXA11-AS	CTNNB1	positively-E	ChIP;RIP	upregulation	microarray;sequencing	TCGA;GSE50710;GSE58828;GSE65801;GSE51575;GSE29431;GSE54002;GSE20842;GSE21510;GSE56140;GSE57957;GSE53624;GSE18842;GSE19188;GSE19804;GSE21933;GSE30219;GSE31210;GSE32863;GSE43458	STAD.zip;GSE50710.zip;GSE58828.zip;GSE65801.zip;GSE51575.zip;GSE29431.zip;GSE54002.zip;GSE20842.zip;GSE21510.zip;GSE56140.zip;GSE57957.zip;GSE53624.zip;GSE18842.zip;GSE19188.zip;GSE19804.zip;GSE21933.zip;GSE30219.zip;GSE31210.zip;GSE32863.zip;GSE43458.zip	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000168036	NA	221883	1499	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID01328	epigenetic regulation
Gastric cancer	HOXA11-AS	KLF2	negatively-E	ChIP;RIP	upregulation	microarray;sequencing	TCGA;GSE50710;GSE58828;GSE65801;GSE51575;GSE29431;GSE54002;GSE20842;GSE21510;GSE56140;GSE57957;GSE53624;GSE18842;GSE19188;GSE19804;GSE21933;GSE30219;GSE31210;GSE32863;GSE43458	STAD.zip;GSE50710.zip;GSE58828.zip;GSE65801.zip;GSE51575.zip;GSE29431.zip;GSE54002.zip;GSE20842.zip;GSE21510.zip;GSE56140.zip;GSE57957.zip;GSE53624.zip;GSE18842.zip;GSE19188.zip;GSE19804.zip;GSE21933.zip;GSE30219.zip;GSE31210.zip;GSE32863.zip;GSE43458.zip	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000127528	NA	221883	10365	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	LKLF	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID01329	epigenetic regulation
Colorectal cancer	RP11-708H21.4	AKT1	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);cell apoptosis(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01330	expression association
Colorectal cancer	RP11-708H21.4	MTOR	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);cell apoptosis(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000198793	NA	NA	2475	NA	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01331	expression association
Colorectal cancer	RP11-708H21.4	RPS6KB1	negatively-E	RNAi	downregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(-);cell invasion(-);cell apoptosis(+)	NA	regulation	NA	5-fluorouracil	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000262973	GRCh38_17:49171895-49173246	ENSG00000108443	NA	NA	6198	NA	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway.up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. Finally, increased RP11-708H21.4 expression blocked AKT/mTOR pathway, and repressed in vivo CRC xenograft tumor growth. As demonstrated in Figure 6, phosphorylation of AKT, mTOR, as well as S6K1, was significantly suppressed after transfection of pcDNA3.1-RP11-708H21.4 in HT-29 and HCT-116 cells. These results suggested that RP11-708H21.4 blocks AKT/mTOR pathway in CRC cells.	28427191	RID01332	expression association
Non-small cell lung cancer	LUCAT1	CDKN1A	negatively-E	ChIP;RIP	upregulation	sequencing	TCGA	LUSC_LUAD.zip	cell proliferation(+);cell growth(+);cell apoptosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000124762	NA	100505994	1026	SCAL1|SCAT5	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.	28423699	RID01333	epigenetic regulation
Non-small cell lung cancer	LUCAT1	CDKN1C	negatively-E	ChIP;RIP	upregulation	sequencing	TCGA	LUSC_LUAD.zip	cell proliferation(+);cell growth(+);cell apoptosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000129757	NA	100505994	1028	SCAL1|SCAT5	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.	28423699	RID01334	epigenetic regulation
Esophagus squamous cell carcinoma	PHBP1	PHB	positively-F	RNase protection assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell cycle(+);tumour groth(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000213091	GRCh38_6:150042546-150043353	ENSG00000167085	NA	5246	5245	NA	HEL-215|HEL-S-54e|PHB1	Pseudogene PHBP1 promotes esophageal squamous cell carcinoma proliferation by increasing its cognate gene PHB expression.we reported that human prohibitin gene pseudogene 1 (PHBP1) was upregulation in ESCC. Mechanisms analysis revealed that PHBP1 transcript as an antisense transcript of PHB is partially complementary to PHB mRNA and formed an RNA-RNA hybrid with PHB, consequently inducing an increase of PHB expression at both the mRNA and protein levels.	28404970	RID01335	interact with mRNA
Hepatocellular carcinoma	MALAT1	TRAF6	positively-E	RNAi;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-146b-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000175104	NA	378938	7189	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MGC:3310|RNF85	Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis.we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b 5p to down-regulate its expression in HCC.TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6.	28404923	RID01336	ceRNA or sponge
Hepatocellular carcinoma	UC.134	LATS1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;microarray	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:158526708-158528574	ENSG00000131023	NA	110599565	9113	NA	WARTS|wts	A novel lncRNA uc.134 represses hepatocellular carcinoma progression by inhibiting CUL4A-mediated ubiquitination of LATS1.The overexpression of uc.134 inhibited HCC cell proliferation, invasion, and metastasis in vitro and in vivo, whereas the knockdown of uc.134 produced the opposite results.we demonstrated that uc.134 inhibits the CUL4A-mediated ubiquitination of LATS1 and increases YAPS127 phosphorylation to silence the target genes of YAP.	28420424	RID01337	expression association
Hepatocellular carcinoma	UC.134	YAP1	negatively-E	RNA pull-down assay	downregulation	qRT-PCR;microarray	NA	NA	cell proliferation(-);cell metastasis(-);cell invasion(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_3:158526708-158528574	ENSG00000137693	NA	110599565	10413	NA	COB1|YAP|YAP2|YAP65|YKI	A novel lncRNA uc.134 represses hepatocellular carcinoma progression by inhibiting CUL4A-mediated ubiquitination of LATS1.The overexpression of uc.134 inhibited HCC cell proliferation, invasion, and metastasis in vitro and in vivo, whereas the knockdown of uc.134 produced the opposite results.we demonstrated that uc.134 inhibits the CUL4A-mediated ubiquitination of LATS1 and increases YAPS127 phosphorylation to silence the target genes of YAP. The use of this lncRNA may offer a promising treatment approach by inhibiting YAP and activating Hippo kinase signaling.	28420424	RID01338	expression association
Prostate cancer	CBR3-AS1	TGFB1	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000105329	NA	100506428	7040	PlncRNA-1|PlncRNA1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01339	expression association
Prostate cancer	CBR3-AS1	CDH2	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000170558	NA	100506428	1000	PlncRNA-1|PlncRNA1	CD325|CDHN|CDw325|NCAD	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01340	expression association
Prostate cancer	CBR3-AS1	CCND1	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000110092	NA	100506428	595	PlncRNA-1|PlncRNA1	BCL1|D11S287E|PRAD1|U21B31	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01341	expression association
Prostate cancer	CBR3-AS1	CDH1	negatively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000039068	NA	100506428	999	PlncRNA-1|PlncRNA1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.TGF-beta1, N-cadherin and CCND1 were downregulated and E-Cadherin was upregulation in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot.The effects of TGF-beta1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. PlncRNA-1 is an oncogene that regulates the cell cycle, CCND1 and EMT in prostate cancer cells through the TGF-beta1 pathway.	28212533	RID01342	expression association
Gastric cancer	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	tumor-suppressive function(+);cell growth(-);cell apoptosis(+)	ceRNA(miR-106b;miR-93)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay. Thus, we revealed a tumor suppressive role of PTENP1 as ceRNA in GC and pinpointed the specific miRNAs decoyed by PTENP1, highlighting the emerging roles of ceRNAs in the biological regulation of GC cells and their possible clinical significance.	28212532	RID01343	ceRNA or sponge
Non-small cell lung cancer	NKILA	SNAI1	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000124216	NA	105416157	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01344	expression association
Non-small cell lung cancer	NKILA	NFKB1	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01345	expression association
Non-small cell lung cancer	NKILA	NFKBIA	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-kB/Snail pathway. Mechanistic study showed that NKILA attenuated Snail expression via inhibiting the phosphorylation of IkBalpha and NF-kB activation, subsequently suppressed the expression of markers of epithelial-mesenchymal transition process.	28412955	RID01346	expression association
Breast cancer	CRNDE	CTNNB1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000168036	NA	NA	1499	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01347	expression association
Breast cancer	CRNDE	MYC	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000136997	NA	NA	4609	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01348	expression association
Breast cancer	CRNDE	CCND1	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000110092	NA	NA	595	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01349	expression association
Breast cancer	CRNDE	miR-136	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);Wnt/beta-catenin signaling pathway(+);tumor growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	Long noncoding RNA CRNDE activates Wnt/beta-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer.We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of beta-catenin, c-myc and CCND1.CRNDE might hyperactivate the Wnt/beta-catenin signaling pathway through directly repressing miR-136 expression in BC;	28469804	RID01350	ceRNA or sponge
Malignant glioma	XIST	RAC1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-137)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000136238	NA	7503	5879	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA XIST exerts oncogenic functions in human glioma by targeting miR-137.our data further showed that XIST could up-regulate the expression of miR-137 targeted gene Rac1 through acting as an endogenous sponge of miR-137. In addition, we found that Rac1 inhibition or miR-137 overexpression could suppress glioma cells proliferation induced by XIST overexpression.	28469789	RID01351	ceRNA or sponge
Gastric cancer	HNRNPKP2	CXCR4	negatively-E	RNAi;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227347	GRCh38_2:136199114-136200503	ENSG00000121966	NA	389053	7852	NA	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	DC-SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis.DC-SIGNR promoted gastric cancer liver metastasis mediated with HNRNPKP2 which expression was regulated by STAT5A. And HNRNPKP2 decreased the expression of downstream target gene CXCR4.	28403883	RID01352	expression association
Gastric cancer	STAT5A	HNRNPKP2	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000126561	NA	ENSG00000227347	GRCh38_2:136199114-136200503	6776	389053	MGF|STAT5	NA	DC-SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis.DC-SIGNR promoted gastric cancer liver metastasis mediated with HNRNPKP2 which expression was regulated by STAT5A. And HNRNPKP2 decreased the expression of downstream target gene CXCR4.STAT5A promoted HNRNPKP2 expression after knockdown DC-SIGNR.	28403883	RID01353	expression association
Hepatocellular carcinoma	TP73-AS1	HMGB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000189403	NA	57212	3146	KIAA0495|PDAM	HMG-1|HMG1|HMG3|SBP-1	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation. Knockdown of TP73-AS1 inhibited the HCC proliferation and the expression levels of HMGB1, RAGE and NF-kB in HCC cells.we confirmed that miR-200a could directly bind to TP73-AS1 and the 3'UTR of HMGB1; TP73-AS1 competed with HMGB1 for miR-200a binding.	28403886	RID01354	ceRNA or sponge
Hepatocellular carcinoma	TP73-AS1	AGER	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000204305	NA	57212	177	KIAA0495|PDAM	NA	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation. Knockdown of TP73-AS1 inhibited the HCC proliferation and the expression levels of HMGB1, RAGE and NF-kB in HCC cells.we confirmed that miR-200a could directly bind to TP73-AS1 and the 3'UTR of HMGB1; TP73-AS1 competed with HMGB1 for miR-200a binding.	28403886	RID01355	expression association
Lung cancer	PRAL	TP53	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000279296	GRCh38_17:6772831-6776116	ENSG00000141510	NA	109245082	7157	lncRNA-PRAL	BCC7|BMFS5|LFS1|P53|TRP53	P53 Regulation-Association Long Non-Coding RNA (LncRNA PRAL) Inhibits Cell Proliferation by Regulation of P53 in Human Lung Cancer.Overexpression of PRAL inhibited cell proliferation by upregulating the expression of P53.	28396580	RID01356	expression association
Hepatocellular carcinoma	XIST	PTEN	positively-E	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-181a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171862	NA	7503	5728	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression.The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects.MiR-181a can promote HCC metastasis by targeting PTEN, which is regulated by lncRNA XIST.	28388883	RID01357	ceRNA or sponge
Endometrial cancer	LINC00672	LASP1	negatively-E	RNAi;western blot;immunofluorescence assay	downregulation	qRT-PCR	NA	NA	paclitaxel chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000263874	GRCh38_17:38925168-38929384	ENSG00000002834	NA	100505576	3927	NA	Lasp-1|MLN50	Long non-coding RNA LINC00672 contributes to p53 protein-mediated gene suppression and promotes endometrial cancer chemosensitivity. Here, we report that a lincRNA, LINC00672, which possesses an ultra-conserved region, is aberrantly down-regulated during the development of EC. LINC00672 overexpression could lower the levels of LASP1 and slow the development of malignant phenotypes of EC both in vitro and in vivo Moreover, LINC00672 significantly increased the 50% inhibitory concentration of paclitaxel in EC cells and increased the sensitivity of xenograft mice to paclitaxel. These findings indicate that LINC00672 can influence LASP1 expression as a locus-restricted cofactor for p53-mediated gene suppression, thus impacting EC malignancies and chemosensitivity to paclitaxel.	28232485	RID01358	expression association
Esophagus squamous cell carcinoma	CCAT1	SPRY4	negatively-E	ChIP;RNA pull-down assay;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000187678	NA	100507056	81848	CARLO5|CARLo-5|onco-lncRNA-40	HH17	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.	27956498	RID01359	epigenetic regulation
Esophagus squamous cell carcinoma	CCAT1	HOXB13	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000159184	NA	100507056	10481	CARLO5|CARLo-5|onco-lncRNA-40	HPC9|PSGD	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.CCAT1 regulates HOXB13 as a molecular decoy for miR-7, a microRNA that targets both CCAT1 and HOXB13, thus facilitating cell growth and migration. Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.	27956498	RID01360	ceRNA or sponge
Renal cell carcinoma	LNCSRLR	IL6	positively-E	ChIP	upregulation	microarray	GSE87121	GSE87121.zip	sorafenib tolerance(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000240032	GRCh38_3:146066344-146069185	ENSG00000136244	NA	109729161	3569	lncRNA-SRLR	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long noncoding RNA-SRLR elicits intrinsic sorafenib resistance via evoking IL-6/STAT3 axis in renal cell carcinoma.Herein, we identified a long non-coding RNA referred to as lncRNA-SRLR (sorafenib resistance-associated lncRNA in RCC) that is upregulation in intrinsically sorafenib-resistant RCCs. lncRNA-SRLR directly binds to NF-kB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance.	27841868	RID01361	expression association
Renal cell carcinoma	LNCSRLR	STAT3	positively-E	RNAi;western blot	upregulation	microarray	GSE87121	GSE87121.zip	sorafenib tolerance(+)	NA	regulation	NA	sorafenib	NA	NA	Cancer	Kidney cancer	lncRNA	TF	ENSG00000240032	GRCh38_3:146066344-146069185	ENSG00000168610	NA	109729161	6774	lncRNA-SRLR	ADMIO|ADMIO1|APRF|HIES	Long noncoding RNA-SRLR elicits intrinsic sorafenib resistance via evoking IL-6/STAT3 axis in renal cell carcinoma.Herein, we identified a long non-coding RNA referred to as lncRNA-SRLR (sorafenib resistance-associated lncRNA in RCC) that is upregulation in intrinsically sorafenib-resistant RCCs. lncRNA-SRLR directly binds to NF-kB and promotes IL-6 transcription, leading to the activation of STAT3 and the development of sorafenib tolerance.	27841868	RID01362	expression association
Liver cancer	GASAL1	E2F1	negatively-E	RNAi	downregulation	NA	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000253669	GRCh38_8:102805517-102810039	ENSG00000101412	NA	401472	1869	NA	E2F-1|RBAP1|RBBP3|RBP3	A novel lncRNA, GASL1, inhibits cell proliferation and restricts E2F1 activity. GASL1 silencing enhanced cell proliferation, while, conversely, its ectopic expression inhibited proliferation. Knockdown of GASL1 also enhanced E2F1-induced apoptosis, suggesting the existence of an E2F/GASL1 negative feedback loop.low levels of GASL1 are associated with decreased survival of liver cancer patients.	28423601	RID01363	expression association
Colorectal cancer	lncRNA-BCAT1	CCND1	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG		GRCh38_12:24810022-24949459	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01364	expression association
Colorectal cancer	lncRNA-BCAT1	MYC	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF		GRCh38_12:24810022-24949459	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01365	expression association
Colorectal cancer	lncRNA-BCAT1	MMP2	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG		GRCh38_12:24810022-24949459	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.lncRNA-BCAT1 overexpression suppressed CRC cell growth and invasion by downregulating CCND1, c-Myc, and MMP-2.	28416735	RID01366	expression association
Colorectal cancer	lncRNA-BCAT1	CTNNB1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE18560;GSE44097	GSE18560.zip;GSE44097.zip	cell growth(-);cell invasion(-);WNT/beta-catenin signaling pathway(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG		GRCh38_12:24810022-24949459	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Reciprocal control of lncRNA-BCAT1 and beta-catenin pathway reveals lncRNA-BCAT1 long non-coding RNA acts as a tumor suppressor in colorectal cancer.We focused on AK091631, a novel lncRNA, which we named lncRNA-beta-catenin associated transcript 1 (LncRNA-BCAT1). lncRNA-BCAT1 expression was decreased in CRC tissues, and was negatively associated with beta-catenin in both CRC tissues and cell lines.These results suggest that lncRNA-BCAT1 overexpression inhibits CRC cell growth and invasion via Wnt/beta-catenin pathway blockade, and that lncRNA-BCAT1 is repressed by Wnt/beta-catenin signaling.	28416735	RID01367	expression association
Glioblastoma	MALAT1	TYMS	positively-E	RNAi;luciferase reporter assay	downregulation	sequencing;qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-203)	regulation	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000176890	NA	378938	7298	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HST422|TMS|TS	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. MALAT1 is down-regulated in GBM patients showing response to TMZ treatment by RT-qPCR. The gain and loss-function experiments revealed that miR-203 was down-regulated by MALAT1 and this interaction has reciprocal effects. Besides, thymidylate synthase (TS) mRNA was identified as a direct target of miR-203. LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression.	28187000	RID01368	ceRNA or sponge
Urinary bladder cancer	TUG1	HMGB1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell apoptosis(-);radiosensitivity(-)	NA	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000189403	NA	55000	3146	LINC00080|NCRNA00080|TI-227H	HMG-1|HMG1|HMG3|SBP-1	Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression. The expression level of TUG1 and HMGB1 mRNA and protein was about twice higher in bladder cancer tissues than that in adjacent normal tissues. LncRNA TUG1 knockdown enhances radiosensitivity of bladder cancer by suppressing HMGB1 expression. TUG1 acts as a potential regulator of radioresistance of bladder cancer, and it may represent a promising therapeutic target for bladder cancer patients.	28376901	RID01369	expression association
Osteosarcoma	AK093407	STAT3	positively-F	RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	NA	GRCh38_8:125613468-125614465	ENSG00000168610	NA	NA	6774	NA	ADMIO|ADMIO1|APRF|HIES	Long non-coding RNA AK093407 promotes proliferation and inhibits apoptosis of human osteosarcoma cells via STAT3 activation.we showed that AK093407 interacted with STAT3, and promoted its phosphorylation. Lastly, we showed that STAT3 activation was essential for the effects of AK093407 on cell proliferation and apoptosis as the overexpression of AK093407 in the presence of STAT3 inhibitor did not promote cell proliferation and inhibit cell apoptosis.	28469961	RID01370	interact with protein
Breast cancer	SNHG16	E2F5	positively-E	qRT-PCR;RIP;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell migration(+)	ceRNA(miR-98)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000133740	NA	100507246	1875	Nbla10727|Nbla12061|ncRAN	E2F-5	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.We predicted SNHG16 as a competitive endogenous RNA (ceRNA) of E2F transcription factor 5 protein (E2F5) via competition for the shared miR-98 through bioinformatics analysis, and proved this regulation using relative quantitative real-time PCR (qRT-PCR).we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues.	28232182	RID01371	ceRNA or sponge
Malignant glioma	PSMD6-AS1	MDM2	interact	RNAi;luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cell proliferation(-);cell migration(-);cell apoptosis(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243410	GRCh38_3:64011964-64016246	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	Long non-coding RNA ENST00462717 suppresses the proliferation, survival, and migration by inhibiting MDM2/MAPK pathway in glioma.we identified MDM2 as a direct target of lnc00462717 and lnc00462717 played a role by partially regulating the MDM2/MAPK pathway. Bioinformatics analysis revealed that ENST00462717 is located on chromosome 12 upstream of the MDM2 promoter region and the lnc00462717 and MDM2 are transcribed from the same DNA strand in UCSC genome database.	28189682	RID01372	transcriptional regulation
Tongue cancer	lnc-Sox5	ELAVL1	positively-F	RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+);tumor growth(+);cell apoptosis(-);cell cycle(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000115934	GRCh38_12:23181334-23251499	ENSG00000066044	NA	NA	1994	NA	ELAV1|HUR|Hua|MelG	HuR Stabilizes lnc-Sox5 mRNA to Promote Tongue Carcinogenesis. RNA immunoprecipitation suggested that HuR directly bound to and stabilized lnc-Sox5 RNA. Consistently, HuR knockdown reduced the level of lnc-Sox5 in Tca8113 cells.Both lnc-Sox5 knockdown and HuR knockdown suppressed Tca8113 cell tumorigenesis in xenograft models.	28371600	RID01373	interact with protein
Gastric cancer	PVT1	HIF1A	positively-E	luciferase reporter assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-186)	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000100644	NA	5820	3091	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer.Further functional experiments indicated up-regulation of PVT1 promoted the GC cell proliferation and invasion, while down-regulation of PVT1 inhibited cell proliferation and invasion. In addition, PVT1 could directly interact with miR-186 in GC cells and this interaction lead to the inhibition of downstream of HIF-1alpha expression.Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	28122299	RID01374	ceRNA or sponge
Cervical cancer	UCA1	CASP3	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-);cell proliferation(+)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000164305	NA	652995	836	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CPP32|CPP32B|SCA-1	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01375	expression association
Cervical cancer	UCA1	CDK2	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000123374	NA	652995	1017	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN2|p33(CDK2)	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01376	expression association
Cervical cancer	UCA1	CDKN1A	negatively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	chemoresistance(+);cell proliferation(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer. UCA1 expression in the DDP-treated group significantly decreased by 31% and 53%, respectively, in comparison with the control group. This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. UCA1 suppressed apoptosis by downregulating caspase 3 and upregulating CDK2, whereas enhanced cell proliferation by increased level of survivin and decreased level of p21.	28414550	RID01377	expression association
Colorectal cancer	LINC-ROR	TP53	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000141510	NA	100885779	7157	ROR|lincRNA-RoR|lincRNA-ST8SIA3	BCC7|BMFS5|LFS1|P53|TRP53	The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway. We discovered that lincRNA-ROR was upregulation in CRC cell lines and tissue samples. LincRNA-ROR decreases sensitivity to radiotherapy via the negative regulation of p53/miR-145 and may represent a potential target for the treatment of CRC.Long Non-Coding RNA Reprogramming (ROR) Promotes Cell Proliferation in Colorectal Cancer via Affecting P53. The expression level of lncRNA-ROR was elevated in CRC tissues when compared to adjacent tissues (n=78). Protein levels of p53 and p53 target genes were affected by lncRNA-ROR in vitro, and downregulation of lncRNA-ROR impeded tumorigenesis in vivo. Our study demonstrates that lncRNA-ROR participates in controlling CRC proliferation, viability, and apoptosis, partially by modulating p53, which provides potential and prospective therapeutic targets for CRC.	27696511;28216611	RID01378	expression association
Colorectal cancer	LINC-ROR	miR-145	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	radioresistance(+);cell proliferation(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway.LincRNA-ROR decreases sensitivity to radiotherapy via the negative regulation of p53/miR-145 and may represent a potential target for the treatment of CRC.	27696511	RID01379	expression association
Prostate cancer	LINC01116	GAPDH	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000111640	NA	375295	2597	TALNEC2	G3PD|GAPD|HEL-S-162eP	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01380	expression association
Prostate cancer	LINC01116	MAP1LC3B2	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000258102	NA	375295	643246	TALNEC2	ATG8G	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01381	expression association
Prostate cancer	LINC01116	H2AFY	negatively-E	RNAi	upregulation	sequencing;qRT-PCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	sulforaphane	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000163364	GRCh38_2:176629572-176637931	ENSG00000113648	NA	375295	9555	TALNEC2	H2A.y|H2A/y|H2AF12M|MACROH2A1.1|mH2A1|macroH2A1.2	Long noncoding RNAs and sulforaphane: a target for chemoprevention and suppression of prostate cancer. Knockdown of LINC01116 with siRNA decreased proliferation of prostate cancer cells and significantly up-regulated several genes including GAPDH (regulates glycolysis), MAP1LC3B2 (autophagy) and H2AFY (chromatin structure).	28131897	RID01382	expression association
Malignant glioma	FTX	MTDH	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000147649	NA	100302692	92140	LINC00182|MIR374AHG|NCRNA00182	3D3|AEG-1|AEG1|LYRIC|LYRIC/3D3	Long noncoding RNA FTX is upregulation in gliomas and promotes proliferation and invasion of glioma cells by negatively regulating miR-342-3p.FTX directly inhibited the expression of miR-342-3p, which subsequently regulates the expression of AEG-1. miR-342-3p Directly Targeted AEG-1. Collectively, FTX is critical for proliferation and invasion of glioma cells by regulating miR-342-3p and AEG-1.	28112756	RID01383	ceRNA or sponge
Colorectal cancer	MALAT1	CDH1	negatively-E	qRT-PCR;RNAi;western blot;RIP	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2.MALAT1 is overexpressed in colorectal cancer patients and correlated with tumor metastasis. LncRNA MALAT1 knockdown enhances E-cadherin expression and inhibits oxaliplatin-induced EMT in colorectal cancer cells. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin.	28069878	RID01384	epigenetic regulation
Non-small cell lung cancer	HAGLR	CDKN1A	positively-E	RNAi;western blot	upregulation	qRT-qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000124762	NA	401022	1026	HOXD-AS1|MIR7704HG|Mdgt	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Increased HAGLR expression promotes non-small cell lung cancer proliferation and invasion via enhanced de novo lipogenesis. Furthermore, the expression levels of p21 and matrix metallopeptidase-9 (MMP-9) were dysregulated when HAGLR expression was suppressed.	28443464	RID01385	expression association
Colorectal cancer	PVT1	MYC	positively-E	RNAi;qRT-PCR	upregulation	qRT-qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	The expression pattern of long non-coding RNA PVT1 in tumor tissues and in extracellular vesicles of colorectal cancer correlates with cancer progression.The results also showed that by down-regulating the PVT1 expression, the c-Myc expression was suppressed, the cell proliferation was inhibited, and cell apoptosis was increased. Taken together, these findings implicated that PVT1 may be a new oncogene co-amplified with c-Myc in colorectal cancer tissues and extracellular vesicles and functionally correlated with the proliferation and apoptosis of colorectal cancer cells.Taken together, these findings implicated that PVT1 may be a new oncogene co-amplified with c-Myc in colorectal cancer tissues and extracellular vesicles and functionally correlated with the proliferation and apoptosis of colorectal cancer cells.	28381186	RID01386	expression association
Malignant glioma	KCNQ1OT1	CCNE2	positively-E	RNAi;qRT-PCR;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumor-suppressive function(-)	ceRNA(miR-370)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000269821	GRCh38_11:2608328-2699994	ENSG00000175305	NA	10984	9134	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	CYCE2	Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells' Malignancy by Activating miR-370/CCNE2 Axis.Knockdown of KCNQ1OT1 decreased the expression level of Cyclin E2 (CCNE2) by binding to miR-370. Further, miR-370 bound to CCNE2 3'UTR region and decreased the expression of CCNE2. These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.	28381990	RID01387	ceRNA or sponge
Anaplastic large cell lymphoma	LINC01013	SNAI1	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lymphoma	lncRNA	TF	ENSG00000228495	GRCh38_6:132131888-132169374	ENSG00000124216	NA	100507254	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma. LINC01013 induced snail, resulting in activation of fibronectin and enhanced ALCL cell invasion.	28331184	RID01388	expression association
Nasopharynx carcinoma	LOC100129148	KLF12	positively-E	RNAi;qRT-PCR;luciferase reporter assay;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth(+)	ceRNA(miR-539-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	TF	NA	GRCh38_7:139417462-139427526	ENSG00000118922	NA	100129148	11278	NA	AP-2rep|AP2REP|HSPC122	Long non-coding RNA LOC100129148 functions as an oncogene in human nasopharyngeal carcinoma by targeting miR-539-5p.Over-expressed LOC100129148 favored, but silenced LOC100129148 hampered cell proliferation in NPC cells. Additionally, LOC100129148 enhanced the KLF12 expression through functioning as a competitive 'sponge' for miR-539-5p.	28328537	RID01389	ceRNA or sponge
Osteosarcoma	MALAT1	HMGB1	positively-E	RNAi;luciferase reporter assay;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	ceRNA(miR-142-3p;miR-129-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000189403	NA	378938	3146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HMG-1|HMG1|HMG3|SBP-1	MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.By using online tools, we screen out 2 candidate miRNAs, miR-142-3p and miR-129-5p which may be associated with both MALAT1 and HMGB1. Luciferase reporter assay revealed a direct interaction between the 2 miRNAs and MALAT1, respectively, via a putative binding site within MALAT1. Meanwhile,both the 2 miRNAs could bind to HMGB1 3'-untranslated region (3'-UTR) and regulate HMGB1 expression. Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis.	28346809	RID01390	ceRNA or sponge
Hepatocellular carcinoma	RB1-DT	RB1	negatively-E	RIP;RNA pull-down assay;5-aza-2'-deoxycytidine treatment;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-);tumor growth(+)	DNA methylation	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231473	GRCh38_13:48296162-48303661	ENSG00000139687	NA	100862704	5925	LINC00441|ncRNA-RB1	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.Here we focused on the bidirectional transcripted long noncoding RNA (Linc00441) with neighbor gene RB1 to investigate whether Linc00441 is involved in the suppression of RB1 in HCC. We found that aberrant upregulation intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement.	28300839	RID01391	epigenetic regulation
Ovarian cancer	LINC00092	PFKFB2	interact	RNAi;RNA pull-down assay;western blot	upregulation	microarray	GSE82059	GSE82059.zip	cell metastasis(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000225194	GRCh38_9:96019724-96027993	ENSG00000123836	NA	100188953	5208	NCRNA00092	PFK-2/FBPase-2	Long Noncoding RNA LINC00092 Acts in Cancer-Associated Fibroblasts to Drive Glycolysis and Progression of Ovarian Cancer. CXCL14 is over-expressed in CAFs of metastatic lesion of ovarian cancer and predicts clinical outcome. Mechanistic studies showed that LINC00092 bound a glycolytic enzyme, the fructose-2,6-biphosphatase PFKFB2, thereby promoting metastasis by altering glycolysis and sustaining the local supportive function of CAFs.	28087599	RID01392	interact with protein
Prostate cancer	UCA1	BCL2	positively-E	RNAi;qRT-PCR	NA	NA	NA	NA	cell viability(+);cell motility(+)	ceRNA(miR-184)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000171791	NA	652995	596	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Bcl-2|PPP1R50	Artesunate suppresses the viability and mobility of prostate cancer cells through UCA1, the sponge of miR-184.Then we determined that the miR-184/Bcl-2 axis might be the downstream signaling pathway of UCA1 upon ART treatment. UCA1 binds to miR-184 through its seed sequences and may function as a sponge for miR-184. Bcl-2, a key anti-apoptotic factor and one of the verified direct targets of miR-184.	28209917	RID01393	ceRNA or sponge
Urinary bladder cancer	CASC2	CTNNB1	negatively-E	RNAi;western blot;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);WNT/beta-catenin signaling pathway(-);cell apoptosis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000168036	NA	255082	1499	C10orf5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Down-regulation of lncRNA CASC2 promotes cell proliferation and metastasis of bladder cancer by activation of the Wnt/beta-catenin signaling pathway.	28199978	RID01394	expression association
Non-small cell lung cancer	SNHG1	SOX9	positively-E	luciferase reporter assay;RNAi	upregulation	sequencing;qRT-PCR	TCGA	LUSC_LUAD.zip	WNT/beta-catenin signaling pathway(+);cancer progression(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000125398	NA	23642	6662	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CMD1|CMPD1|SRA1|SRXX2|SRXY10	upregulation lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/beta-catenin signaling pathway.We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p. In addition, we identified that SOX9 acted as a target of miR-101-3p, and SOX9 played the oncogenic role in NSCLC by activating Wnt/beta-catenin signaling pathway.	28147312	RID01395	ceRNA or sponge
Astrocytoma	CASC2c	miR-101	negatively-F	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Astrocytoma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046821-118210153	NA	NA	NA	NA	NA	NA	CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis. We investigated the role of a new long non-coding RNA CASC2c binding with miR-101. CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1.	28252647	RID01396	ceRNA or sponge
Ovarian cancer	MEG3	miR-214	negatively-F	RNAi;luciferase reporter assay	NA	NA	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer.There were at least two binding sites between MEG3 and miR-214. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance.Curcumin can restore MEG3 levels via demethylation. MEG3 upregulation can decrease EVs mediated transfer of miR-214 in ovarian cancer cells, thereby reducing drug resistance.	28175963	RID01397	ceRNA or sponge
Urinary bladder cancer	SPRY4-IT1	EZH2	positively-E	RNAi;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2. human EZH2 3'UTR fragment containing putative binding sites for miR-101-3p reporter vector and the EZH2 promoter reporter vector were adopted forDual-luciferase Reporter Assays.	27998761	RID01398	ceRNA or sponge
Hepatocellular carcinoma	MALAT1	SRSF1	positively-E	RNAi;western blot;qRT-PCR	upregulation	sequencing	NA	NA	cancer progression(+);WNT signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136450	NA	378938	6426	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASF|SF2|SF2p33|SFRS1|SRp30a	Long Noncoding RNA MALAT1 Promotes Hepatocellular Carcinoma Development by SRSF1 Upregulation and mTOR Activation. Here we report that the lncRNA MALAT1 is upregulation in hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induction of the oncogenic splicing factor SRSF1. Our results reveal a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulation.	27993818	RID01399	expression association
Breast cancer	NEAT1	CTNNB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000168036	NA	283131	1499	LINC00084|NCRNA00084|TncRNA|VINC	CTNNB|EVR7|MRD19|NEDSDV|armadillo	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed.lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01400	expression association
Breast cancer	NEAT1	CDH2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000170558	NA	283131	1000	LINC00084|NCRNA00084|TncRNA|VINC	CD325|CDHN|CDw325|NCAD	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed.lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01401	expression association
Breast cancer	NEAT1	CDH1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000039068	NA	283131	999	LINC00084|NCRNA00084|TncRNA|VINC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. Western blot also showed that beta-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed. lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis.	28338194	RID01402	expression association
Gastric cancer	SNHG5	KLF4	positively-E	RNAi;qRT-PCR;luciferase reporter assay;immunohistochemical assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-32)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000136826	NA	387066	9314	C6orf160|LINC00044|NCRNA00044|U50HG	EZF|GKLF	The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.it was reported that Kruppel-like factor 4 (KLF4) is a target gene of miR-32. In agreement with SNHG5 being a decoy for miR-32, we showed that KLF4 suppression by miR-32 could be partially rescued by SNHG5 overexpression, whereas miR-32 mimic rescued SNHG5 overexpression-mediated suppression of GC cell migration.	27871067	RID01403	ceRNA or sponge
Colon cancer	H19	VDR	positively-E	RNAi;luciferase reporter assay;western blot	NA	NA	NA	NA	chemoresistance(+)	ceRNA(miR-675-5p)	regulation	NA	"1,25(OH)2D3"	NA	NA	Cancer	Colon cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111424	NA	283120	7421	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NR1I1|PPP1R163	H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells. H19, on the other hand, was able to inhibit the expression of VDR through microRNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo.A potential binding site of miR-675-5p was identified in the 3'UTR of VDR mRNA utilizing the online prediction system Targetscan.	28189050	RID01404	ceRNA or sponge
Malignant glioma	PVT1	ATG7	positively-E	RNAi;western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration;angiogenesis(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000197548	NA	5820	10533	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	APG7-LIKE|APG7L|GSA7	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186.The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.MiR-186 binds to the 3' untranslated regions of Atg7 and Beclin1.	28351322	RID01405	ceRNA or sponge
Malignant glioma	PVT1	BECN1	positively-E	RNAi;western blot;RIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration;angiogenesis(+)	ceRNA(miR-186)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000126581	NA	5820	8678	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ATG6|VPS30|beclin1	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186.The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.MiR-186 binds to the 3' untranslated regions of Atg7 and Beclin1.	28351322	RID01406	ceRNA or sponge
Epithelial ovarian cancer	RP11-190D6.2	WWOX	positively-E	RNAi;qRT-PCR	downregulation	qRT-PCR	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_16:78237362-78241218	ENSG00000186153	NA	NA	51741	NA	D16S432E|EIEE28|FOR|FRA16D|HHCMA56|PRO0128|SCAR12|SDR41C1|WOX1	A new tumor suppressor lncRNA RP11-190D6.2 inhibits the proliferation, migration, and invasion of epithelial ovarian cancer cells.We found that RP11-190D6.2 expression was positively correlated with WWOX expression. The WWOX antisense transcript RP11-190D6.2 expression was markedly downregulated in tumor tissues compared with normal tissues.The analyses in EOC implicate that RP11-190D6.2 may play a pivotal role in the regulation of tumor metastasis, suggesting that RP11-190D6.2 may serve as a potential biomarker and therapeutic target for EOC.	28280357	RID01407	expression association
Cervical cancer	MALAT1	VIM	positively-E	RNAi;qRT-PCR	upregulation	RT-PCR;qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000026025	NA	378938	7431	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells.miRNA-143 decreased cell invasion and migration potency, downregulated vimentin and upregulation E-cadherin expression, while MALAT1 had the opposite effects. In conclusion, the low expression of miRNA-143 and high expression of MALAT1 in cervical cancer cells could possibly potentiate cell invasion/migration and alter the levels of vimentin and E-cadherin. Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	28252165;26798987	RID01408	expression association
Cervical cancer	MALAT1	CDH1	negatively-E	RNAi;qRT-PCR	upregulation	RT-PCR;qRT-PCR	NA	NA	cell invasion(+);cell migration(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells.miRNA-143 decreased cell invasion and migration potency, downregulated vimentin and upregulation E-cadherin expression, while MALAT1 had the opposite effects. In conclusion, the low expression of miRNA-143 and high expression of MALAT1 in cervical cancer cells could possibly potentiate cell invasion/migration and alter the levels of vimentin and E-cadherin. Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	28252165;26798987;27658300	RID01409	expression association
Hepatocellular carcinoma	SNHG6-003	MAP3K7	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR;microarray	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-26a;miR-26b)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921690-66925541	ENSG00000135341	NA	NA	6885	NA	NA	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-beta-activated kinase 1 (TAK1). TAK1 was a directtarget of miR-26a/b. Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulation in human cancers, exhibiting a co-expression pattern. Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis. In contrast, SNHG6-003-overexpressing cells were protected from5-fluorouracil toxicity as shown by lower levels of apoptosis,cleaved PARP and cleaved caspase-3 (Figures 2e and f). Thissuggested that SNHG6-003 may boost the resistance of HCC cellsto chemotherapy with 5-fluorouracil	27530352	RID01410	ceRNA or sponge
Liposarcoma	PILRLS	TCL1A	interact	RNA pull-down assay;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lipomatous cancer	lncRNA	PCG	NA	GRCh38_5:66563850-66566010	ENSG00000100721	NA	NA	8115	NA	TCL1	A novel long noncoding RNA PILRLS promote proliferation through TCL1A by activing MDM2 in Retroperitoneal liposarcoma.RNA pull-down assay found PILRLS can specific binding with TCL1A which also regulate the expression level of TCL1A. Our work for the first time demonstrated PILRLS can activating the MDM2 by binding with TCL1A which suppress the P53 pathway to promote the unlimited growth of retroperitoneal Liposarcoma cells.	28129655	RID01411	interact with protein
Liposarcoma	PILRLS	MDM2	positively-E	RNAi;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lipomatous cancer	lncRNA	PCG	NA	GRCh38_5:66563850-66566010	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	A novel long noncoding RNA PILRLS promote proliferation through TCL1A by activing MDM2 in Retroperitoneal liposarcoma.RNA pull-down assay found PILRLS can specific binding with TCL1A which also regulate the expression level of TCL1A. Our work for the first time demonstrated PILRLS can activating the MDM2 by binding with TCL1A which suppress the P53 pathway to promote the unlimited growth of retroperitoneal Liposarcoma cells.	28129655	RID01412	expression association
Hepatocellular carcinoma	AK058003	SNCG	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	host(miR-15a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_10:86948677-87023220	ENSG00000173267	NA	NA	6623	NA	BCSG1|SR	Long non-coding RNA AK058003, as a precursor of miR-15a, interacts with HuR to inhibit the expression of gamma-synuclein in hepatocellular carcinoma cells.lncRNA-AK058003 can reduce the expression of mRNA stabilizing protein HuR and act as a precursor of miR-15a to suppress gamma-synuclein-mediated cell proliferation and the metastasis of hepatocellular carcinoma.	28035067	RID01413	expression association
Pancreatic cancer	miR-216a	MALAT1	negatively-F	luciferase reporter assay	NA	NA	NA	NA	apoptosis process(-);cell cycle(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression.Based on these findings, we infer that miR-216a induces apoptosis both in the presence and absence of gemcitabine in pancreatic cancer cells by silencing MALAT1 expression.	28034748	RID01414	ceRNA or sponge
Breast cancer	LINC-ROR	miR-205	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell invasion(+)	NA	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205. In MDA-MB-231 cells, down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	28063065	RID01415	expression association
Breast cancer	LINC-ROR	ZEB1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+);cell invasion(+)	NA	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205.down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.	28063065	RID01416	expression association
Breast cancer	CCAT2	TGFB1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000105329	NA	101805488	7040	LINC00873|NCCP1	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01417	expression association
Breast cancer	CCAT2	SMAD2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000175387	NA	101805488	4087	LINC00873|NCCP1	JV18|JV18-1|MADH2|MADR2|hMAD-2|hSMAD2	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01418	expression association
Breast cancer	CCAT2	SMN1	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	TGF-beta signaling pathway(+);cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000172062	NA	101805488	6606	LINC00873|NCCP1	BCD541|GEMIN1|SMA|SMA1|SMA2|SMA3|SMA4|SMA@|SMN|SMNT|T-BCD541|TDRD16A	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-beta, Smad2 and alpha-SMA in breast cancer cells.	28272713	RID01419	expression association
Thyroid carcinoma	NEAT1	miR-214	negatively-E	RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214.NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced beta-catenin (a direct target of miRNA-214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA-214, presenting a reciprocal repression correlation.	28000845	RID01420	expression association
Gallbladder cancer	AFAP1-AS1	TWIST1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000122691	NA	84740	7291	AFAP1-AS|AFAP1AS	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01421	expression association
Gallbladder cancer	AFAP1-AS1	VIM	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000026025	NA	84740	7431	AFAP1-AS|AFAP1AS	NA	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01422	expression association
Gallbladder cancer	AFAP1-AS1	CDH1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000039068	NA	84740	999	AFAP1-AS|AFAP1AS	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	RID01423	expression association
Prostate cancer	PVT1	miR-146a	negatively-E	RNAi;qRT-PCR;5-azacytidine	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter. Our study suggested a regulatory relationship between lncRNA PVT1 and miR-146a during the process of the prostate cancer tumorigenesis. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a.	27794184	RID01424	epigenetic regulation
Non-small cell lung cancer	LncRNA-HIT	ZEB1	interact	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	NA	GRCh38_7:27195637-27197624	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulation of LncRNA-HIT promotes migration and invasion of non-small cell lung cancer cells by association with ZEB1. LncRNA-HIT (HOXA transcript induced by TGFbeta) was recently identified. LncRNA-HIT functions as a prometastasis oncogene by directly associating with ZEB1 to regulate NSCLC.	27790864	RID01425	interact with protein
Cervical cancer	HOTAIR	miR-22	negatively-F	luciferase reporter assay	upregulation	amplicon sequencing	NA	NA	cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Identification of genetic variation in the lncRNA HOTAIR associated with HPV16-related cervical cancer pathogenesis.This genetic variant showed the propensity of a secondary structure alteration and gain of a miR-22 binding site in HOTAIR, which was found to be concordant with miR-22 over-expression in low HOTAIR CaCx cases compared to controls. We found that miR-22 expression negatively correlated with HOTAIR and E7 expression. Reduced luciferase activity of a HOTAIR rs2366152C expression plasmid in C33A cells through miR-22 co-transfection confirmed the ability of miR-22 to specifically target rs2366152C-harbouring HOTAIR lncRNA in CaCx cells, ultimately leading to its down-regulation.Here, we aimed at identifying functionally relevant genetic variants that may be employed to differentiate between clinically distinct CaCx subtypes, i.e., those exhibiting high HOTAIR levels and molecular signatures of metastasis and those lacking such signatures in the presence of low HOTAIR expression levels.	27683269	RID01426	ceRNA or sponge
Gallbladder cancer	MALAT1	MCL1	positively-E	luciferase reporter assay;RNA pull-down assay;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-363-3p)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143384	NA	378938	4170	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells. Furthermore, MALAT1 silencing decreased GBC cell proliferation and the S phase cell population and induced apoptosis in vitro. These data demonstrated that the MALAT1/miR-363-3p/MCL-1 regulatory pathway controls the progression of GBC.	27420766	RID01427	ceRNA or sponge
Malignant glioma	RP5-833A20.1	NFIA	negatively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-);cell cycle(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000237853	GRCh38_1:61248945-61253510	ENSG00000162599	NA	NA	4774	NA	BRMUTD|CTF|NF-I/A|NF1-A|NFI-A|NFI-L	Long non-coding RNA RP5-833A20.1 inhibits proliferation, metastasis and cell cycle progression by suppressing the expression of NFIA in U251 cells.The mRNA and protein levels of NFIA were markedly inhibited by overexpression of RP5-833A20.1 in the U251 cells.	27779670	RID01428	expression association
Lung adenocarcinoma	RMRP	miR-206	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000269900	GRCh38_9:35657751-35658018	NA	NA	6023	NA	CHH|NME1|RMRPR|RRP2	NA	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01429	expression association
Lung adenocarcinoma	RMRP	FMNL2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000157827	NA	6023	114793	CHH|NME1|RMRPR|RRP2	FHOD2	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01430	expression association
Lung adenocarcinoma	RMRP	KRAS	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000133703	NA	6023	3845	CHH|NME1|RMRPR|RRP2	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01431	expression association
Lung adenocarcinoma	RMRP	SOX9	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	oncogenic role(+);cell proliferation(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000125398	NA	6023	6662	CHH|NME1|RMRPR|RRP2	CMD1|CMPD1|SRA1|SRXX2|SRXY10	LncRNA-RMRP Acts as an Oncogene in Lung Cancer. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulation in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulation in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	27906963	RID01432	expression association
Osteosarcoma	LINC00161	IFIT2	positively-E	luciferase reporter assay;RIP	NA	NA	NA	NA	chemosensitivity(+);cisplatin-induced apoptosis process(+)	ceRNA(miR-645)	regulation	NA	cisplatin	NA	Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226935	GRCh38_21:28539318-28540355	ENSG00000119922	NA	118421	3433	C21orf100|Linc-USP16|NCRNA00161	G10P2|GARG-39|IFI-54|IFI-54K|IFI54|IFIT-2|ISG-54 K|ISG-54K|ISG54|P54|cig42	Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. the same sequence-specific binding of miR-645 to LINC00161 or IFIT2 3'UTR	27609068	RID01433	ceRNA or sponge
Hepatocellular carcinoma	lncRNA-Unigene56159	SNAI2	negatively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	sequencing;qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-645)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_3:78597238-79767998	ENSG00000019549	NA	NA	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells. We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues.Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug.	27597739	RID01434	ceRNA or sponge
Malignant glioma	CCAT1	miR-410	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1 promotes glioma cell proliferation via inhibiting microRNA-410. Luciferase reporter assay confirmed that CCAT1 targeted miR-410. Correlation analysis showed that CCAT1 expression was negatively related to miR-410 expression in glioma cancer tissues. In addition, down-regulation of miR-410 reversed the inhibitory effect of si-CCAT1 on glioma proliferation. These data demonstrated that lncRNA-CCAT1 promoted glioma cell proliferation via inhibiting miR-410, providing a new insight about the pathogenesis of glioma proliferation.	27765628	RID01435	ceRNA or sponge
Renal cell carcinoma	LNCARSR	YAP1	interact	RNA pull-down assay;RIP;RNA-FISH	upregulation	qRT-PCR	NA	NA	self-renewal(+);tumorigenesis(+);cell metastasis(+)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000137693	NA	112577459	10413	NA	COB1|YAP|YAP2|YAP65|YKI	A feed-forward loop between lncARSR and YAP activity promotes expansion of renal tumour-initiating cells.Knockdown of lncARSR attenuates the self-renewal, tumorigenicity and metastasis of renal T-ICs. Mechanistically,the binding of lncARSR to YAP impedes LATS1-induced YAP phosphorylation and facilitates YAP nuclear translocation.	27886176	RID01436	interact with protein
Hepatocellular carcinoma	linc-cdh4-2	CDH4	positively-F	RNAi;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_20:61252261-61940617	ENSG00000179242	NA	NA	1002	NA	CAD4|R-CAD|RCAD	Long non-coding RNA linc-cdh4-2 inhibits the migration and invasion of HCC cells by targeting R-cadherin pathway.Mechanistically, the linc cdh4-2 could up-regulate the protein level of R-cadherin through direct binding that might improve the protein stability. Over expression of linc-cdh4-2 could significantly increase the protein levels of R-cadherin and decrease the protein levels of small GTPase RAC1. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway.	27765630	RID01437	interact with protein
Hepatocellular carcinoma	linc-cdh4-2	RAC1	negatively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_20:61252261-61940617	ENSG00000136238	NA	NA	5879	NA	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA linc-cdh4-2 inhibits the migration and invasion of HCC cells by targeting R-cadherin pathway.Mechanistically, the linc cdh4-2 could up-regulate the protein level of R-cadherin through direct binding that might improve the protein stability. Over expression of linc-cdh4-2 could significantly increase the protein levels of R-cadherin and decrease the protein levels of small GTPase RAC1. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway.	27765630	RID01438	expression association
Malignant glioma	SNHG18	SEMA5A	negatively-E	RNAi;western blot;qRT-PCR	upregulation	microarray;qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000250786	GRCh38_5:9546200-9550609	ENSG00000112902	NA	100505806	9037	NA	SEMAF|semF	Upregulation of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 Promotes Radioresistance of Glioma by Repressing Semaphorin 5A.	27788958	RID01439	expression association
Cholangiocarcinoma	H19	IL6	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	sequencing;qRT-PCR	GSE76743;GSE57539;GSE67106;GSE55146	GSE76743.zip;GSE57539.zip;GSE67106.zip;GSE55146.zip	cell migration(+);cell invasion(+)	ceRNA(let-7a;let-7b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136244	NA	283120	3569	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	27809873	RID01440	ceRNA or sponge
Cholangiocarcinoma	HULC	CXCR4	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	sequencing;qRT-PCR	GSE76743;GSE57539;GSE67106;GSE55146	GSE76743.zip;GSE57539.zip;GSE67106.zip;GSE55146.zip	cell migration(+);cell invasion(+)	ceRNA(miR-372;miR-373)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000121966	NA	728655	7852	HCCAT1|LINC00078|NCRNA00078	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	27809873	RID01441	ceRNA or sponge
Gastric cancer	SNHG5	MTA2	interact	RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	epigenetic regulation	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000149480	NA	387066	9219	C6orf160|LINC00044|NCRNA00044|U50HG	MTA1L1|PID	Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex.	27065326	RID01442	epigenetic regulation
Colorectal cancer	H19	RB1	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139687	NA	283120	5925	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01443	expression association
Colorectal cancer	H19	E2F1	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000101412	NA	283120	1869	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	E2F-1|RBAP1|RBBP3|RBP3	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01444	expression association
Colorectal cancer	H19	CDK8	positively-E	RNAi	upregulation	sequencing	TCGA	COAD.zip	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000132964	NA	283120	1024	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	K35	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	27789274	RID01445	expression association
Colorectal cancer	H19	CTNNB1	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell growth;cell migration(+)	ceRNA(miR-200a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168036	NA	283120	1499	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing beta-Catenin Expression in Colorectal Cancer. H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues.beta-Catenin was identified as a target gene of miR-200a. H19 regulated beta-catenin expression and activity by competitively binding to miR-200a. H19 promotes cell proliferation by competitively binding to miR-200a and derepressing beta-catenin in CRC. H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-beta-Catenin Signaling in Colorectal Cancer.Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. A scheme of H19 action: we provided additional insights of H19 on Rb-E2F1 signaling and CDK-beta-catenin activity. We propose that H19 interacts with macroH2A, and this may consequently lead to de-repression of genes including CDK8, CDK4, and CCND1. Increased CDK4-cyclin D1 complex phosphorylates Rb to disrupt Rb-E2F1 interaction, leading to E2F1 activation. The increase of CDK8 expression enhances the function of mediator complex including MED1, and facilitates the gene regulation by beta-catenin. These downstream targets could work in a synergistic way of promoting cell proliferation and increasing cell motility in CRC.	28164117;27789274	RID01446	ceRNA or sponge
Hepatocellular carcinoma	GIHCG	miR-200b	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01447	epigenetic regulation
Hepatocellular carcinoma	GIHCG	miR-200a	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01448	epigenetic regulation
Hepatocellular carcinoma	GIHCG	miR-429	negatively-E	ChIRP;qRT-PCR	upregulation	microarray;qRT-PCR	GSE54238;GSE55191;GSE58043	GSE54238.zip;GSE55191.zip;GSE58043.zip	cancer progression(+);cell proliferation(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000257698	GRCh38_12:57930115-57936345	NA	NA	100506844	NA	NA	NA	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID01449	epigenetic regulation
Hepatocellular carcinoma	HOTAIR	miR-1	negatively-F	luciferase reporter assay;RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues; The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1.	27895772	RID01450	ceRNA or sponge
Esophageal cancer	UCA1	SOX4	positively-E	RNAi;qRT-PCR;western blot;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124766	NA	652995	6659	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	EVI16	lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer.Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA).	27667646	RID01451	ceRNA or sponge
Breast cancer	UCA1	HIF1A	positively-E	qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	ceRNA(miR-18a)	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000100644	NA	652995	3091	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1alpha feedback regulatory loop.The upregulation UCA1 sponges miR-18a, which is a negative regulator of HIF1alpha. One recent study found that miR-18a can directly targetthree prime untranslated region (3'UTR)of HIF1alpha and suppresses its expression.	27629141	RID01453	ceRNA or sponge
Colon cancer	HULC	NKD2	negatively-E	RIP;RNA pull-down assay;RNAi;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000145506	NA	728655	85409	HCCAT1|LINC00078|NCRNA00078	Naked2	Long noncoding RNA HULC promotes colorectal carcinoma progression through epigenetically repressing NKD2 expression. Mechanistically, RNA immunoprecipitation (RIP) and RNA pull-down experiment demonstrated that HULC could simultaneously interact with EZH2 to repress underlying targets NKD2 transcription. In addition, rescue experiments determined that HULC oncogenic function is partly dependent on repressing NKD2.	27496341	RID01454	epigenetic regulation
Malignant glioma	H19	VASH2	positively-E	RNAi;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-29a)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000143494	NA	283120	79805	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a.Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a. In addition, miR-29a targeted 3'-UTR region of vasohibin 2 (VASH2) and decreased its expression. VASH2 has been identified as an angiogenic factor. Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a. In conclusion, the results indicated that knockdown of H19 suppressed glioma induced angiogenesis by inhibiting microRNA-29a, which may modulate the onset of glioma by regulating biological behaviors of glioma vascular endothelial cells.	27543358	RID01455	ceRNA or sponge
Liver cancer	HULC	TERF2	positively-E	ChIP;western blot;qRT-PCR;luciferase reporter assay;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000132604	NA	728655	7014	HCCAT1|LINC00078|NCRNA00078	NA	HULC cooperates with MALAT1 to aggravate liver cancer stem cells growth through telomere repeat-binding factor 2. Mechanistically, both HULC and MALAT1 overexpression enhanced RNA polII, P300,CREPT to load on the promoter region of telomere repeat-binding factor 2(TRF2), triggering the overexpression, phosphorylation and SUMOylation of TRF2.	27782152	RID01456	transcriptional regulation
Liver cancer	MALAT1	TERF2	positively-E	ChIP;western blot;qRT-PCR;luciferase reporter assay;Co-immunoprecipitation	upregulation	qRT-PCR	NA	NA	cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132604	NA	378938	7014	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	HULC cooperates with MALAT1 to aggravate liver cancer stem cells growth through telomere repeat-binding factor 2.Mechanistically, both HULC and MALAT1 overexpression enhanced RNA polII, P300,CREPT to load on the promoter region of telomere repeat-binding factor 2(TRF2), triggering the overexpression, phosphorylation and SUMOylation of TRF2.	27782152	RID01457	transcriptional regulation
Non-small cell lung cancer	FENDRR	EZH2	interact	RIP	downregulation	qRT-PCR;microarray	NA	NA	cell metastasis(-);cell migration(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Limitless Replicative Potential;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000106462	NA	400550	2146	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Loss of long noncoding RNA FOXF1-AS1 regulates epithelial-mesenchymal transition, stemness and metastasis of non-small cell lung cancer cells.Interestingly, we found that FOXF1-AS1 physically associates with PRC2 components EZH2 and loss of FOXF1-AS1 mediates cell migration and stem-like properties require EZH2. These results suggested that FOXF1-AS1 might regulate EMT, stemness and metastasis of NSCLC cells via EZH2, indicating it as a therapeutic target for future treatment of NSCLC.	27577075	RID01458	interact with protein
Hepatocellular carcinoma	FTX	miR-374a	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000230590	GRCh38_X:73940435-74293574	NA	NA	100302692	NA	LINC00182|MIR374AHG|NCRNA00182	NA	Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/beta-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells. In conclusion, these findings suggest that lnc-FTX may act as a tumor suppressor in HCC through physically binding miR-374a and MCM2. It may also be one of the reasons for HCC gender disparity and may potentially contribute to HCC treatment.	27065331	RID01459	ceRNA or sponge
Hepatocellular carcinoma	FTX	MCM2	interact	RIP	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000073111	NA	100302692	4171	LINC00182|MIR374AHG|NCRNA00182	BM28|CCNL1|CDCL1|D3S3194|DFNA70|MITOTIN|cdc19	Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/beta-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells. In conclusion, these findings suggest that lnc-FTX may act as a tumor suppressor in HCC through physically binding miR-374a and MCM2. It may also be one of the reasons for HCC gender disparity and may potentially contribute to HCC treatment.	27065331	RID01460	interact with protein
Liver cancer	UCA1	TP53	interact	RIP	upregulation	RT-PCR	NA	NA	cell growth(+)	interact with protein;mutation(N340Q/L344R)	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000141510	NA	652995	7157	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCC7|BMFS5|LFS1|P53|TRP53	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR. P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1-(TERT-HOTAIR-TERRA).	27167190	RID01461	interact with protein
Liver cancer	UCA1	PIM1	positively-E	ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell growth(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000137193	NA	652995	5292	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	PIM	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR.P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1- (TERT-HOTAIR-TERRA).	27167190	RID01462	epigenetic regulation
Liver cancer	UCA1	PKM	positively-E	RIP;ChIP;luciferase reporter assay	upregulation	RT-PCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000067225	NA	652995	5315	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR.P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation.Moreover, the combination of H3K9me1 and HP1 alpha forms more H3K9me3-HP1alpha complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1alpha)-Pim1- (TERT-HOTAIR-TERRA).	27167190	RID01463	transcriptional regulation
Breast cancer	BRCA1	NEAT1	negatively-E	RNAi;western blot;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protien-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000012048	NA	ENSG00000245532	GRCh38_11:65422774-65445540	672	283131	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	LINC00084|NCRNA00084|TncRNA|VINC	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis.In this study, we delineate the role of the novel BRCA1/lncRNA NEAT1 signaling axis in breast tumorigenesis. BRCA1 inhibits NEAT1 expression potentially through binding to its genomic binding site upstream of the NEAT1 gene. BRCA1 deficiency in human normal/cancerous breast cells and mouse mammary glands leads to NEAT1 overexpression. Our studies show that NEAT1 upregulation resulting from BRCA1 deficiency stimulates in vitro and in vivo breast tumorigenicity.	27556296	RID01464	transcriptional regulation
Breast cancer	NEAT1	miR-129-5p	negatively-E	luciferase reporter assay;RNAi;qRT-PCR;ChIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency	27556296	RID01465	epigenetic regulation
Breast cancer	NEAT1	WNT4	positively-E	western blot;RNAi	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000162552	NA	283131	54361	LINC00084|NCRNA00084|TncRNA|VINC	SERKAL|WNT-4	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency	27556296	RID01466	expression association
Colorectal cancer	LINC01133	SRSF6	interact	RIP;western blot;RNA pull-down assay	downregulation	microarray	NA	NA	cell metastasis(-);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124193	NA	100505633	6431	NA	B52|HEL-S-91|SFRS6|SRP55	Long non-coding RNA LINC01133 inhibits epithelial-mesenchymal transition and metastasis in colorectal cancer by interacting with SRSF6. we confirmed that the EMT process was regulated by LINC01133 in CRC cells dependent on the presence of SRSF6. These data suggest that LINC01133 inhibits the EMT and metastasis by directly binding to SRSF6 as a target mimic, and may serve as a prognostic biomarker and an effective target for anti-metastasis therapies for CRC.	27443606	RID01467	interact with protein
Gastric cancer	LINC-ROR	POU5F1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000204531	NA	100885779	5460	ROR|lincRNA-RoR|lincRNA-ST8SIA3	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01468	expression association
Gastric cancer	LINC-ROR	SOX2	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000181449	NA	100885779	6657	ROR|lincRNA-RoR|lincRNA-ST8SIA3	ANOP3|MCOPS3	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01469	expression association
Gastric cancer	LINC-ROR	NANOG	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000111704	NA	100885779	79923	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01470	expression association
Gastric cancer	LINC-ROR	PROM1	positively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell stemness(+)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000007062	NA	100885779	8842	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC. Our data demonstrated that lncRNA ROR was associated with core stemness transcriptional factors and the pluripotent state of GCSCs.	27602437	RID01471	expression association
Hepatocellular carcinoma	GPC3-AS1	GPC3	positively-E	RNA pull-down assay;ChIP;RIP;ChIRP	upregulation	qRT-PCR	NA	NA	cancer progression(+);cell proliferation(+);cell migration(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000286096	GRCh38_X:133897443-133897934	ENSG00000147257	NA	110806308	2719	NA	DGSX|GTR2-2|MXR7|OCI-5|SDYS|SGB|SGBS|SGBS1	Long noncoding RNA glypican 3 (GPC3) antisense transcript 1 promotes hepatocellular carcinoma progression via epigenetically activating GPC3. Furthermore, we found that GPC3-AS1 physically associated with P300/CBP-associated factor and recruited it to the GPC3 gene body region, consequently inducing an increase in euchromatic histone marks and activating GPC3 transcription. Moreover, the effects of GPC3-AS1 on HCC cell proliferation and migration were dependent on the upregulation of GPC3.	27573079	RID01472	epigenetic regulation
Osteosarcoma	MFI2	FOXP4	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	lncRNA	TF	NA	GRCh38_3:196987559-197029816	ENSG00000137166	NA	NA	116113	NA	hFKHLA	Overexpression of long non-coding RNA MFI2 promotes cell proliferation and suppresses apoptosis in human osteosarcoma.Furthermore, the expression of forkhead box P4 (FOXP4) was significantly increased and it was positively associated with lncRNA MFI2 expression in tumor tissues. All the results indicated lncRNA MFI2 could promote proliferation and migration of osteosarcoma cells by regulating FOXP4 expression, which suggested critical roles of lncRNA MFI2 and FOXP4 in occurrence and development of human osteosarcoma.	27513470	RID01473	expression association
Osteosarcoma	BCAR4	GLI2	positively-E	ChIRP;luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000074047	NA	400500	2736	NA	CJS|HPE9|PHS2|THP1|THP2	Long noncoding RNA BCAR4 promotes osteosarcoma progression through activating GLI2-dependent gene transcription. Chromatin isolation by RNA purification assay showed that BCAR4 physically associates with the promoters of GLI2 target genes.	27460090	RID01474	transcriptional regulation
Lung adenocarcinoma	HOTAIR	miR-326	negatively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1. Decreased miR-326 expression was also detected in tumor tissues sampled from LAD patients treated with cisplatin-based chemotherapy and was proved to be correlated with high expression of SP1 and decreased sensitivity to cisplatin. Furthermore, we show that the long noncoding RNA HOTAIR repression reverses chemoresistance of LAD cells partially through modulation of miR-326/SP1 pathway. In summary, we unveil a branch of the HOTAIR/miR-326/SP1 pathway that regulates chemoresistance of LAD cells. Results showed that si-HOTAIR increased miR-326 expression (Fig.6b) and synergistically reduced SP1 expression (Fig.6c),ultimately enhanced sensitivity to cisplatin in A549/CDDPcells. HOTAIR regulates cisplatin resistance via miR-326/SP1 pathway.	27460077	RID01475	expression association
Lung adenocarcinoma	HOTAIR	SP1	negatively-E	RNAi;western blot;qRT-PCR	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000185591	NA	100124700	6667	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1. Decreased miR-326 expression was also detected in tumor tissues sampled from LAD patients treated with cisplatin-based chemotherapy and was proved to be correlated with high expression of SP1 and decreased sensitivity to cisplatin. Furthermore, we show that the long noncoding RNA HOTAIR repression reverses chemoresistance of LAD cells partially through modulation of miR-326/SP1 pathway. In summary, we unveil a branch of the HOTAIR/miR-326/SP1 pathway that regulates chemoresistance of LAD cells. Results showed that si-HOTAIR increased miR-326 expression (Fig.6b) and synergistically reduced SP1 expression (Fig.6c),ultimately enhanced sensitivity to cisplatin in A549/CDDPcells. HOTAIR regulates cisplatin resistance via miR-326/SP1 pathway.	27460077	RID01476	expression association
Melanoma	MALAT1	MMP14	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000157227	NA	378938	4323	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.	27564100	RID01477	ceRNA or sponge
Melanoma	MALAT1	SNAI1	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-22)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124216	NA	378938	6615	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.	27564100	RID01478	ceRNA or sponge
Hepatocellular carcinoma	CAMTA1-DT	CAMTA1	negatively-E	RNAi;qRT-PCR;western blot;ChIRP	upregulation	microarray;qRT-PCR	GSE58043;GSE55191	GSE58043.zip;GSE55191.zip	cell proliferation(+)	epigenetic regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Limitless Replicative Potential	Cancer	Liver cancer	lncRNA	TF	ENSG00000237436	GRCh38_1:6783892-6784843	ENSG00000171735	NA	110841581	23261	lncCAMTA1	CANPMR	Long Noncoding RNA lncCAMTA1 Promotes Proliferation and Cancer Stem Cell-Like Properties of Liver Cancer by Inhibiting CAMTA1. Mechanistically, we demonstrated that lncCAMTA1 physically associates with the calmodulin binding transcription activator 1 (CAMTA1) promoter, induces a repressive chromatin structure, and inhibits CAMTA1 transcription.	27669232	RID01479	epigenetic regulation
Malignant glioma	NEAT1	NRAS	positively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	ceRNA(let-7e)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000213281	NA	283131	4893	LINC00084|NCRNA00084|TncRNA|VINC	ALPS4|CMNS|N-ras|NCMS|NRAS1|NS6	Knockdown of NEAT1 restrained the malignant progression of glioma stem cells by activating microRNA let-7e.A potential binding region between NEAT1 and microRNA let-7e was confirmed by dual-luciferase assays. Upregulation of NEAT1 reduced the expression of let-7e. NEAT1 knockdown and let-7e overexpression both reduced NRAS protein expression. NRAS was identified as a direct target of let-7e and promoted oncogenesis in GSCs.	27556696;26306906	RID01480	ceRNA or sponge
Non-small cell lung cancer	XIST	KLF2	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell growth(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000127528	NA	7503	10365	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	LKLF	Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression.Mechanistically, RNA immune-precipitation (RIP) and RNA pull-down experiment demonstrated that XIST could simultaneously interact with EZH2 to suppress transcription of its potential target KLF2.	27501756	RID01481	epigenetic regulation
Endometrial carcinoma	FER1L4	PTEN	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-);cell cycle(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA FER1L4 suppresses cancer cell proliferation and cycle by regulating PTEN expression in endometrial carcinoma. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition. We conclude that one mechanism by which lncRNAs function in in tumorigenesis is as ceRNAs for tumor suppressor mRNAs.	27381864	RID01482	ceRNA or sponge
Gallbladder cancer	miR-17-3p	GCASPC	negatively-F	luciferase reporter assay;RNAi;RNA pull-down assay	downregulation	microarray;qRT-PCR	GSE62335	GSE62335.zip	cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gallbladder cancer	miRNA	lncRNA	NA	NA	ENSG00000224073	GRCh38_6:159639307-159640101	NA	112441427	NA	lnc-SOD2-1	Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase-Dependent Cell Proliferation in Gallbladder Cancer.	27450454	RID01483	ceRNA or sponge
Gastric cancer	KRT7-AS	KRT7	positively-F	RNAi;qRT-PCR;western blot;RIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000257671	GRCh38_12:52245048-52247448	ENSG00000135480	NA	109729127	3855	NA	CK7|K2C7|K7|SCL	Long non-coding antisense RNA KRT7-AS is activated in gastric cancers and supports cancer cell progression by increasing KRT7 expression.KRT7-AS formed an RNA-RNA hybrid with KRT7 and controlled KRT7 expression at both the mRNA and the post-transcriptional levels.We conclude that lncRNA KRT7-AS promotes GC, at least in part, by increasing KRT7 expression.	26876208	RID01484	interact with mRNA
Gastric cancer	XIST	EZH2	positively-E	luciferase reporter assay;RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cancer progression(+)	ceRNA(miR-101)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression. Furthermore, an inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted.	27620004	RID01485	ceRNA or sponge
Acute myeloid leukemia	linc-223	IRF4	positively-E	luciferase reporter assay;qRT-PCR	upregulation	qRT-PCR	NA	NA	cell differentiation(-);tumorigenesis(-)	ceRNA(miR-125-5p)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	TF	ENSG00000274536	GRCh38_X:66015461-66020422	ENSG00000137265	NA	NA	3662	NA	LSIRF|MUM1|NF-EM5|SHEP8	The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA. Here, we identify the host transcript of miR-223, linc-223, as a novel functional long non-coding RNA (lncRNA) in AML. We also demonstrate that endogenous linc-223 localizes in the cytoplasm and acts as a competing endogenous RNA for miR-125-5p, an oncogenic microRNA in leukemia. Among the validated miR-125-5p target mRNAs, we focused on the transcription factor IRF4 (interferon regulatory factor 4).In particular, we show that linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo.Therein, these findings indicate that the newly identified lncRNA linc-223 may have an important role in myeloid differentiation and leukemogenesis, at least in part, by cross-talking with IRF4 mRNA.	27517498	RID01486	ceRNA or sponge
Colorectal cancer	CLMAT3	CDKN1B	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249035	GRCh38_5:151676945-151725473	ENSG00000111276	NA	101927096	1027	CTB-113P19.1|SPARC-AS1	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Downregulated long non-coding RNA CLMAT3 promotes the proliferation of colorectal cancer cells by targeting regulators of the cell cycle pathway. In this study, we demonstrate that lncRNA-CLMAT3 expression was significantly increased in colorectal cancer cells compared with a normal intestinal mucous cell line and that inhibition of lncRNA-CLMAT3 suppressed colorectal cancer cell proliferation in vitro. We also found that this reduced colorectal cancer cell proliferation due to lncRNA-CLMAT3 knockdown is associated with G0/G1 cell-cycle arrest induction and apoptosis enhancement. Furthermore, lncRNA-CLMAT3 knockdown enhanced Cdh1 expression and resulted in p27Kip accumulation via increased Skp2 protein ubiquitination.	27391344	RID01487	expression association
Colorectal cancer	CLMAT3	CDH1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249035	GRCh38_5:151676945-151725473	ENSG00000039068	NA	101927096	999	CTB-113P19.1|SPARC-AS1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Downregulated long non-coding RNA CLMAT3 promotes the proliferation of colorectal cancer cells by targeting regulators of the cell cycle pathway. In this study, we demonstrate that lncRNA-CLMAT3 expression was significantly increased in colorectal cancer cells compared with a normal intestinal mucous cell line and that inhibition of lncRNA-CLMAT3 suppressed colorectal cancer cell proliferation in vitro. We also found that this reduced colorectal cancer cell proliferation due to lncRNA-CLMAT3 knockdown is associated with G0/G1 cell-cycle arrest induction and apoptosis enhancement. Furthermore, lncRNA-CLMAT3 knockdown enhanced Cdh1 expression and resulted in p27Kip accumulation via increased Skp2 protein ubiquitination.	27391344	RID01488	expression association
Lung cancer	CAR10	EGFR	positively-E	RNAi;qRT-PCR;western blot	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000148848	GRCh38_10:126012381-126388455	ENSG00000146648	NA	NA	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. The lncRNA CAR intergenic 10 (CAR10) was up-regulated. CAR10 bound and stabilized transcription factor Y-box-binding protein 1 (YB-1), leading to up-regulation of the epidermal growth factor receptor (EGFR) and proliferation of lung cancer cells. Knockdown of CAR10 inhibited cell growth in vitro and tumor growth in vivo. These results demonstrate the role of lncRNAs in environmental lung carcinogenesis, and CAR10-YB-1 represents a potential therapeutic target.	27322209	RID01489	expression association
Lung cancer	CAR10	YBX1	interact	RNAi;RNA pull-down assay;RIP	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+);tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000148848	GRCh38_10:126012381-126388455	ENSG00000065978	NA	NA	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. The lncRNA CAR intergenic 10 (CAR10) was up-regulated. CAR10 bound and stabilized transcription factor Y-box-binding protein 1 (YB-1), leading to up-regulation of the epidermal growth factor receptor (EGFR) and proliferation of lung cancer cells. Knockdown of CAR10 inhibited cell growth in vitro and tumor growth in vivo. These results demonstrate the role of lncRNAs in environmental lung carcinogenesis, and CAR10-YB-1 represents a potential therapeutic target.	27322209	RID01490	interact with protein
Hepatocellular carcinoma	XIST	PDK1	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+)	ceRNA(miR-139-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000152256	NA	7503	5163	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma. In this study, we found that XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p. We proposed that XIST was responsible for hepatocellular carcinoma cell proliferation, and XIST exerted its function through the miR-139-5p/PDK1 axis.	28231734	RID01491	ceRNA or sponge
Non-small cell lung cancer	TRPM2-AS	SHC1	negatively-E	RNAi;qRT-PCR;western blot	upregulation	sequencing	TCGA	LUSC_LUAD.zip	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230061	GRCh38_21:44414588-44425272	ENSG00000160691	NA	101928607	6464	TRPM2-AS1	SHC|SHCA	Downregulation of a novel long noncoding RNA TRPM2-AS promotes apoptosis in non-small cell lung cancer. Here, we identified a novel long noncoding RNA TRPM2-AS from published dataset and found TRPM2-AS is widely upregulated in non-small cell lung cancer tissues compared with adjacent non-tumor tissues. Further experiments showed that silence of TRPM2-AS upregulated SHC1 and silence of SHC1 partially reversed cell apoptosis after TRPM2-AS knockdown. In summary, the novel long noncoding RNA TRPM2-AS upregulated in non-small cell lung cancer, and downregulation of TRPM2-AS promotes apoptosis in vitro.	28231726	RID01492	expression association
Colorectal adenocarcinoma	miR-491-5p	PRINS	negatively-F	luciferase reporter assay	downregulation	qRT-PCR	NA	NA	apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	NA	GRCh38_10:24247125-24256046	NA	100169750	NA	NCRNA00074	TFF3-dependent resistance of human colorectal adenocarcinoma cells HT-29/B6 to apoptosis is mediated by miR-491-5p regulation of lncRNA PRINS. In silico-based expression analysis revealed TFF3-mediated regulation of selected microRNAs as well as long non-coding RNAs (lncRNAs), whereas miR-491-5p was identified to target the lncRNA 'psoriasis susceptibility-related RNA gene induced by stress' (PRINS).Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS. Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS.	28149533	RID01493	ceRNA or sponge
Breast cancer	HOTAIR	TP53	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	self-renewal(+);cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141510	NA	100124700	7157	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCC7|BMFS5|LFS1|P53|TRP53	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024;28407576	RID01494	expression association
Breast cancer	HOTAIR	CDKN1A	negatively-E	RNAi;qRT-PCR;western blot	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124762	NA	100124700	1026	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024	RID01495	expression association
Breast cancer	HOTAIR	SOX2	positively-E	RNAi;qRT-PCR;western blot;ChIP	upregulation	qRT-PCR	NA	NA	self-renewal(+);cell proliferation(+);cell invasion(+)	ceRNA(miR-34a)	regulation	NA	NA	CSC	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000181449	NA	100124700	6657	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ANOP3|MCOPS3	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity,Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.Moreover, full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a.Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a. Interestingly, tight transcriptional regulation of p53 by HOTAIR was found; accordingly, p21 is indirectly regulated by HOTAIR, resulting in cell cycle entry.These results suggest that HOTAIR is a key regulator of proliferation, colony formation, invasion and self-renewal capacity in breast CSCs, which occurs in part through regulation of Sox2 and p53.	28122024;25512558	RID01496	ceRNA or sponge
Neuroblastoma	GAS5	BRCA1	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000012048	NA	60674	672	NCRNA00030|SNHG2	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma.Global sequencing and ELISA arrays revealed that the loss of GAS5 induced p53, BRCA1, and GADD45A, which appeared to modulate cell cycle arrest in concert. Complementation with only the FL GAS5 clone could rescue cell cycle arrest, stabilizing HDM2, and leading to the loss of p53.	28035057	RID01497	expression association
Neuroblastoma	GAS5	TP53	negatively-E	RNAi;qRT-PCR;western blot	downregulation	qRT-PCR	NA	NA	cell cycle(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	BCC7|BMFS5|LFS1|P53|TRP53	The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma.Global sequencing and ELISA arrays revealed that the loss of GAS5 induced p53, BRCA1, and GADD45A, which appeared to modulate cell cycle arrest in concert. Complementation with only the FL GAS5 clone could rescue cell cycle arrest, stabilizing HDM2, and leading to the loss of p53.	28035057	RID01498	expression association
Lung adenocarcinoma	CYTOR	IL24	negatively-E	RIP;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000162892	NA	112597	11009	C2orf59|LINC00152|NCRNA00152	C49A|FISP|IL10B|MDA7|MOB5|ST16	Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression.LINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. EZH2 was shown to bind the promoter region of IL24, while LINC00152 knockdown reduced the histone H3 lysine 27 trimethylation (H3K27me3) occupancy of the IL24 promoter locus (Fig. 5h). However, LSD1 did not bind the IL24 promoter locus (Additional file 5: Figure S3d). These results indicated that LINC00152 repression of target IL24 expression occured, at least partially, through interaction with EZH2.	28109288	RID01499	epigenetic regulation
Breast cancer	H19	LIN28A	positively-E	luciferase reporter assay;RNAi	downregulation	qPCR	NA	NA	cell stemness(+)	ceRNA(let-7)	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Breast cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000131914	NA	283120	79727	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.Here we show that breast cancer stem cells (BCSCs) express high levels of H19. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples.	28102845	RID01500	ceRNA or sponge
Glioblastoma	TUG1	VEGFA	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-299)	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	LINC00080|NCRNA00080|TI-227H	MVCD1|VEGF|VPF	Long non-coding RNA taurine upregulated 1 enhances tumor-induced angiogenesis through inhibiting microRNA-299 in human glioblastoma.Bioinformatics analysis and luciferase reporter assay revealed that TUG1 influenced tumor angiogenesis via directly binding to the miR-299 and there was a reciprocal repression between TUG1 and miR-299 in the same RNA-induced silencing complex. Moreover, knockdown of TUG1 reduced the expression of vascular endothelial growth factor A (VEGFA), which was defined as a functional downstream target of miR-299.Overall, the results demonstrated that TUG1 enhances tumor-induced angiogenesis and VEGF expression through inhibiting miR-299. Also, the inhibition of TUG1 could provide a novel therapeutic target for glioblastoma treatment.	27345398	RID01501	ceRNA or sponge
Papillary thyroid carcinoma	HIT000218960	HMGA2	negatively-E	western blot;RNAi	downregulation	qPCR;microarray	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	TF	NA	GRCh38_12:66352406-66352634	ENSG00000149948	NA	NA	8091	NA	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long noncoding RNA HIT000218960 promotes papillary thyroid cancer oncogenesis and tumor progression by upregulating the expression of high mobility group AT-hook 2 (HMGA2) gene.In the microarray data, we observed that a newly identified lncRNA, HIT000218960, was significantly upregulated in PTC tissues and associated with a well-known oncogene, high mobility group AT-hook 2 (HMGA2) gene. Both in normal thyroid tissues and PTC tissues, the expression of HIT000218960 was significantly positively correlated with that of HMGA2 mRNA. Those findings suggest that HIT000218960 might acts as a tumor promoter through regulating the expression of HMGA2.	27929737	RID01502	expression association
Gastric cancer	XIST	MACC1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	ceRNA(miR-497)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000183742	NA	7503	346389	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	7A5|SH3BP4L	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.In the present study, we found that XIST expression was significantly increased in GC tissues and cell lines. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis.	27911852	RID01503	ceRNA or sponge
Papillary thyroid carcinoma	PTCSC2	FOXE1	negatively-F	luciferase reporter assay;RIP;ChIP	downregulation	qPCR;sequencing	TCGA	THCA.zip	p53 signaling pathway(-);predisposition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Thyroid cancer	lncRNA	TF	ENSG00000236130	GRCh38_9:97699625-97853080	ENSG00000178919	NA	101928337	2304	NA	FKHL15|FOXE2|HFKH4|HFKL5|NMTC4|TITF2|TTF-2|TTF2	MYH9 binds to lncRNA gene PTCSC2 and regulates FOXE1 in the 9q22 thyroid cancer risk locus. We propose that the interaction between the lncRNA, its binding protein MYH9, and the coding gene FOXE1 underlies the predisposition to PTC triggered by rs965513.	28049826	RID01504	interact with protein
Colorectal cancer	CRNDE	TCF4	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	5-fluorouracil;oxaliplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000196628	NA	NA	6925	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	E2-2|FECD3|ITF-2|ITF2|PTHS|SEF-2|SEF2|SEF2-1|SEF2-1A|SEF2-1B|SEF2-1D|TCF-4|bHLHb19	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/beta-catenin signaling.In this study, we found that the expression levels of the CRNDE were upregulated in CRC clinical tissue samples.We identified microRNA miR-181a-5p as an inhibitory target of CRNDE.CRNDE binds to miR-181a-5p and represses its expression. We also determined that beta-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/beta-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression.We found that CRNDE knockdown (Fig. 4a) and miR-181a-5p overexpression (Fig. 4b) appeared to increase the sensitivity of CRC cells to 5-Fu treatment and therefore further inhibited cell growth. Consistently, CRNDE knockdown (Fig. 4c) and miR-181a-5p overexpression (Fig. 4d) led to increased sensitivity of CRC cells to Oxa treatment, and CRNDE overexpression (Additional file 4c) and miR-181a-5p knockdown (Additional file 4d) led to decreased Oxa sensitivity of CRC cells.	28086904	RID01505	ceRNA or sponge
Colorectal cancer	CRNDE	CTNNB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-181a-5p)	regulation	NA	5-fluorouracil;oxaliplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000168036	NA	NA	1499	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/beta-catenin signaling.In this study, we found that the expression levels of the CRNDE were upregulated in CRC clinical tissue samples.We identified microRNA miR-181a-5p as an inhibitory target of CRNDE.CRNDE binds to miR-181a-5p and represses its expression. We also determined that beta-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/beta-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression.We found that CRNDE knockdown (Fig. 4a) and miR-181a-5p overexpression (Fig. 4b) appeared to increase the sensitivity of CRC cells to 5-Fu treatment and therefore further inhibited cell growth. Consistently, CRNDE knockdown (Fig. 4c) and miR-181a-5p overexpression (Fig. 4d) led to increased sensitivity of CRC cells to Oxa treatment, and CRNDE overexpression (Additional file 4c) and miR-181a-5p knockdown (Additional file 4d) led to decreased Oxa sensitivity of CRC cells.	28086904	RID01506	ceRNA or sponge
Hepatocellular carcinoma	SNHG12	MAP3K11	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);tumorigenesis(+);cell metastasis(+)	ceRNA(miR-199a-5p;miR-199b-5p)	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000173327	NA	85028	4296	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma.SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues. There were direct interactions between miR-199a/b-5p and the binding site of SNHG12. SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-kB pathway. Eventually, SNHG12 was able to modulate the expression of the miR-199a/b-5p target gene, MLK3, and thus affected the NF-kB pathway.	28073380	RID01507	ceRNA or sponge
Melanoma	MALAT1	ITGB1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-183)	regulation	NA	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150093	NA	378938	3688	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation.Previous studies have demonstrated that MALAT1 (metastasis associated with lung adenocarcinoma transcript-1, also named NEAT2) is over-expressed in multiple carcinomas, consistent with our findings as it was increased in melanoma cancer tissues and cells (Figure 3A and 3B). We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin beta1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1. Collectively, we found a new signaling pathway promoting melanoma development by MALAT1-miR-183-ITGB1 axis, which may be clinically valuable as new targets for malignant melanoma therapy.	27966454	RID01508	ceRNA or sponge
Small cell lung cancer	TUG1	LIMK2	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+)	histone modification	regulation	NA	cisplatin;adriamycin;etoposide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000182541	NA	55000	3985	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 is involved in cell growth and chemoresistance of small cell lung cancer by regulating LIMK2b via EZH2.We found that TUG1 was overexpressed in SCLC tissues.We further demonstrated that TUG1 can regulate the expression of LIMK2b (a splice variant of LIM-kinase 2) via binding with enhancer of zeste homolog 2 (EZH2), and then promoted cell growth and chemoresistance of SCLC.After knockdown of TUG1, the IC50 values of H446DDP and H69AR cells significantly decreased with treatment of chemotherapeutic drugs including DDP, ADM or VP-16 (Fig. 4a). Three chemotherapy drugs [Cisplatin (DDP; Shandong, China), Adriamycin (ADM; Jiangsu, China) Etoposide (VP-16; Jiangsu, China),] were used. Furthermore, we conducted ChIP assays and found that knockdown of TUG1 decreased the binding of EZH2 and H3K27me3 levels across the LIMK2b promoter compared to cells transfected with siNC (Fig. 6f). Taken together, these data suggest that TUG1 is required to target EZH2 occupancy and activity to epigenetically modulate the expression of LIMK2b.	28069000	RID01509	epigenetic regulation
Lung cancer	MEG3	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000039068	NA	55384	999	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression.	27852821	RID01510	epigenetic regulation
Lung cancer	MEG3	miR-200b	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01511	epigenetic regulation
Lung cancer	MEG3	miR-200a	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01512	epigenetic regulation
Lung cancer	MEG3	miR-429	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01513	epigenetic regulation
Lung cancer	MEG3	miR-200c	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01514	epigenetic regulation
Lung cancer	MEG3	miR-141	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID01515	epigenetic regulation
Laryngeal squamous cell carcinoma	HOTAIR	EZH2	interact	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The role of long non-coding RNA HOTAIR in the progression and development of laryngeal squamous cell carcinoma interacting with EZH2.HOTAIR and EZH2 were over-expressed in LSCC tissue. The higher expression was significantly related to T phase, pathological grades, and risk of lymphatic metastasis of LSCC. Suppressing HOTAIR expression stimulated EZH2 expressing, promoted the proliferation of AMC-HN8 cells, and increased the sensitivity to cis-platinum of the LSCC cells.	27542077	RID01516	interact with protein
Gastric cancer	MALAT1	GLI2	positively-E	luciferase reporter assay;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-202)	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000074047	NA	378938	2736	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CJS|HPE9|PHS2|THP1|THP2	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression.We found that MALAT1 was upregulated in GC tissues and higher MALAT1 expression was correlated with larger tumor size, lymph node metastasis, and TNM stage. Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202.	27887846	RID01517	ceRNA or sponge
Lung adenocarcinoma	XIST	BAG1	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(let-7i)	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000107262	NA	7503	573	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	BAG-1|HAP|RAP46	LncRNA XIST promotes human lung adenocarcinoma cells to cisplatin resistance via let-7i/BAG-1 axis.LncRNA XIST expression was markedly increased in cisplatin-resistant A549/DDP cells compared with parental A549 cells as shown by qRT-PCR.LncRNA XIST overexpression in A549 cells increased their chemosensitivity to cisplatin both in vitro and in vivo by protecting cells from apoptosis and promoting cell proliferation. By contrast, LncRNA XIST knockdown in A549/DDP cells decreased the chemoresistance. We revealed that XIST functioned as competing endogenous RNA to repress let-7i, which controlled its down-stream target BAG-1. We proposed that XIST was responsible for cisplatin resistance of LAD cells and XIST exerted its function through the let-7i/BAG-1 axis.	28961027	RID01518	ceRNA or sponge
Renal cell carcinoma	DLX6-AS1	PTEN	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000171862	NA	285987	5728	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis. In this study, we identified an upregulated lncRNA, DLX6-AS1, in RCC tumor tissues compared with normal kidney tissues. Our data suggested that DLX6-AS1 promoted RCC cell growth and tumorigenesis via targeting miR-26a. PTEN is the direct target of miR-26a in RCC cells. In addition, we observed that PTEN overexpression restored the renal cancer cell growth and also rescued the RCC tumorigenesis. In summary, we conclude that DLX6-AS1 promotes renal cell carcinoma development via regulation of miR-26a/PTEN axis.	28881158	RID01519	ceRNA or sponge
Breast cancer	ANCR	EZH2	negatively-E	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell metastasis(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	282	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The degradation of EZH2 mediated by lncRNA ANCR attenuated the invasion and metastasis of breast cancer.Here we report the discovery of ANCR modulating the stability of EZH2, and hence in the invasion and metastasis of breast cancer cells. We determined that ANCR potentiated the CDK1-EZH2 interaction, which then increased the intensity of phosphorylation at Thr-345 and Thr-487 sites of EZH2, facilitating EZH2 ubiquitination and hence its degradation.	27716745	RID01520	interact with protein
Hepatocellular carcinoma	LINC00161	PTEN	negatively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-21;miR-590-5p)	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226935	GRCh38_21:28539318-28540355	ENSG00000171862	NA	118421	5728	C21orf100|Linc-USP16|NCRNA00161	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression.Here, we found that Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p. These interactions led to repression of AKT pathway and inhibition of HCC cell proliferation and migration.	29179215	RID01521	ceRNA or sponge
Breast cancer	H19	CBL	negatively-E	western blot;RNAi	upregulation	qPCR;microarray	NA	NA	chemosensitivity(-);cell viability(+);apoptosis process(-);tumorigenesis(+);cell metastasis(+)	host(miR-675-5p)	regulation	NA	Huaier	NA	Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000110395	NA	283120	867	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	C-CBL|CBL2|FRA11B|NSLL|RNF55	Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway.MiR-675-5p was identified as a mature product of H19. Upregulating miR-675-5p reversed the inhibitory effects of Huaier extract, whereas downregulating miR-675-5p sensitized breast cancer cells to the effect of Huaier extract. In addition, Huaier extract increased the expression of CBL protein, a direct target of miR-675-5p. Collectively, the data demonstrate that Huaier extract reduces viability and induces apoptosis in breast cancer cells via H19-miR-675-5p-CBL axis regulation.H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b. We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested. In addition, H19 is also a precursor for microRNA-675 (miR-675) and generates two mature miRNAs, miR-675-5p (miR-675) and miR-675-3p (miR-675*)	29145193	RID01522	expression association
Pancreatic neuroendocrine tumor	MEG3	BRI3	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-183)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000164713	NA	55384	25798	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	I3	MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183.MEG3 was low expressed in BON1 and QGP-1 cells. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/beta-Catenin signaling in BON1 cells.	29132136	RID01523	ceRNA or sponge
Urinary bladder cancer	UCA1	ARL2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell growth(+);mitochondrial function(+)	ceRNA(miR-195)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000213465	NA	652995	402	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ARFL2	LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway. UCA1, as a competing endogenous RNA (ceRNA), regulates mitochondrial function through upregulating ARL2. ARL2 is a direct target of miR-195 and can be repressed by either miR-195 overexpression or UCA1 inhibition. Animal experiments further indicated that UCA1 promoted bladder tumor growth by regulating miR-195 /ARL2. These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo.	29130995	RID01524	ceRNA or sponge
Hepatocellular carcinoma	HANR	GSK3B	interact	RNA pull-down assay;western blot	upregulation	qPCR;microarray	NA	NA	chemoresistance(+);tumorigenesis(+)	phosphorylation	binding/interaction	RNA-protein	doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_12:12875477-12876136	ENSG00000082701	NA	NA	2932	NA	NA	LncRNA HANR Promotes Tumorigenesis and Increase of Chemoresistance in Hepatocellular Carcinoma.HANR was demonstrated to be up-regulated in HCC patients and HCC cell lines.Increased HANR expression in HCC predicted short survival of patients. Knock-down of HANR markedly retarded cell proliferation, suppressed HCC xenograft/orthotopic tumor growth, induced apoptosis and enhanced chemosensitivity to doxorubicin, while over-expression of HANR showed the opposite effects. It was found that HANR bind to GSKIP for regulating the phosphorylation of GSK3beta in HCC.	29055955	RID01525	interact with protein
Gastric cancer	UPF1	MALAT1	negatively-E	RIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(-)	RNA stability	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000005007	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5976	378938	HUPF1|NORF1|RENT1|pNORF1|smg-2	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1.The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1.	28942451	RID01526	interact with protein
Urinary bladder cancer	XIST	AR	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+);cell migration(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000169083	NA	7503	367	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR).XIST and AR were upregulated in bladder cancer tissues and positively correlated. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3'UTR of AR to regulate its expression. These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.	28869948	RID01527	ceRNA or sponge
Non-small cell lung cancer	PVT1	miR-195	negatively-F	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	radiosensitivity(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195. PVT1 directly interacted with miR-195 and regulated its expression. Moreover, PVT1 knockdown improved radiosensitivity of NSCLC cells in vitro and in vivo by sponging miR-195.	28848163	RID01528	ceRNA or sponge
Pancreatic carcinoma	TUG1	EZH2	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-382)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation,Migration and EMT Phenotype Formation Through Sponging Mir-382. In this study, we reported that TUG1 was overexpressed in PC tissues and cell lines, and high expression of TUG1 predicted poor prognosis. Collectively, these findings revealed that TUG1 functions as an oncogenic lncRNA that promotes tumor progression, at least partially, by functioning as an endogenous 'sponge' and competing for miR-382 binding to the miRNA target EZH2.	28813705	RID01529	ceRNA or sponge
Gastric cancer	SNHG6	ZEB1	positively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000148516	NA	641638	6935	HBII-276HG|NCRNA00058|U87HG	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.In this study, we revealed that SNHG6 was overexpressed in gastric cancer tissues and cell lines. Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446	RID01530	ceRNA or sponge
Gastric cancer	SNHG6	CDKN1B	negatively-E	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000111276	NA	641638	1027	HBII-276HG|NCRNA00058|U87HG	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446	RID01531	epigenetic regulation
Cholangiocarcinoma	AFAP1-AS1	MMP2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000087245	NA	84740	4313	AFAP1-AS|AFAP1AS	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma.In this study, we found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. AFAP1-AS1 silencing inhibited cell migration partly due to decrease the expression of MMP-2 and MMP-9.	28535506	RID01532	expression association
Cholangiocarcinoma	AFAP1-AS1	MMP9	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000100985	NA	84740	4318	AFAP1-AS|AFAP1AS	CLG4B|GELB|MANDP2|MMP-9	Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma.In this study, we found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. AFAP1-AS1 silencing inhibited cell migration partly due to decrease the expression of MMP-2 and MMP-9.	28535506	RID01533	expression association
Non-small cell lung cancer	XLOC_008466	MMP2	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-874)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG		GRCh38_10:43323011-43327969	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.XLOC_008466 is up-regulated in NSCLC patients. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression. A bioinformatics analysis using TargetScan, microRNA.org, and miRanda indicated that MMP2 and XIAP were potential targets of miR-874.	28501870	RID01534	ceRNA or sponge
Non-small cell lung cancer	XLOC_008466	XIAP	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-874)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG		GRCh38_10:43323011-43327969	ENSG00000101966	NA	NA	331	NA	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.XLOC_008466 is up-regulated in NSCLC patients. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression. A bioinformatics analysis using TargetScan, microRNA.org, and miRanda indicated that MMP2 and XIAP were potential targets of miR-874.	28501870	RID01535	ceRNA or sponge
Gastric cancer	CRNDE	E2F3	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-45)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000112242	NA	NA	1871	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	E2F-3	Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145.CRNDE was highly expressed in GC cell lines and tissues;Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145.	28490034	RID01536	ceRNA or sponge
Colorectal cancer	CRNDE	TCF7L2	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-217)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000148737	NA	NA	6934	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	TCF-4|TCF4	The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/beta-Catenin Signaling Pathway.In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells.The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/beta-catenin signaling through binding miR-217 competitively.	28472810	RID01537	ceRNA or sponge
Urinary bladder cancer	LINC-ROR	ZEB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition.ZEB1 was a target gene of ROR and was positive correlation with the level of ROR in cancer tissues.ZEB1 is target of ROR.Rescue assays were performed to further confirm that ROR contributes to the progression of BC cells through targeting ZEB1.	28463831	RID01538	transcriptional regulation
Non-small cell lung cancer	XIST	miR-186-5p	negatively-F	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000229807	GRCh38_X:73820649-73852723	NA	NA	7503	NA	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	NA	The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p.We confirmed that XIST was upregulated in NSCLC cell lines and tissues.Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p. Furthermore, we showed that miR-186-5p has a binding site for XIST.	28448993	RID01539	ceRNA or sponge
Colorectal cancer	TUSC7	CDK6	positively-E	western blot;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-211-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000105810	NA	285194	1021	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	MCPH12|PLSTIRE	The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer.In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p.	28214867	RID01540	ceRNA or sponge
Esophagus squamous cell carcinoma	H19	CDH1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01541	expression association
Esophagus squamous cell carcinoma	H19	VIM	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01542	expression association
Esophagus squamous cell carcinoma	H19	MMP9	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000100985	NA	283120	4318	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CLG4B|GELB|MANDP2|MMP-9	Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis.silencing of H19 up-regulated epithelial marker E-cadherin while down-regulating mesenchymal marker vimentin and metastasis-associated protein such as MMP-9.	27247022	RID01543	expression association
Esophagus squamous cell carcinoma	NEAT1	CTBP2	positively-E	RIP;western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	ceRNA(miR-129)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000175029	NA	283131	1488	LINC00084|NCRNA00084|TncRNA|VINC	NA	LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis.NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells. Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129. CTBP2 restoration overturned cell viability and invasion suppression mediated by NEAT1 knockdown or miR-129 overexpression.	29147064	RID01544	ceRNA or sponge
Chronic myeloid leukemia	UCA1	ABCB1	positively-E	western blot;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-16)	regulation	NA	imatinib	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000085563	NA	652995	5243	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	lncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.The function of drug efflux mediated by multidrug resistance protein-1 (MDR1) is considered as a main reason for IM drug resistance in CML cells.UCA1 was significantly upregulated in K562/IM and K562/IM-R cells compared with K562 cells, and UCA1 in K562/IM cells was higher than that in K562/IM-R cells. In the present study, long noncoding RNA (lncRNA) UCA1 was identified as an important modulator of MDR1 by a model system of leukemia cell lines with a gradual increase of MDR1 expression and IM resistance. Overexpression of UCA1 increased MDR1 expression to promote IM resistance of CML cells.we demonstrated that UCA1 functions as a competitive endogenous (ceRNA) of MDR1 through completely binding the common miR-16.	27854515	RID01545	ceRNA or sponge
Pancreatic ductal adenocarcinoma	HOTAIR	miR-34a	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma.Loss of miR-34a contributed to EZH2-mediated cell growth in PDAC cells. As HOTAIR was shown to be overexpressed in PDAC.	27594424	RID01546	epigenetic regulation
Hepatocellular carcinoma	PCBP2-OT1	RASAL1	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with mRNA	binding/interaction	RNA-RNA	sorafenib	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000111344	NA	102157401	8437	NA	RASAL	Long non-coding RNA TUC338 is functionally involved in sorafenib-sensitized hepatocarcinoma cells by targeting RASAL1.Higher levels of TUC338 were found both in HCC tissues and cell lines. Higher levels of TUC338 were found both in HCC tissues and cell lines, knockdown of TUC338 was accompanied with increased expression of RASAL1 in HCC cell line with increased proliferation and invasion ability, knockdown of TUC338 could activate the RASAL1 pathway and inhibit tumor growth genes by directly targeting RASAL1 3'-UTR. These findings provide direct evidence that the TUC338/RASAL1 axis might play an essential role in sorafenib-resistance of liver cancer cells, suggesting the signaling cohort could serve as a novel therapeutic target for the treatment of chemotherapy resistant liver cancer.	27878301	RID01547	interact with mRNA
Gallbladder cancer	CYTOR	HIF1A	positively-E	RIP;western blot;luciferase reporter assay;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000100644	NA	112597	3091	C2orf59|LINC00152|NCRNA00152	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1alpha via miR-138. LINC00152 is significantly upregulated in gallbladder cancer and associated with clinicopathologic characteristics. Mechanistic analyses indicated that LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of hypoxia inducible factor-1alpha (HIF-1alpha). LINC00152 positively regulates HIF-1alpha, a target of miR-138.	28077595	RID01548	ceRNA or sponge
Pancreatic cancer	PVT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124762	NA	5820	1026	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long Noncoding RNA PVT1 Promotes EMT and Cell Proliferation and Migration Through Downregulating p21 in Pancreatic Cancer Cells. It showed that plasmacytoma variant translocation 1 expression was significantly upregulated in pancreatic cancer tissues or cell line compared to normal groups. Plasmacytoma variant translocation 1 downregulation significantly inhibited zinc finger E-box-binding protein 1/Snail expression but promoted p21 expression, and it also inhibited the cell proliferation and migration.	28355965	RID01549	expression association
Pancreatic cancer	HOTAIR	miR-663b	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter.Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.	27895308	RID01550	epigenetic regulation
Pancreatic cancer	HOTAIR	IGF2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000167244	NA	100124700	3481	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C11orf43|GRDF|IGF-II|PP9974	Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter.Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.	27895308	RID01551	expression association
Colorectal cancer	SNHG5	STAU1	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell survival(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000203875	GRCh38_6:85650491-85678932	ENSG00000124214	NA	387066	6780	C6orf160|LINC00044|NCRNA00044|U50HG	PPP1R150|STAU	SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization. Here, we identify and characterize SNHG5 as a stable cytoplasmic lncRNA with up-regulated expression in colorectal cancer. Importantly, knockdown of key SNHG5 target transcripts, including SPATS2, induces apoptosis and thus mimics the effect seen following SNHG5 depletion. Mechanistically, we suggest that SNHG5 stabilizes the target transcripts by blocking their degradation by STAU1.	28004750	RID01552	expression association
Ovarian cancer	MALAT1	PPP1R13L	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-506)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104881	NA	378938	10848	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	IASPP|NKIP1|RAI|RAI4	Long noncoding RNA MALAT1-regulated microRNA 506 modulates ovarian cancer growth by targeting iASPP.lncRNA-MALAT1 was specifically upregulated in ovarian cancer cell lines and promoted ovarian cancer-cell growth through targeting microRNA (miR)-506. In addition, miR-506-dependent iASPP regulation was required in MALAT1-induced ovarian cancer-cell growth. MalaT1 regulated mir-506 by direct targeting. mir-506 regulated iASPP expression by direct targeting.	28031721	RID01553	ceRNA or sponge
Colorectal cancer	miR-376c-3p	CYTOR	negatively-F	RNAi;bioinformatics	downregulation	qPCR	NA	NA	apoptosis process(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	ENSG00000222041	GRCh38_2:87454781-87636740	NA	112597	NA	C2orf59|LINC00152|NCRNA00152	LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.we found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Interestingly, microRNA (miR)-376c-3p down-regulated the expression of LINC00152 in CSC cells.	28078002	RID01554	ceRNA or sponge
Gastric cancer	AC009084.3	MUC2	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	NA	NA	cell proliferation(-);cell invasion(-)	ceRNA(miR-34c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000280416	GRCh38_16:66944660-66945096	NA	NA	NA	4583	NA	MLP|MUC-2|SMUC	Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c. LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression.we searched from miRanda database and found that miR-34c might be one regulatory gene of MUC2.	27835575	RID01555	ceRNA or sponge
Hepatocellular carcinoma	SNHG1	miR-195	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000255717	GRCh38_11:62851984-62855953	NA	NA	23642	NA	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	NA	Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1(SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195. The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration in vitro through the inhibition of miR-195. This suggests that miR-195 is a direct downstream target of lncRNA SNHG1. lncRNA SNHG1 may contribute to the aggravation of HCC through the inhibition of miR-195.	27932778	RID01556	ceRNA or sponge
Colorectal cancer	lnc-GNAT1-1	PEBP1	positively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000204282	GRCh38_3:50191612-50196516	ENSG00000089220	NA	NA	5037	NA	NA	A novel long non-coding RNA lnc-GNAT1-1 is low expressed in colorectal cancer and acts as a tumor suppressor through regulating RKIP-NF-kB-Snail circuit.In vivo study showed that overexpression of lnc-GNAT1-1 could suppress the liver metastasis of CRC cells. Finally, we explored the underlying mechanism of the role lnc-GNAT1-1 plays in CRC, and found a positive correlation between lnc-GNAT1-1 and Raf kinase inhibitor protein (RKIP) expression both in cells and in patients' tissues. We further found that lnc-GNAT1-1 could regulate the RKIP-NF-kB-Snail circuit in CRC.	27912775	RID01557	expression association
Hepatocellular carcinoma	MALAT1	SIRT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-204)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000096717	NA	378938	23411	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SIR2|SIR2L1|SIR2alpha	The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1.	28720061	RID01558	ceRNA or sponge
Cervical cancer	GAS5	FOXO1	negatively-E	luciferase reporter assay;RIP;RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	ceRNA(miR-205;miR-196a)	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150907	NA	60674	2308	NCRNA00030|SNHG2	FKH1|FKHR|FOXO1A	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression. Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively.	28671039	RID01559	ceRNA or sponge
Osteosarcoma	FOXC2-AS1	FOXC2	positively-F	luciferase reporter assay;RIP;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with mRNA	binding/interaction	RNA-RNA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000176692	NA	103752587	2303	ODRUL	FKHL14|LD|MFH-1|MFH1	Antisense lncRNA FOXC2-AS1 promotes doxorubicin resistance in osteosarcoma by increasing the expression of FOXC2.FOXC2-AS1 and FOXC2 are mainly located in the cytoplasm and form an RNA-RNA double-stranded structure in the overlapping region, which is necessary for FOXC2-AS1 to regulate the expression of FOXC2 at both the transcription and post-transcription levels. In addition, transcription factor FOXC2 also contributes to doxorubicin resistance through inducing the expression of the classical multi-drug resistance-related ABCB1 gene similar to FOXC2-AS1. Thus, we concluded that the lncRNA FOXC2-AS1 may promote doxorubicin resistance in OS by increasing the expression of transcription factor FOXC2, further facilitating ABCB1 expression.	28323030	RID01560	interact with mRNA
Clear cell renal cell carcinoma	MRCCAT1	NPR3	negatively-E	luciferase reporter assay;RIP;RNAi	upregulation	qPCR;microarray	GSE88948	GSE88948.zip	cell metastasis(+);P38/MAPK signaling pathway(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	ENST00000237853	GRCh38_5:95885098-95962071	ENSG00000113389	NA	NA	4883	NA	ANP-C|ANPR-C|ANPRC|C5orf23|GUCY2B|NPR-C|NPRC	Long noncoding RNA MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 and activating p38-MAPK signaling. The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway.	28659173	RID01561	epigenetic regulation
Malignant glioma	CYTOR	FEZF1	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-103a-3p)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	TF	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000128610	NA	112597	389549	C2orf59|LINC00152|NCRNA00152	FEZ|HH22|ZNF312B	Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway.Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs by binding to miR-103a-3p, which functions as a tumor suppressor.In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1), a direct target of miR-103a-3p which played an oncogenic role in GSCs. FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A). CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.	28651608	RID01563	ceRNA or sponge
Pancreatic cancer	HOTAIR	TNFRSF10B	negatively-E	ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	conatumumab;tigatuzumab	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000120889	NA	100124700	8795	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CD262|DR5|KILLER|KILLER/DR5|TRAIL-R2|TRAILR2|TRICK2|TRICK2A|TRICK2B|TRICKB|ZTNFR9	The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer.These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression.Some TRAIL and DR4/DR5 agonist antibodies, including conatumumab (AMG655, antibody for DR5) and tigatuzumab (CS-1008/TRA-8, antibody for DR5), have also been used for treating several types of cancers	28476883	RID01564	epigenetic regulation
Esophagus squamous cell carcinoma	LNCRNA-ATB	FERMT2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-200b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000073712	NA	114004396	10979	NA	KIND2|MIG2|PLEKHC1|UNC112|UNC112B|mig-2	Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis.Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts.Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC.	28640252	RID01565	ceRNA or sponge
Melanoma	HEIH	miR-200a	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes' promoters and modulate the expression of EZH2 target genes in HCC. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC.	28487474	RID01566	epigenetic regulation
Melanoma	HEIH	miR-200b	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes'promoters and modulate the expression of EZH2 target genes in HCC [27]. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC [28,29].	28487474	RID01567	epigenetic regulation
Melanoma	HEIH	miR-429	negatively-E	ChIRP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	miRNA	ENSG00000278970	GRCh38_5:180826871-180831605	NA	NA	100859930	NA	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	NA	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes'promoters and modulate the expression of EZH2 target genes in HCC [27]. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC [28,29].	28487474	RID01568	epigenetic regulation
Colorectal cancer	FBXL19-AS1	miR-203	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000260852	GRCh38_16:30919319-30923269	NA	NA	283932	NA	NCRNA00095	NA	Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203. Among these dysregulated lncRNAs, FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors.Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development.	28479250	RID01569	ceRNA or sponge
Lung cancer	POU5F1	NEAT1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000204531	NA	ENSG00000245532	GRCh38_11:65422774-65445540	5460	283131	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	LINC00084|NCRNA00084|TncRNA|VINC	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression.Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.	28615056	RID01570	transcriptional regulation
Lung cancer	POU5F1	MALAT1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell proliferation(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000204531	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5460	378938	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression.Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.	28615056	RID01571	transcriptional regulation
Lung adenocarcinoma	CDKN2B-AS1	PARP1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);mitochondrial signaling pathway(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000143799	NA	100048912	142	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells.Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2.ANRIL decreases Bcl-2 expression and increases PARP expression.	28402932	RID01572	expression association
Lung adenocarcinoma	CDKN2B-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);mitochondrial signaling pathway(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells.Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2.ANRIL decreases Bcl-2 expression and increases PARP expression.	28402932	RID01573	expression association
Breast cancer	H19	CYTH3	positively-E	RNAi;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-200b;miR-200c)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000008256	NA	283120	9265	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ARNO3|GRP1|PSCD3|cytohesin-3	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b. We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (lncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b. We found that this ability enabled H19 to modulate the expression of the microRNA targets Git2 and Cyth3, respectively, which encode regulators of the RAS superfamily member adenosine 5'-diphosphate (ADP) ribosylation factor (ARF), a guanosine triphosphatase (GTPase) that promotes cell migration associated with EMT and disseminating tumor cells.	28611183	RID01574	ceRNA or sponge
Breast cancer	H19	GIT2	positively-E	RNAi;RIP	upregulation	qPCR	NA	NA	mesenchymal to epithelial transition(+)	ceRNA(let-7b)	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000139436	NA	283120	9815	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CAT-2|CAT2|PKL	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b. We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (lncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b. We found that this ability enabled H19 to modulate the expression of the microRNA targets Git2 and Cyth3, respectively, which encode regulators of the RAS superfamily member adenosine 6'-diphosphate (ADP) ribosylation factor (ARF), a guanosine triphosphatase (GTPase) that promotes cell migration associated with EMT and disseminating tumor cells.	28611183	RID01575	ceRNA or sponge
Non-small cell lung cancer	HOXA11-AS	miR-200b	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	epigenetic regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID01576	epigenetic regulation
Colon cancer	CRNDE	HNRNPUL2	interact	RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);RAS/MAPK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000214753	NA	NA	221092	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HNRPUL2|SAF-A2	Long noncoding RNA CRNDE stabilized by hnRNPUL2 accelerates cell proliferation and migration in colorectal carcinoma via activating Ras/MAPK signaling pathways.The promoting effects of CRNDE on the cell proliferation, cell cycling and metastasis of CRC cells were confirmed both in vitro and in vivo by gain-of-function and loss-of-function experiments. Mechanistically, it was demonstrated that CRNDE could form a functional complex with heterogeneous nuclear ribonucleoprotein U-like 2 protein (hnRNPUL2) and direct the transport of hnRNPUL2 between the nucleus and cytoplasm. hnRNPUL2 that was accumulated in the cytoplasm could interact with CRNDE both physically and functionally, increasing the stability of CRNDE RNA.	28594403	RID01577	interact with protein
Cervical cancer	CASC2	PTEN	positively-E	luciferase reporter assay;RNAi;western blot	downregulation	qPCR	NA	NA	chemosensitivity(+)	ceRNA(miR-21)	regulation	NA	cisplatin	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Modulation of CASC2/miR-21/PTEN pathway sensitizes cervical cancer to cisplatin. CASC2 expression was down-regulated in cervical cancer tissues.CACS2 overexpression could sensitize DDP-resistant cervical cancer cell (HeLa/DDP and CaSki/DDP) to DDP. Further functional experiments indicate that CASC2 upregulated PTEN expression by direct inhibiting miR-21 in the DDP-resistant cancer cells, leading to the down-regulation of p-AKT protein.	28495512	RID01578	ceRNA or sponge
Esophageal cancer	HOTAIR	SNAI2	positively-E	western blot;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000019549	NA	100124700	6591	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.Mechanistic investigations revealed lncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.LncRNA-HOTAIR acts as a miR-148a sponge to positively regulate Snail2 expression, enhance cell invasion and metastasis, and promote the EMT in EC.	28441714;30223861	RID01579	ceRNA or sponge
Lung squamous cell carcinoma	SNHG1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000148516	NA	23642	6935	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA SNHG1 regulates zinc finger E-box binding homeobox 1 expression by interacting with TAp63 and promotes cell metastasis and invasion in Lung squamous cell carcinoma. SNHG1 was one of over-expressed lncRNAs in SCC tissues. Rather than direct interaction, SNHG1 regulated ZEB1 expression by suppressing the activity of p63 TA isoform (TAp63), which is a repressor of ZEB1 and physically associates with SNHG1. Furthermore, SNHG1 promoted ZEB1 expression and promoted cell proliferation, metastasis, invasive but inhibited apoptosis of SCC cells via the TAp63/ZEB1 pathway.	28415044	RID01580	expression association
Cervical cancer	TCONS_00026907	ELK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	ceRNA(miR-203)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	TF	NA	GRCh38_19:14792302-14792753	ENSG00000126767	NA	NA	2002	NA	NA	LncRNA-TCONS_00026907 is involved in the progression and prognosis of cervical cancer through inhibiting miR-143-5p.To confirm TCONS_00026907 regulates expression of ELK1 through inhibiting miR-143-5p, overexpression of miR-143-5p and silencing of ELK1 were, respectively, performed in HeLa and SiHa cells. Results showed that TCONS_00026907 level was significantly higher in cervical cancer tissues compared to noncancerous tissues and the survival rate was lower in the high expression group. Our study identifies TCONS_00026907 as a potent proto-oncogene and indicates that TCONS_00026907/miR143-5p/ELK1 regulatory pathway plays an important role in cervical cancer.TCONS_00026907 serving as a ceRNA accelerates ELK1 expression through inhibition of miR-143-5p and regulates C-fos, Cyclin D1, and Bcl-2 expression.	28544557	RID01581	ceRNA or sponge
Hepatocellular carcinoma	PVT1	YAP1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	ceRNA(miR-186-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000137693	NA	5820	10413	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	COB1|YAP|YAP2|YAP65|YKI	Long non-coding RNA PVT1 serves as a competing endogenous RNA for miR-186-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma.It was found that there was direct interaction between miR-186-5p and the binding site of plasmacytoma variant translocation 1 by performing dual-luciferase assay and RNA immunoprecipitation assay. Furthermore, it was identified that plasmacytoma variant translocation 1 regulated the expression of the miR-186-5p target gene, yes-associated protein 1. Taken together, plasmacytoma variant translocation 1 served as an endogenous sponge for miR-186-5p to reduce its inhibiting effect on yes-associated protein 1 and thus promoted the tumorigenesis of hepatocellular carcinoma.	28656879	RID01582	ceRNA or sponge
Endometrial carcinoma	TUSC7	miR-23b	negatively-F	RNA pull-down assay	downregulation	qPCR	NA	NA	chemosensitivity(+)	sponge	binding/interaction	RNA-RNA	cisplatin;paclitaxel	NA	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Long non-coding RNA tumor suppressor candidate 7 advances chemotherapy sensitivity of endometrial carcinoma through targeted silencing of miR-23b.the low expression of TUSC7 was confirmed in endometrial carcinoma tissues. TUSC7 upregulation inhibited proliferation, blocked cells at G1 phase, and advanced apoptosis and chemotherapy sensitivity to cisplatin (CDDP) and paclitaxel (Taxol) in HEC1A/CR cell line. Furthermore, miR-23b was upregulated in endometrial carcinoma and negatively correlated with the expression of TUSC7. RNA pull-down assay indicated that TUSC7 could specifically silence the expression of miR-23b in HEC1A/CR cell line; miR-23b was a target gene of TUSC7. In summary, long non-coding RNA TUSC7 was underexpressed in endometrial carcinoma, especially in endometrial carcinoma chemotherapy-resistant tissues and cell lines and acted as a potential tumor suppressor gene to inhibit cell growth as well as advance the chemotherapy sensitivity through targeted silencing of miR-23b, which might provide a new therapeutic target to endometrial carcinoma.	28653877	RID01583	ceRNA or sponge
Gastric cancer	MSTO2P	miR-335	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);colony formation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000203761	GRCh38_1:155745829-155750137	NA	NA	100129405	NA	MSTO2	NA	Long non-coding RNA MSTO2P promotes the proliferation and colony formation in gastric cancer by indirectly regulating miR-335 expression. LncRNA MSTO2P showed the highest expression level and was upregulated in gastric cancer and metastatic tissues. Long non-coding RNA misato family member 2, pseudogene influenced biologic functions in gastric cancer cells via indirectly regulating the activation of miR-335.	28618927	RID01584	expression association
Esophageal cancer	SNHG1	CST3	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-338)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000101439	NA	23642	1471	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ARMD11|HEL-S-2	LncRNA Snhg1, a non-degradable sponge for miR-338, promotes expression of proto-oncogene CST3 in primary esophageal cancer cells.lncRNA-Snhg1 was significantly upregulated in esophageal carcinoma tissues and promoted esophageal carcinoma cell growth. Furthermore, our results from bioinformatics, luciferase reporter gene and RNA pull-down assays indicated that Snhg1 could be directly bound by miR-338. Snhg1 acted as a non-degradable sponge to relieve the suppression on CST3 caused by miR-338. In conclusion, lncRNA-Snhg1 promoted cell proliferation by acting as a non-degradable sponge for the tumor suppressor miR-338 in esophageal cancer cells.	28423738	RID01587	ceRNA or sponge
Gastric cancer	TUG1	miR-145-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p.TUG1 could directly bind to miR-145-5p and repress miR-145-5p expression. TUG1 overexpression significantly relieved the inhibition on GC cell proliferation and invasion in vitro and tumor growth in vivo, mediated by miR-145-5p overexpression.	27983921	RID01588	ceRNA or sponge
Hepatocellular carcinoma	PCAT14	miR-372	negatively-E	RNAi;methylation-specific PCR	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000280623	GRCh38_22:23536881-23547797	NA	NA	NA	NA	NA	NA	Long noncoding RNA PCAT-14 induces proliferation and invasion by hepatocellular carcinoma cells by inducing methylation of miR-372. lncRNA PCAT-14 is overexpressed in patients with hepatocellular carcinoma (HCC). In addition, PCAT-14 inhibits miR-372 expression by inducing methylation of the miR-372 promoter. Simultaneously, miR-372 eliminates the effects of PCAT-14 on proliferation, invasion, and cell cycle in HCC cells.	28415780	RID01589	epigenetic regulation
Esophagus squamous cell carcinoma	PVT1	LASP1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-203)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000002834	NA	5820	3927	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	Lasp-1|MLN50	Upregulation of the long non-coding RNA PVT1 promotes esophageal squamous cell carcinoma progression by acting as a molecular sponge of miR-203 and LASP1. Here, we showed that PVT1 expression is significantly up-regulated in ESCC tumor samples compared with their normal counterparts.miR-203, which has been reported to be down-regulated in ESCC, could bind to PVT1. a significant inverse correlation between PVT1 and miR-203.we firstly confirmed direct binding of miR-203 to the 3'-UTR of LASP1.Our results suggest that PVT1 promote ESCC progression via functioning as a molecular sponge for miR-203 and LASP1 and provide the first evidence of dysregulated PVT1/miR-203/LASP1 axis in ESCC.	28404954	RID01590	ceRNA or sponge
Prostate cancer	SNHG1	CDK7	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-199a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000134058	NA	23642	1022	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	CAK|CAK1|CDKN7|HCAK|MO15|STK1|p39MO15	SNHG1 lncRNA negatively regulates miR-199a-3p to enhance CDK7 expression and promote cell proliferation in prostate cancer.We found that SNHG1 was aberrantly up-regulated in prostate carcinoma tissues; while, miR-199a-3p was abnormally down-regulated. The level of SNHG1 in prostate cancer was significantly negatively correlated with that of miR-199a-3p. Our data indicated that SNHG1 could interact with miR-199a-3p and inhibit the activity of miR-199a-3p in prostate cancer cells. In addition, miR-199a-3p could target the 3' UTR of CDK7 and suppress CDK7 expression. More importantly, SNHG1 increased CDK7 expression by competitively binding miR-199a-3p, and then promoted cell proliferation and cell cycle progression in prostate cancer. 	28400279	RID01591	ceRNA or sponge
Hepatocellular carcinoma	AF113014	EGR2	positively-E	luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	cell proliferation(-)	ceRNA(miR-20a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_10:63527874-63529035	ENSG00000122877	NA	NA	1959	NA	AT591|CHN1|CMT1D|CMT4E|KROX20	LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells.In this study, AF113014 is a new lncRNA identified from Microarray. Expression of AF113014 was down-regulated in HCC cell lines. Functionally, AF113014 inhibited proliferation of HCC cells both in vitro and in vivo, whereas the opposite effect was observed when AF113014 knockdown. Moreover, we identified that Egr2, a tumor suppressor gene, was a downstream target gene of AF113014.Interestingly, we found that there was base complementary relationship between AF113014, miRNA-20a and Egr2-3 'UTR.	28542387	RID01592	ceRNA or sponge
Osteosarcoma	FENDRR	ABCB1	negatively-E	western blot	upregulation	qPCR;microarray	NA	NA	chemosensitivity(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000085563	NA	400550	5243	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1.Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells.	29069754	RID01593	expression association
Osteosarcoma	FENDRR	ABCC1	negatively-E	western blot	upregulation	qPCR;microarray	NA	NA	chemosensitivity(+)	NA	regulation	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000103222	NA	400550	4363	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	ABC29|ABCC|GS-X|MRP|MRP1	LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1.Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells.	29069754	RID01594	expression association
Pancreatic cancer	HOTAIR	NOTCH3	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-613)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000074181	NA	100124700	4854	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CADASIL|CADASIL1|CASIL|IMF2|LMNS	LncRNA HOTAIR acts a competing endogenous RNA to control the expression of notch3 via sponging miR-613 in pancreatic cancer.Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.	28415631	RID01595	ceRNA or sponge
Thyroid cancer	n340790	miR-1254	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	miRNA	NA	GRCh38_8:94427712-94436952	NA	NA	NA	NA	NA	NA	The lncRNA n340790 accelerates carcinogenesis of thyroid cancer by regulating miR-1254. Here, we found that the lncRNA n340790 was highly expressed in human thyroid cancer tissues and was strongly correlated with the clinical characteristics of patients.Furthermore, we discovered that n340790 could act as an endogenous sponge by directly binding to miR-1254 and downregulating miR-1254 expression. In addition, miR-1254 could inhibit the stimulatory effect of n340790 on the growth and invasion of thyroid cancer cells.	28559970	RID01596	ceRNA or sponge
Colorectal cancer	UCC	miR-143	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	GSE75970	GSE75970.zip	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	miRNA	NA	GRCh38_2:9579498-9581745	NA	NA	NA	NA	NA	NA	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. Our results suggest that UCC and miR-143 may be promising molecular targets for CRC therapy.	28492554	RID01597	ceRNA or sponge
Renal cell carcinoma	HOTAIR	HIF1A	positively-E	RIP;western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+);apoptosis process(-)	ceRNA(miR-217)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100644	NA	100124700	3091	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA HOTAIR regulates HIF-1alpha/AXL signaling through inhibition of miR-217 in renal cell carcinoma.In this study, we first demonstrated that HOTAIR expression was upregulated, which was correlated with tumor progression, and miR-217 downregulated in Rcc tissues and cells. Importantly, HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1alpha expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. a direct interaction between miR-217 and the 3'UTR of HIF-1alpha.	28492542	RID01598	ceRNA or sponge
Epithelial ovarian carcinoma	MEG3	ATG3	positively-F	RIP	downregulation	qPCR	NA	NA	cell autophagy(-);tumorigenesis(-);cancer progression(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000144848	NA	55384	64422	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	APG3|APG3-LIKE|APG3L|PC3-96	Upregulation of the lncRNA Meg3 induces autophagy to inhibit tumorigenesis and progression of epithelial ovarian carcinoma by regulating activity of ATG3. we found that the expression of Meg3 was lower in epithelial ovarian carcinoma.Upregulated expression of Meg3 also suppressed tumorigenesis in vivo in a xenograft mouse model through upregulating ATG3 expression. RIP (ribonucleoprotein immunoprecipitation) and RNA pull-down assays showed that Meg3 was co-immunoprecipitated with ATG3. In addition, Meg3 protected ATG3 mRNA from degradation following treatment with actinomycin D. Overall, our results suggest that the lncRNA Meg3 acts as a tumor suppressor in EOC by regulating ATG3 activity and inducing autophagy.	28423647	RID01599	interact with mRNA
Medulloblastoma	MIR100HG	CDK6	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000105810	NA	399959	1021	AGD1|linc-NeD125|lncRNA-N2	MCPH12|PLSTIRE	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01600	ceRNA or sponge
Medulloblastoma	MIR100HG	MYCN	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	TF	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000134323	NA	399959	4613	AGD1|linc-NeD125|lncRNA-N2	MODED|N-myc|NMYC|ODED|bHLHe37	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01601	ceRNA or sponge
Medulloblastoma	MIR100HG	SNCAIP	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000064692	NA	399959	9627	AGD1|linc-NeD125|lncRNA-N2	SYPH1|Sph1	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01602	ceRNA or sponge
Medulloblastoma	MIR100HG	KDM6A	positively-E	RNA pull-down assay;luciferase reporter assay;CLIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-19a-3p;miR-19b-3p;miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000147050	NA	399959	7403	AGD1|linc-NeD125|lncRNA-N2	KABUK2|UTX|bA386N14.2	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.Mechanistically, linc-NeD125 is able to recruit the miRNA-induced silencing complex (miRISC) and to directly bind the microRNAs miR-19a-3p, miR-19b-3p and miR-106a-5p. Functionally, linc-NeD125 acts as a competing endogenous RNA (ceRNA) that, sequestering the three miRNAs, leads to de-repression of their targets CDK6, MYCN, SNCAIP, and KDM6A, which are major driver genes of G4 MB. Accordingly, linc-NeD125 downregulation reduces G4 cell proliferation. Moreover, we also provide evidence that linc-NeD125 ectopic expression in the aggressive Group 3 MB cells attenuates their proliferation, migration and invasion.	28415684	RID01603	ceRNA or sponge
Nasopharynx carcinoma	CDKN2B-AS1	miR-125a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	radiosensitivity(-);cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Downregulation of lncRNA ANRIL inhibits proliferation, induces apoptosis, and enhances radiosensitivity in nasopharyngeal carcinoma cells through regulating miR-125a.Luciferase reporter assay was performed to verity the direct target of miR-125a. LncRNA ANRIL was evidently elevated in NPC tissues and cell lines. Moreover, knockdown of ANRIL repressed proliferation, promoted apoptosis, and improved radiosensitivity in NPC via functioning as a miR-125a sponge.	28402230	RID01604	ceRNA or sponge
Uveal melanoma	CANT1	JPX	positively-E	ChIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000225470	GRCh38_X:73944182-74070408	NA	554203	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	DCBALD06|ENOX|LINC00183|NCRNA00183	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01605	epigenetic regulation
Uveal melanoma	CANT1	FTX	positively-E	ChIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000230590	GRCh38_X:73940435-74293574	NA	100302692	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	LINC00182|MIR374AHG|NCRNA00182	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01606	epigenetic regulation
Uveal melanoma	CANT1	XIST	positively-E	RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	lncRNA	ENSG00000171302	GRCh38_17:78991716-79009867	ENSG00000229807	GRCh38_X:73820649-73852723	NA	7503	DBQD|DBQD1|EDM7|SCAN-1|SCAN1|SHAPY	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CANT1 lncRNA Triggers Efficient Therapeutic Efficacy by Correcting Aberrantlncing Cascade in Malignant Uveal Melanoma.In this study, we identified a novel nuclear CANT1 lncRNA (CASC15-New-Transcript 1) that acts as a necessary UM suppressor. CANT1 significantly reduced tumor metastatic capacity and tumor formation, either in cell culture or in animals harboring tumor xenograft. Intriguingly, XIST lncRNA serves as a potential target of CANT1, and JPX or FTX lncRNA subsequently serves as a contextual hinge to activate a novel CANT1-JPX/FTX-XIST long non-coding (lncing) pathway in UM. Moreover, CANT1 triggers the expression of JPX and FTX by directly binding to their promoters and promoting H3K4 methylation.	28330694	RID01607	expression association
Pancreatic cancer	MEG3	PI3K	negatively-E	RNAi	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	lncRNA MEG3 had anti-cancer effects to suppress pancreatic cancer activity. MEG3 gene expression was negatively correlated with PI3K expression. The MEG3 was negatively correlated with tumor size, Metastasis and Vascular invasion in pancreatic cancer (P<0.05, respectively). MEG3 over-expressing had anti-cancer effects to suppress pancreatic cancer activity by regulation PI3K/AKT/Bcl-2/Bax/Cyclin D1/P53 and PI3K/AKT/MMP-2/MMP-9 signaling pathways.	28320094	RID01608	expression association
Hepatocellular carcinoma	HNF1A-AS1	NKD1	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000140807	NA	283460	85407	C12orf27|HAS1|NCRNA00262	Naked1	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID01609	epigenetic regulation
Hepatocellular carcinoma	HNF1A-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000124762	NA	283460	1026	C12orf27|HAS1|NCRNA00262	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID01610	epigenetic regulation
Hepatocellular carcinoma	SNHG20	CDH1	negatively-E	RIP;RNAi;western blot	upregulation	qPCR	NA	NA	cell invasion(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000039068	NA	654434	999	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA SNHG20 predicts a poor prognosis for HCC and promotes cell invasion by regulating the epithelial-to-mesenchymal transition.In vitro, loss-function assays revealed that knockdown of SNHG20 inhibited cell proliferation and invasion, whereas, gain-of-function promoted cell proliferation and invasion.Mechanistic investigation revealed that SNHG20 could bind to enhancer of zeste homolog 2 (EZH2) and regulated E-cadherin expression.Our results showed that the SNHG20/EZH2/E-cadhein regulator pathway might contribute to the development of novel therapeutic strategies for HCC patients.	28282787	RID01611	epigenetic regulation
Osteosarcoma	TUG1	ROCK1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-335-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000067900	NA	55000	6093	LINC00080|NCRNA00080|TI-227H	P160ROCK|ROCK-I	Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells.In our research, we found that TUG1 was elevated and correlated with a poor prognosis in osteosarcoma patients. Moreover, we revealed that TUG1 and Rho-associated coiled-coil-containing protein kinase 1 (ROCK1), a metastasis-related gene targeted by microRNA-335-5p (miR-335-5p), had the same miR-335-5p combining site. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p.	28205334	RID01612	ceRNA or sponge
Nasopharynx carcinoma	CASC9	HIF1A	interact	RNAi	upregulation	qPCR	NA	NA	cell growth(+);glucose metabolic process(+);tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000100644	NA	101805492	3091	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	The Long Noncoding RNA Cancer Susceptibility Candidate 9 Promotes Nasopharyngeal Carcinogenesis via Stabilizing HIF1alpha.In this study, we identified that lncRNA cancer susceptibility candidate 9 (CASC9) is highly expressed in NPC tissues, which facilitates cell growth and is correlated with a poor prognosis of cancer patients. The underlying molecular mechanism revealed that CASC9 interacts with HIF1alpha and enhances the stabilization of HIF1alpha. Activation of HIF1alpha by overexpressed CASC9 promotes the glycolysis and tumorigenesis of NPC cells.Downregulation of CASC9 significantly inhibits NPC cancer cell growth.	28398871	RID01613	interact with protein
Hepatocellular carcinoma	HULC	YBX1	positively-F	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(+);tumorigenesis(+)	phosphorylation	regulation	NA	cisplatin	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000065978	NA	728655	4904	HCCAT1|LINC00078|NCRNA00078	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA HULC modulates the phosphorylation of YB-1 through serving as a scaffold of extracellular signal-regulated kinase and YB-1 to enhance hepatocarcinogenesis. Meanwhile, HULC could promote cell proliferation, migration, and invasion in vitro and inhibit cisplatin-induced apoptosis. YB-1 is a major component of translationally inactive messenger ribonucleoprotein particles which keeps mRNA in a silent state. Our study further demonstrated that HULC could promote the phosphorylation of YB-1 protein, which leads to the release of YB-1 from its bound mRNA.	28027578	RID01614	interact with protein
Colon cancer	H19	HMGA1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	ceRNA(miR-138)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000137309	NA	283120	3159	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HMG-R|HMGA1A|HMGIY	H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1.We found that H19 was overexpressed in colon cancer tissues and cell lines. Moreover, the high-mobility group A (HMGA1) protein was predicted as a target of miR-138. HMGA1 was suppressed by H19 shRNA and could be up-regulated by miR-138 inhibitor. The migration and invasion ability of colon cancer was restrained by H19 shRNA and promoted by miR-138 inhibitor.	28358427	RID01615	ceRNA or sponge
Colorectal cancer	XIST	MAPK1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-132-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000100030	NA	7503	5594	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA XIST functions as an oncogene in human colorectal cancer by targeting miR-132-3p. The expression level of XIST was significantly increased in both CRC tissues sample and CRC cells. XIST promoted CRC cell proliferation by affecting the cell cycle. In addition, XIST and miR-132-3p were inhibited by each other reciprocally. MAPK1 was proved to be a direct target spot of miR-132-3p. We claim that XIST was responsible for CRC cell proliferation working by the miR-132-3p/MAPK1 axis.	28730777	RID01616	ceRNA or sponge
Hepatocellular carcinoma	lncRNA-PE	miR-200a	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	NA	GRCh38_5:132190148-132191509	NA	NA	NA	NA	NA	NA	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01617	transcriptional regulation
Hepatocellular carcinoma	lncRNA-PE	miR-200b	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	NA	GRCh38_5:132190148-132191509	NA	NA	NA	NA	NA	NA	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01618	transcriptional regulation
Hepatocellular carcinoma	lncRNA-PE	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_5:132190148-132191509	ENSG00000148516	NA	NA	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A long non-coding RNA lncRNA-PE promotes invasion and epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway. LncRNA-PE is upregulated in HCC tissues. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial-mesenchymal transition of hepatocellular carcinoma cells. Luciferase assays indicated that lncRNA-PE regulated the expression of miR-200b via its promoter.	28488544	RID01619	expression association
Neuroblastoma	MALAT1	AXL	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000167601	NA	378938	558	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ARK|JTK11|Tyro7|UFO	LncRNA-MALAT1-mediated Axl promotes cell invasion and migration in human neuroblastoma.We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1.Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.	28468579	RID01620	expression association
Renal cell carcinoma	UCA1	CDKN1A	negatively-E	RIP;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124762	NA	652995	1026	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495. In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. n addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR-495. These findings illuminated that urothelial carcinoma-associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495.	28466784	RID01621	epigenetic regulation
Renal cell carcinoma	UCA1	miR-495	negatively-F	RIP;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Kidney cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495. In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. n addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR-495. These findings illuminated that urothelial carcinoma-associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495.	28466784	RID01622	ceRNA or sponge
Neuroblastoma	MYCN	SNHG1	positively-E	bioinformatics	upregulation	qPCR;sequencing	GSE62564	GSE62564.zip	prognosis(-)	amplification	regulation	NA	NA	NA	NA	Cancer	Neuroblastoma	TF	lncRNA	ENSG00000134323	NA	ENSG00000255717	GRCh38_11:62851984-62855953	4613	23642	MODED|N-myc|NMYC|ODED|bHLHe37	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	Co-expression analysis identifies long noncoding RNA SNHG1 as a novel predictor for event-free survival in neuroblastoma. In conclusion, our study unveils that SNHG1 is up-regulated by MYCN amplification and could be a potential prognostic biomarker for high-risk NB intervention.	27517149	RID01623	expression association
Thyroid cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);TGF-beta/SMAD signaling pathway(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA ANRIL promotes the invasion and metastasis of thyroid cancer cells through TGF-beta/Smad signaling pathway.ANRIL expression was significantly up-regulated in TC tissues and cells (P < 0.001). ANRIL may reduce p15INK4B expression through inhibiting TGF-beta/Smad signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 cells.	27507052	RID01624	expression association
Malignant glioma	TUG1	PTEN	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	ceRNA(miR-26a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171862	NA	55000	5728	LINC00080|NCRNA00080|TI-227H	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells.TUG1 expression was confirmed to be upregulated in glioma tissues, and showed an inverse correlation with downregulated miR-26a.The bioinformatics prediction revealed putative miR-26a binding sites within TUG1 transcripts. Further experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3'UTR.TUG1 could serve as a miR-26a sponge in human glioma cells, contributing to the upregulation of PTEN. This study revealed a new TUG1/miR-26a/PTEN regulatory mechanism and provided a further understanding of the tumor-suppressive role of TUG1 in glioma development.	27363339	RID01625	ceRNA or sponge
Nasopharynx carcinoma	RBM24	MALAT1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000112183	NA	ENSG00000251562	GRCh38_11:65497688-65506516	221662	378938	RNPC6|dJ259A10.1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma. In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Overall, these findings suggest a novel role of RBM24 as a tumor suppressor. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.	27584791	RID01626	expression association
Breast cancer	EGF	LINC01089	negatively-E	ChIP	downregulation	qPCR;microarray	E-MTAB-4821	E-MTAB-4821.zip	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000138798	NA	ENSG00000212694	GRCh38_12:121795267-121803906	1950	338799	HOMG4|URG	LIMT	LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis. Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter.We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo. In conclusion, lncRNAs dynamically regulated by growth factors might act as novel drivers of cancer progression and serve as prognostic biomarkers.	27485121	RID01627	epigenetic regulation
Non-small cell lung cancer	H19	MACC1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000183742	NA	283120	346389	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	7A5|SH3BP4L	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01628	expression association
Non-small cell lung cancer	H19	EGFR	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000146648	NA	283120	1956	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01629	expression association
Non-small cell lung cancer	H19	CTNNB1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168036	NA	283120	1499	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01630	expression association
Non-small cell lung cancer	H19	MAPK3	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000102882	NA	283120	5595	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01631	expression association
Non-small cell lung cancer	H19	MAPK1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000100030	NA	283120	5594	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Targeting H19 by lentivirus-mediated RNA interference increases A549 cell migration and invasion. The knockdown of H19 increased the migration and invasion of A549 cells, and knockdown of metastasis-associated in colon cancer 1 (MACC1) decreased the migration and invasion of A549 cells. Furthermore, MACC1 protein targeted by H19 was upregulated as well as the downstream signaling proteins including epidermal growth factor receptor (EGFR), beta-catenin, extracellular-signal-regulated kinase 1/2 (ERK1/2). More importantly, H19 may regulate NSCLC metastasis through modulating cellular signaling pathway proteins related to cell proliferation and cell adhesion, including MACC1, EGFR, beta-catenin and ERK1/2.	27607135	RID01632	expression association
Cervical cancer	HOTAIR	HLA-G	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-148a)	regulation	NA	NA	NA	NA	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204632	NA	100124700	3135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MHC-G	Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer.HOTAIR expression was obviously increased in cervical cancer tissue.Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a. HOTAIR negatively regulated miR-148a expression via direct interaction. These results indicate that HOTAIR-induced downregulation of miR-148a attenuated the post-transcriptional regulation of miR-148a on HLA-G, contributing to HLA-G upregulation.Our data suggest that HOTAIR plays an important oncogenic role in cervical cancer and might serve as a marker for cervical cancer prognosis and a potential target for therapeutic intervention.	27574106	RID01633	ceRNA or sponge
Ovarian cancer	HOTAIR	RAB22A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-124)	regulation	NA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124209	NA	100124700	57403	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR controls the expression of Rab22a by sponging miR-373 in ovarian cancer. In patients with ovarian cancer, HOTAIR was significantly upregulated. HOTAIR functioned as a ceRNA, and acted as a sink for microRNA (miR)-373, thereby regulating the expression of Rab22a. The upregulation of HOTAIR contributed to the malignant progression of ovarian cancer cells. Therefore, the positive regulation between HOTAIR and Rab22a can be partially attributed to the ceRNA regulatory network through miR-373.	27484896	RID01634	ceRNA or sponge
Hepatocellular carcinoma	MEG3	HSPA5	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000044574	NA	55384	3309	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.	27432655	RID01635	expression association
Hepatocellular carcinoma	MEG3	NFKB1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000109320	NA	55384	4790	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus.These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF-kB signaling is required for p53 activation in ER stress.	27432655	RID01636	expression association
Malignant glioma	ZEB1-AS1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000087088	NA	220930	581	NA	BCL2L4	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01637	expression association
Malignant glioma	ZEB1-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000171791	NA	220930	596	NA	Bcl-2|PPP1R50	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01638	expression association
Malignant glioma	ZEB1-AS1	CCND1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000110092	NA	220930	595	NA	BCL1|D11S287E|PRAD1|U21B31	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01639	expression association
Malignant glioma	ZEB1-AS1	CDK2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000123374	NA	220930	1017	NA	CDKN2|p33(CDK2)	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01640	expression association
Malignant glioma	ZEB1-AS1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01641	expression association
Malignant glioma	ZEB1-AS1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000087245	NA	220930	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01642	expression association
Malignant glioma	ZEB1-AS1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000100985	NA	220930	4318	NA	CLG4B|GELB|MANDP2|MMP-9	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01643	expression association
Malignant glioma	ZEB1-AS1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000170558	NA	220930	1000	NA	CD325|CDHN|CDw325|NCAD	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01644	expression association
Malignant glioma	ZEB1-AS1	ITGB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000150093	NA	220930	3688	NA	CD29|FNRB|GPIIA|MDF2|MSK12|VLA-BETA|VLAB	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01645	expression association
Malignant glioma	ZEB1-AS1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000039068	NA	220930	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating epithelial to mesenchymal transition (EMT) through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-beta1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. Additionally, forced down-regulation of ZEB1-AS1 could dramatically promote apoptosis by increasing the expression level of Bax and reducing Bcl-2 expression in glioma.	27589728	RID01646	expression association
Osteosarcoma	MALAT1	TGFA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cancer progression(+)	ceRNA(miR-376a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163235	NA	378938	7039	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TFGA	MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A.Here, we showed that MALAT1 was increased in human OS cell lines and tissues and promoted OS cell growth, while MALAT1 knockdown suppressed OS cell growth. There was a direct interaction between MIR376A and MALAT1 via a putative MIR376A binding site within the MALAT1 3'-untranslated region (3'-UTR). There was also a direct interaction between MIR376A and the TGFA 3'-UTR. Thus, MALAT1 may promote OS cell growth through inhibition of MIR376A, leading to increased expression of TGFA. Our results suggest a MALAT1/MIR376A/TGFA axis mediates OS cell proliferation and tumor progression.	27458156	RID01647	ceRNA or sponge
Prostate cancer	SOCS2-AS1	TNFSF10	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+);apoptosis process(-)	epigenetic regulation	association	NA	docetaxel	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000246985	GRCh38_12:93542022-93571768	ENSG00000121858	NA	144481	8743	NA	APO2L|Apo-2L|CD253|TL2|TNLG6A|TRAIL	Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.suppressor of cytokine signaling 2-antisense transcript 1 (SOCS2-AS1), the expression of which was higher in castration-resistant prostate cancer model cells.SOCS2-AS1 promoted castration-resistant and androgen-dependent cell growth. We found that SOCS2-AS1 knockdown up-regulated genes related to the apoptosis pathway, including tumor necrosis factor superfamily 10 (TNFSF10), and sensitized prostate cancer cells to docetaxel treatment. Moreover, we also demonstrated that SOCS2-AS1 promotes androgen signaling by modulating the epigenetic control for AR target genes including TNFSF10 These findings suggest that SOCS2-AS1 plays an important role in the development of castration-resistant prostate cancer by repressing apoptosis.	27342777	RID01648	epigenetic regulation
Non-small cell lung cancer	NEAT1	E2F3	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-377-3p)	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000112242	NA	283131	1871	LINC00084|NCRNA00084|TncRNA|VINC	E2F-3	Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.In our studies, we identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression.we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression.	27351135	RID01649	ceRNA or sponge
Non-small cell lung cancer	TUG1	CELF1	negatively-E	RIP;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000149187	NA	55000	10658	LINC00080|NCRNA00080|TI-227H	BRUNOL2|CUG-BP|CUGBP|CUGBP1|EDEN-BP|NAB50|NAPOR|hNab50	Long noncoding RNA TUG1 is downregulated in non-small cell lung cancer and can regulate CELF1 on binding to PRC2. Knockdown of TUG1 significantly promoted the proliferation of NSCLC cells. The results demonstrated that TUG1 RNA was bound to enhancer of zeste protein 2/embryonic ectoderm development (EZH2/EED), which is essential for PRC2. Finally, our designed ChIP assay revealed that the EZH2/EED was bound to the promotor region of CELF1 within 992 bp upstream of the transcript start site.	27485439	RID01650	epigenetic regulation
Cervical cancer	PVT1	miR-200b	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b.Our results revealed that PVT1 is upregulated in cervical cancer tissues.Mechanistically, we verified that PVT1 binds to EZH2, recruits EZH2 to the miR-200b promoter, increases histone H3K27 trimethylation level on the miR-200b promoter, and inhibits miR-200b expression. Furthermore, the effects of PVT1 on cervical cell proliferation and migration depend upon silencing of miR-200b.	27272214	RID01651	epigenetic regulation
Endometrial carcinoma	MEG3	NOTCH1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000148400	NA	55384	4851	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AOS5|AOVD1|TAN1|hN1	LncRNA-MEG3 inhibits cell proliferation of endometrial carcinoma by repressing Notch signaling.Significant downregulation of MEG3 was observed in EC samples compared to control, while the protein levels of Notch1 and Hes1 were both upregulated. Cell proliferation was obviously inhibited by MEG3 overexpression, while opposite improved result was obtained in MEG3 knockout cells. Interestingly, MEG3-induced changes could be reversed by Notch1 regulators.Downregulated MEG3 exhibited an anti-proliferative role in EC by repressing Notch signaling pathway.	27470401	RID01652	expression association
Endometrial carcinoma	MEG3	HES1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);Notch signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000114315	NA	55384	3280	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HES-1|HHL|HRY|bHLHb39	LncRNA-MEG3 inhibits cell proliferation of endometrial carcinoma by repressing Notch signaling.Significant downregulation of MEG3 was observed in EC samples compared to control, while the protein levels of Notch1 and Hes1 were both upregulated. Cell proliferation was obviously inhibited by MEG3 overexpression, while opposite improved result was obtained in MEG3 knockout cells. Interestingly, MEG3-induced changes could be reversed by Notch1 regulators.Downregulated MEG3 exhibited an anti-proliferative role in EC by repressing Notch signaling pathway.	27470401	RID01653	expression association
Her2-receptor positive breast cancer	HOTAIR	FOXM1	positively-E	RNAi;luciferase reporter assay	upregulation	sequencing	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000111206	NA	100124700	2305	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.HOTAIR is a long non-coding RNA that is overexpressed, promotes metastasis and is predictive of decreased survival.HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. Analysis of breast cancer gene expression data indicates that HOTAIR is co-expressed with FOXA1 and FOXM1 in HER2-enriched tumours, and these factors enhance the prognostic power of HOTAIR in aggressive HER2+ breast tumours.	27378691	RID01654	expression association
Her2-receptor positive breast cancer	HOTAIR	FOXA1	positively-E	RNAi;luciferase reporter assay	upregulation	sequencing	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129514	NA	100124700	3169	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3A|TCF3A	Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.HOTAIR is a long non-coding RNA that is overexpressed, promotes metastasis and is predictive of decreased survival.HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. Analysis of breast cancer gene expression data indicates that HOTAIR is co-expressed with FOXA1 and FOXM1 in HER2-enriched tumours, and these factors enhance the prognostic power of HOTAIR in aggressive HER2+ breast tumours.	27378691	RID01655	expression association
Glioblastoma	HOTAIR	PDCD4	negatively-E	ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000150593	NA	100124700	27250	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	H731	Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	27277755	RID01656	epigenetic regulation
Skin squamous cell carcinoma	PICSAR	DUSP6	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000139318	NA	378825	1848	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	HH19|MKP3|PYST1	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01657	expression association
Skin squamous cell carcinoma	PICSAR	MAPK3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000102882	NA	378825	5595	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01658	expression association
Skin squamous cell carcinoma	PICSAR	MAPK1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Skin carcinoma	lncRNA	PCG	ENSG00000275874	GRCh38_21:44999208-45004727	ENSG00000100030	NA	378825	5594	C21orf113|LINC00162|NCRNA00162|NLC1-C|NLC1C|PRED74	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long Noncoding RNA PICSAR Promotes Growth of Cutaneous Squamous Cell Carcinoma by Regulating ERK1/2 Activity.Whole transcriptome analysis of cSCC cells (n = 8) and normal human epidermal keratinocytes (n = 4) revealed overexpression of long intergenic ncRNA (LINC00162) in cSCC cells. Furthermore, knockdown of LINC00162 inhibited extracellular signal-regulated kinase 1/2 activity and upregulated expression of dual specificity phosphatase 6 (DUSP6) in cSCC cells. Our results provide mechanistic evidence for the role of PICSAR in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 signaling pathway by downregulating DUSP6 expression.	27049681	RID01659	expression association
Melanoma	UCA1	FOXM1	positively-E	western blot;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-507)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111206	NA	652995	2305	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma.UCA1 expression was discovered to be upregulated in melanoma tissues and cells.We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507.	27389544	RID01660	ceRNA or sponge
Malignant glioma	CRNDE	PIWIL4	positively-E	western blot;IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-384)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000134627	NA	NA	143689	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	HIWI2|MIWI2	CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis.Colorectal neoplasia differentially expressed (CRNDE) is the most upregulated long noncoding RNA (lncRNA) in glioma.In addition, the expression of miR-384 was negatively correlated with CRNDE expression. A binding region between CRNDE and miR-384 was confirmed using luciferase assays.Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression.PIWIL4 was identified as a target of miR-384 and plays an oncogenic role in glioma.	27058823	RID01661	ceRNA or sponge
Malignant glioma	miR-148b-3p	HOTAIR	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cancer progression(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.RT-qPCR revealed that the expression level of miR-148b-3p was significantly lower in A172 cells compared with HA1800 cells. Bioinformatics and luciferase reporter assays showed that miR-148b-3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence. In summary, the results indicated that miR-148b-3p inhibits malignant biological behaviors of glioma cells by directly targeting HOTAIR.	27446363	RID01662	ceRNA or sponge
Hepatocellular carcinoma	TUSC7	EPHA4	negatively-E	luciferase reporter assay;IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	ceRNA(miR-10a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000116106	NA	285194	2043	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	EK8|HEK8|SEK|TYRO1	Long non-coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma.In this study, we observed that the expression of TUSC7 was immensely decreased in HCC. Moreover, TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis.	27002617	RID01663	ceRNA or sponge
Epithelial ovarian cancer	UCA1	MMP14	positively-E	luciferase reporter assay;RIP;IHC	upregulation	qPCR	NA	NA	cell metastasis(-)	ceRNA(miR-485-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000157227	NA	652995	4323	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	UCA1 functions as a competing endogenous RNA to suppress epithelial ovarian cancer metastasis.UCA1 was aberrantly upregulated in EOC tissues and cells.The results showed that UCA1 could function as an endogenous sponge by directly binding to miR-485-5p. Depletion of UCA1 was involved in the downregulation of matrix metallopeptidase 14 (MMP14) expression, a target gene of miR-485-5p.	26867765	RID01664	ceRNA or sponge
Osteosarcoma	TUSC7	BCL2	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000171791	NA	285194	596	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Bcl-2|PPP1R50	Long non-coding RNA tumor suppressor candidate 7 functions as a tumor suppressor and inhibits proliferation in osteosarcoma.Here, we reported a novel lncRNA, tumor suppressor candidate 7 (TUSC7), was significantly downregulated in osteosarcoma tissues compared with paired non-tumor tissues and low expression of TUSC7 indicated poor survival.Western blot showed that after silence of TUSC7, the proapoptotic Bcl2 expression was downregulated.	26781978	RID01665	expression association
Hepatoblastoma	TUG1	VEGFA	positively-E	luciferase reporter assay;western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(-);angiogenesis(-)	ceRNA(miR-34a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000112715	NA	55000	7422	LINC00080|NCRNA00080|TI-227H	MVCD1|VEGF|VPF	Targeting long non-coding RNA-TUG1 inhibits tumor growth and angiogenesis in hepatoblastoma. We previously reveal that lnRNA-TUG1 is upregulated in hepatoblastoma specimens by microarray analysis. TUG1, miR-34a-5p, and VEGFA constitutes to a regulatory network, and participates in regulating hepatoblastoma cell function, tumor progression, and tumor angiogenesis.LncRNA-TUG1 functions as miR-34a-5p sponge in hepatoblastoma cell.LncRNA-TUG1 regulates the expression of miR-34a-5p target gene, VEGFA, in hepatoblastoma cell.	27362796	RID01666	ceRNA or sponge
Colorectal cancer	CASC11	HNRNPK	interact	RNA pull-down assay;RIP;IHC	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000249375	GRCh38_8:127686343-127738987	ENSG00000165119	NA	100270680	3190	CARLO7|CARLo-7|LINC00990|TCONS_00014535	AUKS|CSBP|HNRPK|TUNP	Long non-coding RNA CASC11 interacts with hnRNP-K and activates the WNT/beta-catenin pathway to promote growth and metastasis in colorectal cancer.Here, we report that cancer susceptibility candidate 11 (CASC11) was upregulated in CRC tissues;Furthermore, CASC11 can target heterogeneous ribonucleoprotein K (hnRNP-K) to activate WNT/beta-catenin signaling in CRC cells. In addition, we found that c-Myc directly bound to the promoter regions of CASC11 and increased promoter histone acetylation to enhance CASC11 expression.	27012187	RID01667	transcriptional regulation
Colorectal cancer	MYC	CASC11	positively-E	RNA pull-down assay;RIP;IHC	NA	NA	NA	NA	cell growth(+);cell metastasis(+);WNT/beta-catenin signaling pathway(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000249375	GRCh38_8:127686343-127738987	4609	100270680	MRTL|MYCC|bHLHe39|c-Myc	CARLO7|CARLo-7|LINC00990|TCONS_00014535	Long non-coding RNA CASC11 interacts with hnRNP-K and activates the WNT/beta-catenin pathway to promote growth and metastasis in colorectal cancer.Here, we report that cancer susceptibility candidate 11 (CASC11) was upregulated in CRC tissues;Furthermore, CASC11 can target heterogeneous ribonucleoprotein K (hnRNP-K) to activate WNT/beta-catenin signaling in CRC cells. In addition, we found that c-Myc directly bound to the promoter regions of CASC11 and increased promoter histone acetylation to enhance CASC11 expression.	27012187	RID01668	epigenetic regulation
Gastric cancer	RMRP	CCND2	positively-E	RNAi;miRcode	downregulation	qPCR;microarray	GSE47850	GSE47850.zip	cell growth(+);biomarker	ceRNA(miR-206)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000269900	GRCh38_9:35657751-35658018	ENSG00000118971	NA	6023	894	CHH|NME1|RMRPR|RRP2	KIAK0002|MPPH3	LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.RMRP is downregulated during gastric carcinogenesis. Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression.miR-206 is a potential tumor suppressor with G0/G1 cell cycle arrest by targeting the Cyclin D2.	27192121	RID01669	ceRNA or sponge
Prostate cancer	DANCR	TIMP2	negatively-E	western blot;RNA pull-down assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000035862	NA	57291	7077	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CSC-21K|DDC8	Long noncoding RNA DANCR promotes invasion of prostate cancer through epigenetically silencing expression of TIMP2/3.In the present study, we found the expression of DANCR increases in prostate cancer tissues and cells compared to normal prostate tissues and cells.Mechanistically, we found that TIMP2/3, which are critical metastasis inhibitor of prostate cancer, were down-regulated by DANCR synergistically with EZH2 through epigenetically silencing their promoter by chromatin immunoprecipitation assay.	27191265	RID01670	epigenetic regulation
Prostate cancer	DANCR	TIMP3	negatively-E	western blot;RNA pull-down assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000100234	NA	57291	7078	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	HSMRK222|K222|K222TA2|SFD	Long noncoding RNA DANCR promotes invasion of prostate cancer through epigenetically silencing expression of TIMP2/3.In the present study, we found the expression of DANCR increases in prostate cancer tissues and cells compared to normal prostate tissues and cells.Mechanistically, we found that TIMP2/3, which are critical metastasis inhibitor of prostate cancer, were down-regulated by DANCR synergistically with EZH2 through epigenetically silencing their promoter by chromatin immunoprecipitation assay.	27191265	RID01671	epigenetic regulation
Glioblastoma	HIF1A-AS2	HMGA1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell stemness(+)	NA	regulation	NA	NA	CSC	Limitless Replicative Potential	Cancer	Brain glioma	lncRNA	TF	NA	GRCh38_14:61715558-61751097	ENSG00000137309	NA	100750247	3159	3'aHIF-1A|aHIF	HMG-R|HMGA1A|HMGIY	The Long Non-coding RNA HIF1A-AS2 Facilitates the Maintenance of Mesenchymal Glioblastoma Stem-like Cells in Hypoxic Niches.We identified hypoxia-inducible factor 1 alpha-antisense RNA 2 (HIF1A-AS2) as a subtype-specific hypoxia-inducible lncRNA, upregulated in mesenchymal GSCs.Among the HIF1A-AS2 interactome, IGF2BP2 and DHX9 were identified as direct partners. This association was needed for maintenance of expression of their target gene, HMGA1. Downregulation of HIF1A-AS2 led to delayed growth of mesenchymal GSC tumors, survival benefits, and impaired expression of HMGA1 in vivo.	27264189	RID01672	expression association
Gastric cancer	HOXA13	HOTTIP	positively-E	luciferase reporter assay;ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000106031	NA	ENSG00000243766	GRCh38_7:27198575-27207259	3209	100316868	HOX1|HOX1J	HOXA-AS6|HOXA13-AS1|NCRNA00213	Oncogenic function of the homeobox A13-long noncoding RNA HOTTIP-insulin growth factor-binding protein 3 axis in human gastric cancer. Knockdown of HoxA13 caused the downregulation of long non-coding RNA HOTTIP and insulin growth factor-binding protein 3 (IGFBP-3) genes, indicating that both were targets of HoxA13. Concurrent regulation of HoxA13-HOTTIP was mediated by the mixed lineage leukemia-WD repeat domain 5 complex, which caused the trimethylation of H3K4 and then stimulated cell proliferation. HoxA13 transactivated the IGFBP-3 promoter through the HOX-binding site.	27144338	RID01673	epigenetic regulation
Malignant glioma	H19	ABCB1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01674	expression association
Malignant glioma	H19	ABCC1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000103222	NA	283120	4363	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC29|ABCC|GS-X|MRP|MRP1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01675	expression association
Malignant glioma	H19	ABCG2	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-)	NA	association	NA	temozolomide	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000118777	NA	283120	9429	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.the expression level of H19 transcripts was increased compared to wild-type or nonresistant clones.Furthermore, the reduced expression of H19 altered major drug resistance genes, such as ABCB1 (MDR1), ABCC (MRP), and ABCG2 (BCRP), both at the mRNA and protein levels. Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas.Our results suggested that knockdown of H19 significantly downregulated the expression of these drug-resistant genes, both at the mRNA (P<0.001 vs respective control siRNA, Figure 4A) and protein (Figure 4B) levels. These data confirm that the H19-induced TMZ resistance is in part mediated by MDR, MRP, and ABCG2.	27366087	RID01676	expression association
Breast cancer	BCYRN1	BCL2L1	negatively-F	RIP;ChIP;IHC	upregulation	qPCR	NA	NA	oncogenic role(+)	alternative splicing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000236824	GRCh38_2:47335315-47335514	ENSG00000171552	NA	618	598	BC200|BC200a|LINC00004|NCRNA00004	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Regulation of alternative splicing of Bcl-x by BC200 contributes to breast cancer pathogenesis.In this study, we show that BC200 is upregulated in breast cancer. Mechanistically, BC200 contains a 17-nucleotide sequence complementary to Bcl-x pre-mRNA, which may facilitate its binding to Bcl-x pre-mRNA and recruitment of heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1, a known splicing factor. Together, these results suggest that BC200 plays an oncogenic role in breast cancer. Thus, BC200 may serve as a prognostic marker and possible target for attenuating deregulated cell proliferation in estrogen-dependent breast cancer.	27277684	RID01677	interact with mRNA
Malignant glioma	LNCRNA-ATB	TGFB2	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-200a)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000092969	NA	114004396	7042	NA	G-TSF|LDS4|TGF-beta2	Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time.ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-beta2.Recent study has reported that miR-200a suppresses renal cell carcinoma development by directly targeting TGF-beta2.	27267902	RID01678	ceRNA or sponge
Medulloblastoma	CRNDE	CASP3	negatively-E	IHC	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000164305	NA	NA	836	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CPP32|CPP32B|SCA-1	Long non-coding RNA CRNDE promotes tumor growth in medulloblastoma.Our data suggest that transcript levels of CRNDE are elevated in clinical medulloblastoma tissues instead of in adjacent non-cancerous tissues.In vivo data further showed that proliferating cell nuclei antigen (PCNA) was decreased, whereas the apoptosis initiator cleaved-caspase-3 was increased upon CRNDE knockdown in cancerous tissues from the mouse model.	27383309	RID01679	expression association
Medulloblastoma	CRNDE	PCNA	negatively-E	IHC	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Medulloblastoma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000132646	NA	NA	5111	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ATLD2	Long non-coding RNA CRNDE promotes tumor growth in medulloblastoma.Our data suggest that transcript levels of CRNDE are elevated in clinical medulloblastoma tissues instead of in adjacent non-cancerous tissues.In vivo data further showed that proliferating cell nuclei antigen (PCNA) was decreased, whereas the apoptosis initiator cleaved-caspase-3 was increased upon CRNDE knockdown in cancerous tissues from the mouse model.	27383309	RID01680	expression association
Thyroid cancer	H19	YES1	positively-E	luciferase reporter assay;IHC 	upregulation	qPCR	NA	NA	cell cycle(+)	ceRNA(miR-17-5p)	regulation	NA	NA	NA	NA	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000176105	NA	283120	7525	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HsT441|P61-YES|Yes|c-yes	Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer.H19 expression was higher in tumor samples and in thyroid cancer cell lines than nontumor tissues and normal thyroid cells.H19 was identified as a target of miR-17-5p, by Dual-Luciferase Reporter assays and RNA-binding protein immunoprecipitation assays. H19 antagonized the function of miR-17-5p on upregulation of its target YES1 and inhibited miR-17-5p-induced cell cycle progression.	27093644	RID01681	ceRNA or sponge
Uveal melanoma	PAUPAR	HES1	negatively-E	ChIP;western blot	downregulation	qPCR	NA	NA	tumorigenesis(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Uveal cancer	lncRNA	TF	ENSG00000281880	GRCh38_11:31812307-32002405	ENSG00000114315	NA	103157000	3280	NA	HES-1|HHL|HRY|bHLHb39	PAUPAR lncRNA suppresses tumourigenesis by H3K4 demethylation in uveal melanoma.We show that lncRNA PAUPAR is present at low levels in UM tissues and cell lines and modulates the tumourigenesis of UM in vitro and in vivo. The ectopic expression of PAUPAR in UM cells revealed that PAUPAR acts as a necessary UM suppressor and induces the silencing of HES1 expression, which significantly reduces tumour metastasis. Mechanistically, PAUPAR modulates HES1 expression by inhibiting histone H3K4 methylation.	27214741	RID01682	epigenetic regulation
Colorectal cancer	DUXAP9	TWIST1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000122691	NA	503638	7291	NA	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01683	ceRNA or sponge
Colorectal cancer	DUXAP9	SNAI1	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000124216	NA	503638	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01684	ceRNA or sponge
Colorectal cancer	DUXAP9	VIM	negatively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000026025	NA	503638	7431	NA	NA	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01685	ceRNA or sponge
Colorectal cancer	DUXAP9	TJP1	positively-E	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(-);cell migration(-);WNT/beta-catenin signaling pathway(-)	ceRNA(miR-145)	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000225210	GRCh38_14:19062316-19131167	ENSG00000104067	NA	503638	7082	NA	ZO-1	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/beta-catenin signaling and predicts favorable prognosis. Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues.Furthermore, downregulation of CTD903 enhanced Wnt/beta-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	RID01686	ceRNA or sponge
Gastric cancer	HOTTIP	HOXA13	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	HOTTIP and HOXA13 are oncogenes associated with gastric cancer progression.We found that HOTTIP was upregulated in gastric cancer cell lines. Moreover, downregulation of HOTTIP led to decreased expression of homeobox protein Hox-A13 (HOXA13) in gastric cancer cell lines. HOXA13 was involved in HOTTIP-induced malignant phenotypes of gastric cancer cells.	27108607	RID01687	expression association
Epithelial ovarian cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC). Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation.	27095571	RID01688	expression association
Epithelial ovarian cancer	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC). Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation.	27095571	RID01689	expression association
Ovarian cancer	MALAT1	MMP13	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137745	NA	378938	4322	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG3|MANDP1|MDST|MMP-13	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01690	expression association
Ovarian cancer	MALAT1	MMP19	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000123342	NA	378938	4327	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CODA|MMP18|RASI-1	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01691	expression association
Ovarian cancer	MALAT1	ADAMTS1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000154734	NA	378938	9510	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C3-C5|METH1	The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration.Overexpressed MALAT-1 expression in SKOV3 cells promoted cell proliferation, migration and invasion. Downregulation of MALAT-1 resulted in significant change of gene expression (at least 2-fold) in 449 genes, which regulate proliferation, cell cycle, and adhesion. As a consequence of MALAT-1 knockdown, MMP13 protein expression decreased, while the expression of MMP19 and ADAMTS1 was increased.	27227769	RID01692	expression association
Colorectal cancer	linc-UFC1	CTNNB1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01693	expression association
Colorectal cancer	linc-UFC1	MAPK1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01694	expression association
Colorectal cancer	linc-UFC1	CDK4	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000135446	NA	NA	1019	NA	CMM3|PSK-J3	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01695	expression association
Colorectal cancer	linc-UFC1	CCND1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01696	expression association
Colorectal cancer	linc-UFC1	RB1	negatively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_1:161152776-161158856	ENSG00000139687	NA	NA	5925	NA	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage.Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of beta-catenin and activation of phosphorylated P38. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and beta-catenin and P38 signaling.	27195675	RID01697	expression association
Non-small cell lung cancer	AGAP2-AS1	LATS2	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000150457	NA	100130776	26524	PUNISHER	KPM	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID01698	epigenetic regulation
Non-small cell lung cancer	AGAP2-AS1	KLF2	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE19188;GSE18842	GSE19188.zip;GSE18842.zip	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	TF	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000127528	NA	100130776	10365	PUNISHER	LKLF	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID01699	epigenetic regulation
Hepatocellular carcinoma	HNF1A-AS1	BCL2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(+)	ceRNA(miR-30b-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000171791	NA	283460	596	C12orf27|HAS1|NCRNA00262	Bcl-2|PPP1R50	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p. HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines. HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. ATG5 is a direct target of miR-30b and thereby a ceRNA for HNF1A-AS1.	27084450	RID01700	ceRNA or sponge
Hepatocellular carcinoma	HNF1A-AS1	ATG5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell autophagy(+)	ceRNA(miR-30b-5p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000057663	NA	283460	9474	C12orf27|HAS1|NCRNA00262	APG5|APG5-LIKE|APG5L|ASP|SCAR25|hAPG5	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p. HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines. HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. ATG5 is a direct target of miR-30b and thereby a ceRNA for HNF1A-AS1.	27084450	RID01701	ceRNA or sponge
Nasopharynx carcinoma	H19	EZH2	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+)	ceRNA(miR-630)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma.Herein, we found that H19 was overexpressed in NPC tissues and poorly differentiated cell lines.Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner.	27040767	RID01702	ceRNA or sponge
Her2-receptor positive breast cancer	GAS5	PTEN	positively-E	IHC;RNAi	downregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-21)	regulation	NA	trastuzumab	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer.Expression of the lncRNA GAS5 was decreased in trastuzumab-resistant SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. This work identifies GAS5 as a novel prognostic marker and candidate drug target for HER2-positive breast cancer.	27034004	RID01703	ceRNA or sponge
Renal cell carcinoma	LNCARSR	AXL	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34;miR-449)	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000167601	NA	112577459	558	NA	ARK|JTK11|Tyro7|UFO	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA. Here we identified an lncRNA, named lncARSR (lncRNA Activated in RCC with Sunitinib Resistance), which correlated with clinically poor sunitinib response. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	27117758	RID01704	ceRNA or sponge
Renal cell carcinoma	LNCARSR	MET	positively-E	RNAi;luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	ceRNA(miR-34;miR-449)	regulation	NA	sunitinib	NA	NA	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000233086	GRCh38_9:79505804-79567802	ENSG00000105976	NA	112577459	4233	NA	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA. Here we identified an lncRNA, named lncARSR (lncRNA Activated in RCC with Sunitinib Resistance), which correlated with clinically poor sunitinib response. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	27117758	RID01705	ceRNA or sponge
Non-small cell lung cancer	LINC00673	NCALD	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	microarray	GSE18842	GSE18842.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000104490	NA	100499467	83988	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	NA	Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer.We identified an oncogene, linc00673, whose expression level was upregulated by bioinformatics analyses and qRT-PCR analyses in NSCLC. Further mechanistic analyses indicated that the oncogenic activity of linc00673 is partially attributable to its repression of NCALD through association with the epigenetic repressor LSD1, Histone demethylase lysine specific demethylase 1.	27027352	RID01706	epigenetic regulation
Esophagus squamous cell carcinoma	MALAT1	CTNNB1	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01707	expression association
Esophagus squamous cell carcinoma	MALAT1	EZH2	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01708	expression association
Esophagus squamous cell carcinoma	MALAT1	LIN28A	positively-E	RNAi;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131914	NA	378938	79727	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues. Down-regulation of MALAT1 decreased the expression of beta-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of beta-catenin and Lin28 in esophageal cancer cells.	27015363	RID01709	expression association
Hepatocellular carcinoma	FTX	DDX58	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	host(miR-545)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000230590	GRCh38_X:73940435-74293574	ENSG00000107201	NA	100302692	23586	LINC00182|MIR374AHG|NCRNA00182	RIG-I|RIG1|RIGI|RLR-1|SGMRT2	Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.We demonstrated that the lncRNA Ftx and Ftx-derived miR-545 were up-regulated in both HCC tissues and cells. MiR-545 was positively correlated with lncRNA Ftx expression.We found that miR-545 was a pivotal mediator in Ftx-induced promotion of HCC cell growth. Subsequently, we identified RIG-I as a direct target of miR-545. The expression of RIG-I was downregulated in HCC tissues and was inversely correlated with miR-545 expression. In conclusion, our study demonstrates that the novel pathway lncRNA Ftx/miR-545/RIG-I promotes HCC development by activating PI3K/Akt signaling, and it may serve as a novel prognostic biomarker and therapeutic target for HCC.	26992218	RID01710	expression association
Hepatocellular carcinoma	SNHG1	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000141510	NA	23642	7157	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA SNHG1 predicts a poor prognosis and promotes hepatocellular carcinoma tumorigenesis.In this study, we found SNHG1 was upregulated in HCC tissues in comparison with adjacent liver tissues in both publicly available microarray data and our own cohort. Further experiments revealed that SNHG1 promotes HCC cells proliferation through inhibiting p53 and p53-target genes expression.	27133041	RID01711	expression association
Gastric cancer	UCA1	PARP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	association	NA	adriamycin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000143799	NA	652995	142	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Silence of long noncoding RNA UCA1 inhibits malignant proliferation and chemotherapy resistance to adriamycin in gastric cancer.UCA1 was highly expressed in gastric cancer tissues and cells, and its high expression level had a positive correlation with some malignant pathological characteristics of gastric cancer, such as higher grade and poor differentiation. The chemotherapy resistance to adriamycin of SGC7901/ADR cells was depressed by UCA1 silence, and IC50 for adriamycin presented a conspicuous depression.UCA1 silence advanced apoptosis induced by adriamycin in SGC7901/ADR cells, up-regulated cleaved PARP protein expression and depressed the expression of anti-apoptosis protein Bcl-2. These results demonstrated that chemotherapy resistance changes induced by UCA1 silence might be mediated by the cell apoptosis pathway.	27056384	RID01712	expression association
Gastric cancer	UCA1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);apoptosis process(-)	NA	association	NA	adriamycin	NA	Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000171791	NA	652995	596	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Bcl-2|PPP1R50	Silence of long noncoding RNA UCA1 inhibits malignant proliferation and chemotherapy resistance to adriamycin in gastric cancer.UCA1 was highly expressed in gastric cancer tissues and cells, and its high expression level had a positive correlation with some malignant pathological characteristics of gastric cancer, such as higher grade and poor differentiation. The chemotherapy resistance to adriamycin of SGC7901/ADR cells was depressed by UCA1 silence, and IC50 for adriamycin presented a conspicuous depression.UCA1 silence advanced apoptosis induced by adriamycin in SGC7901/ADR cells, up-regulated cleaved PARP protein expression and depressed the expression of anti-apoptosis protein Bcl-2. These results demonstrated that chemotherapy resistance changes induced by UCA1 silence might be mediated by the cell apoptosis pathway.	27056384	RID01713	expression association
Pancreatic cancer	LINC-ROR	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000148516	NA	100885779	6935	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway. In the present study, we found that linc-ROR was upregulated in PC tissues. Mechanistically, we confirmed that linc-ROR up-regulates ZEB1 and then induces epithelial-mesenchymal transition (EMT), which promotes the aggressive biological behaviors of PC.	26898939	RID01714	expression association
Breast cancer	MALAT1	PROM1	negatively-E	IHC;ChIP	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000007062	NA	378938	8842	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	The Ribonucleic Complex HuR-MALAT1 Represses CD133 Expression and Suppresses Epithelial-Mesenchymal Transition in Breast Cancer. In this study, we show that a ribonucleoprotein complex including the long noncoding RNA MALAT1 and the RNA-binding protein HuR (ELAVL1) binds the CD133 promoter region to regulate its expression. In conclusion, our findings suggest that the failure of a repressive complex to form or stabilize in breast cancer promotes CD133 upregulation and an EMT-like program, providing new mechanistic insights underlying the control of prometastatic processes.	27197265	RID01715	transcriptional regulation
Osteosarcoma	H19	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200s)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.	27008415	RID01716	ceRNA or sponge
Osteosarcoma	H19	ZEB2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	ceRNA(miR-200s)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169554	NA	283120	9839	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.	27008415	RID01717	ceRNA or sponge
Osteosarcoma	FGFR3-AS1	FGFR3	positively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	NA	GRCh38_4:1807353-1808406	ENSG00000068078	NA	NA	2261	NA	ACH|CD333|CEK2|HSFGFR3EX|JTK4	Long noncoding RNA FGFR3-AS1 promotes osteosarcoma growth through regulating its natural antisense transcript FGFR3.FGFR3-AS1 was upregulated in osteosarcoma.Through antisense pairing with FGFR3 3'UTR, FGFR3-AS1 increases FGFR3 mRNA stability and upregulates FGFR3 expression. The expression of FGFR3-AS1 and FGFR3 is positively correlated in osteosarcoma tissues.	27022737	RID01718	interact with mRNA
Non-small cell lung cancer	PVT1	LATS2	negatively-E	IHC;RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000150457	NA	5820	26524	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	KPM	Long Noncoding RNA PVT1 Promotes Non-Small Cell Lung Cancer Cell Proliferation through Epigenetically Regulating LATS2 Expression.Here, we found that PVT1 was upregulated in 105 human NSCLC tissues compared with normal samples.RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription.	26908628	RID01719	epigenetic regulation
Acute myeloid leukemia	CCAT1	MYC	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell differentiation(+);cell growth(+)	ceRNA(miR-155)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia.In this study, the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients.By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155.Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155.	26923190	RID01720	ceRNA or sponge
Gastric cancer	LINC00668	CDKN2B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000147883	NA	400643	1030	NA	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01721	epigenetic regulation
Gastric cancer	E2F1	LINC00668	positively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000265933	GRCh38_18:6919496-6929966	1869	400643	E2F-1|RBAP1|RBBP3|RBP3	NA	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01722	transcriptional regulation
Gastric cancer	LINC00668	CDKN2A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000147889	NA	400643	1029	NA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01723	epigenetic regulation
Gastric cancer	LINC00668	CDKN1A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000124762	NA	400643	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01724	epigenetic regulation
Gastric cancer	LINC00668	CDKN1B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000111276	NA	400643	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01725	epigenetic regulation
Gastric cancer	LINC00668	CDKN1C	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000129757	NA	400643	1028	NA	BWCR|BWS|KIP2|WBS|p57|p57Kip2	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	RID01726	epigenetic regulation
Hepatocellular carcinoma	MEG3	GDF15	positively-E	western blot;IHC	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26992211	RID01727	expression association
Hepatocellular carcinoma	MEG3	MDM2	negatively-E	western blot;IHC	downregulation	qPCR	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000135679	NA	55384	4193	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ACTFS|HDMX|hdm2	Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Our study also revealed that the targeted delivery was mainly dependent on clathrin-mediated endocytosis and MEG3 RNA suppresses tumor growth mainly via increasing the expression of p53 and its downstream gene GDF15, but decreasing the expression of MDM2. Thus, this vector is promising as a novel delivery system and may facilitate a new approach to lncRNA based cancer therapy.	26992211	RID01728	expression association
Hepatocellular carcinoma	XIST	SMAD7	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-92b)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000101665	NA	7503	4092	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	CRCS3|MADH7|MADH8	MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XIST.Mechanistic investigations suggested that Smad7, which exhibited an inverse relationship with miR-92b expression in HCC, was a direct target of miR-92b and could reverse its effects on HCC tumorigenesis. Furthermore, long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and miR-92b could directly interact with and repress each other, and XIST could inhibit HCC cell proliferation and metastasis by targeting miR-92b.	27100897	RID01729	ceRNA or sponge
Colorectal cancer	MYC	TINCR	negatively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000223573	GRCh38_19:5558167-5578349	4609	257000	MRTL|MYCC|bHLHe39|c-Myc	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/beta-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression.It reported that c-Myc binding to the Sp1 transcription factor via the c-Myc central region and inhibition of Sp1 transcriptional activity on the cell cycle/growth arrest mechanism [19]. TINCR, transcribed by Sp1, was repressed by c-Myc.	27009809	RID01730	transcriptional regulation
Colorectal cancer	TINCR	EPCAM	negatively-F	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000223573	GRCh38_19:5558167-5578349	ENSG00000119888	NA	257000	4072	LINC00036|NCRNA00036|PLAC2|onco-lncRNA-16	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/beta-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression.TINCR specifically binds to EpCAM and regulates its proteolysis.	27009809	RID01731	interact with protein
Osteosarcoma	miR-141	H19	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.The overexpressed miR-141 suppressed H19 and miR-675 expression in hFOB1.19 cells. Taken together, our study revealed that tumor-suppressor miR-141 overexpression suppressed osteoblasts proliferation but induced apoptosis through down-regulating H19 or miR-675 in osteosarcoma.	27186302	RID01732	expression association
Colon cancer	Lnc34a	miR-34a	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	epigenetic regulation	regulation	NA	NA	CSC	Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	miRNA	NA	NA	NA	NA	NA	NA	NA	NA	A long non-coding RNA targets microRNA miR-34a to regulate colon cancer stem cell asymmetric division.Here we report a novel LncRNA, Lnc34a, that is enriched in colon cancer stem cells (CCSCs) and initiates asymmetric division by directly targeting the microRNA miR-34a to cause its spatial imbalance.Lnc34a recruits Dnmt3a via PHB2 and HDAC1 to methylate and deacetylate the miR-34a promoter simultaneously, hence epigenetically silencing miR-34a expression independent of its upstream regulator, p53. Lnc34a levels affect CCSC self-renewal and colorectal cancer (CRC) growth in xenograft models. Lnc34a is upregulated in late-stage CRCs, contributing to epigenetic miR-34a silencing and CRC proliferation.	27077950	RID01733	epigenetic regulation
Esophagus squamous cell carcinoma	TP73-AS1	BDH2	positively-E	RNAi;western blot	upregulation	qPCR;microarray	NA	NA	chemoresistance(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	5-fluorouracil;cisplatin	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000227372	GRCh38_1:3735511-3747373	ENSG00000164039	NA	57212	56898	KIAA0495|PDAM	DHRS6|EFA6R|PRO20933|SDR15C1|UCPA-OR|UNQ6308	Knockdown of long non-coding RNA TP73-AS1 inhibits cell proliferation and induces apoptosis in esophageal squamous cell carcinoma. Our results show that lncRNA TP73-AS1 and BDH2 levels are generally upregulated in esophageal cancer tissues and are strongly correlated with tumor location or TNM stage in clinical samples. LncRNA TP73-AS1 knockdown inhibited BDH2 expression in EC9706 and KYSE30 cells, whereas BDH2 knockdown repressed esophageal cancer cell proliferation and induced apoptosis via the caspase-3 dependent apoptotic pathway. In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin.	26799587	RID01734	expression association
Non-small cell lung cancer	TATDN1	CDH1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000147687	GRCh38_8:124488485-124539458	ENSG00000039068	NA	NA	999	CDA11	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01735	expression association
Non-small cell lung cancer	TATDN2	ERBB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000157014	GRCh38_3:10248023-10281218	ENSG00000141736	NA	NA	2064	NA	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01736	expression association
Non-small cell lung cancer	TATDN3	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000203705	GRCh38_1:212791828-212816830	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01737	expression association
Non-small cell lung cancer	TATDN1	EZR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000147687	GRCh38_8:124488485-124539458	ENSG00000092820	NA	NA	7430	CDA11	CVIL|CVL|HEL-S-105|VIL2	The role and potential mechanisms of LncRNA-TATDN1 on metastasis and invasion of non-small cell lung cancer.We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, beta-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting beta-catenin and Ezrin.	26943769	RID01738	expression association
Colorectal cancer	UCA1	CREB1	positively-E	RIP;luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	ceRNA(miR-204-5p)	regulation	NA	5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000118260	NA	652995	1385	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CREB|CREB-1	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.We found that UCA1 was up-regulated in CRCs and negatively correlated with survival time in two CRC cohorts. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression. The present work provides the first evidence of a UCA1-miR-204-5p-CREB1/BCL2/RAB22A regulatory network in CRC and reveals that UCA1 and CREB1 are potential new oncogenes and prognostic factors for CRC.	27046651	RID01739	ceRNA or sponge
Hepatocellular carcinoma	AFAP1-AS1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000067560	NA	84740	387	AFAP1-AS|AFAP1AS	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling.Expression of AFAP1-AS1 is increased in human HCC tissues and correlates with poor prognosis.the decreased expression levels of AFAP1-AS1, RhoA and Rac2 in si-AFAP1-AS1 group compared with the si-NC group (P<0.01).	26892468	RID01740	expression association
Hepatocellular carcinoma	AFAP1-AS1	RAC2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000128340	NA	84740	5880	AFAP1-AS|AFAP1AS	EN-7|Gx|HSPC022|p21-Rac2	Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling.Expression of AFAP1-AS1 is increased in human HCC tissues and correlates with poor prognosis.the decreased expression levels of AFAP1-AS1, RhoA and Rac2 in si-AFAP1-AS1 group compared with the si-NC group (P<0.01).	26892468	RID01741	expression association
Melanoma	GAS5	MMP2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000087245	NA	60674	4313	NCRNA00030|SNHG2	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Lentiviral-mediated overexpression of long non-coding RNA GAS5 reduces invasion by mediating MMP2 expression and activity in human melanoma cells.Overexpressing lncRNA GAS5 inhibited the migration and invasion ability of melanoma SK-Mel-110 cells, partially by decreasing the MMP2 expression and its activity.	26846479	RID01742	expression association
Ovarian cancer	BACE1-AS	BACE1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell proliferation(-);cell invasion(-)	NA	association	NA	anisomycin	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000278768	GRCh38_11:117288453-117293571	ENSG00000186318	NA	100379571	23621	BACE1-AS1|BACE1AS|NCRNA00177	ASP2|BACE|HSPC104	Long non-coding RNA BACE1-AS is a novel target for anisomycin-mediated suppression of ovarian cancer stem cell proliferation and invasion.The mRNA expression levels of long non-coding RNA (lncRNA) beta-site APP cleaving enzyme 1 antisense strand (BACE1-AS) were significantly increased in anisomycin-treated OCSCs compared to controls. Finally, when expression of lncRNA BACE1-AS was silenced using siRNA, BACE1 expression was downregulated and the antiproliferative and anti-invasive effects of anisomycin were reduced.	26783004	RID01743	expression association
Breast cancer	MALAT1	CDK4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+)	ceRNA(miR-124)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000135446	NA	378938	1019	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CMM3|PSK-J3	miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells.Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. MALAT1 increased the expression of CDK4, a target of miR-124	26918449	RID01744	ceRNA or sponge
Hepatocellular carcinoma	MT1JP	TP53	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell cycle(-);apoptosis process(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000255986	GRCh38_16:56635739-56637086	ENSG00000141510	NA	4498	7157	MT1|MT1J|MT1NP|MTB	BCC7|BMFS5|LFS1|P53|TRP53	LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway.By associating with the RNA-binding protein TIAR, MT1JP enhanced the translation of the master transcription factor p53, thereby regulating a series of pathways involving p53, such as the cell cycle, apoptosis and proliferation.Taken together, we identified MT1JP as a critical factor in restraining cell transformation by modulating p53 translation through interactions with TIAR, and this finding is likely to shed new light on future investigations about posttranscriptional or translational effects of lncRNAs during cell transformation.	26909858	RID01745	expression association
Melanoma	SAMMSON	C1QBP	interact	RIP;IHC	upregulation	qPCR	NA	NA	mitochondrial function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Melanoma	lncRNA	PCG	ENSG00000240405	GRCh38_3:69999550-70518064	ENSG00000108561	NA	101927152	708	LINC01212	NA	Melanoma addiction to the long non-coding RNA SAMMSON. Mechanistically, SAMMSON interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function.Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted anti-melanoma therapeutic responses.	27008969	RID01746	interact with protein
Hepatocellular carcinoma	UCA1	CDK2	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell cycle phase transition (G1/S)(+)	epigenetic regulation	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000123374	NA	652995	1017	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN2|p33(CDK2)	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID01747	epigenetic regulation
Hepatocellular carcinoma	UCA1	CDKN1B	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);tumorigenesis(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID01748	epigenetic regulation
Malignant glioma	HULC	ESM1	positively-E	IHC	upregulation	qPCR	NA	NA	angiogenesis(+);PI3K/AKT/mTOR signaling pathway(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000164283	NA	728655	11082	HCCAT1|LINC00078|NCRNA00078	endocan	HULC long noncoding RNA silencing suppresses angiogenesis by regulating ESM-1 via the PI3K/Akt/mTOR signaling pathway in human gliomas. This process induced anoikis and blocked the cell cycle at G1/S phase via the PI3K/Akt/mTOR signaling pathway, thus regulating the tumor-related genes involved in the above biological behavior in human glioma U87MG and U251 cells. However, these effects were reversed by ESM-1 overexpression, suggesting a mediating role of ESM-1 in the pro-angiogenesis effect of HULC.	26894862	RID01749	expression association
Gastric cancer	MALAT1	PCDH10	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138650	NA	378938	57575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OL-PCDH|PCDH19	MALAT1 long ncRNA promotes gastric cancer metastasis by suppressing PCDH10.In particular, we found that long noncoding RNA (lncRNA) MALAT1 binds EZH2, suppresses the tumor suppressor PCDH10, and promotes gastric cellular migration and invasion.	26871474	RID01750	epigenetic regulation
Colon cancer	HOTAIR	CASP2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106144	NA	100124700	835	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CASP-2|ICH1|NEDD-2|NEDD2|PPP1R57	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.Luciferase assays identified caspase 2, an initiator caspase, to be a new target of miR-125a-5p.In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. These findings indicate that miR-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	26962687	RID01751	expression association
Colon cancer	HOTAIR	miR-125a-5p	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.Luciferase assays identified caspase 2, an initiator caspase, to be a new target of miR-125a-5p.In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. These findings indicate that miR-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	26962687	RID01752	expression association
Colorectal cancer	MALAT1	AKAP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127914	NA	378938	10142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP-9|AKAP350|AKAP450|CG-NAP|HYPERION|LQT11|MU-RMS-40.16A|PPP1R45|PRKA9|YOTIAO	Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation.These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells.Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro.MALAT1 promotes colorectal cancer cell proliferation/migration/invasion via PRKA kinase anchor protein 9. overexpression of MALAT1 via RNA activation promoted CRC cell proliferation, invasion and migration in vitro, and stimulated tumor growth and metastasis in mice in vivo. Among these genes, PRKA kinase anchor protein 9 (AKAP-9) was significantly up-regulated at both mRNA and protein levels. Importantly, knockdown of AKAP-9 blocked MALAT1-mediated CRC cell proliferation, migration and invasion. These data indicate that MALAT1 may promote CRC tumor development via its target protein AKAP-9.	26887056;25446987	RID01753	expression association
Colorectal cancer	MALAT1	SRSF1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000136450	NA	378938	6426	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ASF|SF2|SF2p33|SFRS1|SRp30a	Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation.These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells.Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro.	26887056	RID01754	expression association
Colon cancer	FEZF1-AS1	FEZF1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	TF	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000128610	NA	154860	389549	NA	FEZ|HH22|ZNF312B	Long non-coding RNA FEZF1-AS1 facilitates cell proliferation and migration in colorectal carcinoma.Here, we discovered a novel long noncoding RNA (lncRNA) FEZF1 antisense RNA1 (FEZF1-AS1) is markedly upregulated in human primary colorectal carcinoma (CRC) and associated with CRC metastasis and poor prognosis.We further discovered that the downregulation of FEZF1-AS1 reduced its sense-cognate gene FEZF1 mRNA and protein expression in CRC cells. There was a positive correlation between FEZF1-AS1 and FEZF1 expression in CRC. Moreover, FEZF1 knockdown also significantly suppressed CRC cell proliferation, migration, and invasion. Our findings indicate that the dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction.	26848625	RID01755	expression association
Non-small cell lung cancer	LINC01133	KLF2	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000127528	NA	100505633	10365	NA	LKLF	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01756	epigenetic regulation
Non-small cell lung cancer	LINC01133	CDKN1A	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000124762	NA	100505633	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01757	epigenetic regulation
Non-small cell lung cancer	LINC01133	CDH1	negatively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000039068	NA	100505633	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID01758	epigenetic regulation
Lung adenocarcinoma	RGMB-AS1	RGMB	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000174136	NA	503569	285704	NA	DRAGON	Long Noncoding RNA RGMB-AS1 Indicates a Poor Prognosis and Modulates Cell Proliferation, Migration and Invasion in Lung Adenocarcinoma.The expression of lncRNA RGMB-AS1 was inversely correlated with that of repulsive guidance molecule b (RGMB) in lung adenocarcinoma tissues, and UCSC analysis and fluorescence detection assay indicated that lncRNA RGMB-AS1 may be involved in the development of human lung adenocarcinoma by regulating RGMB expression though exon2 of RGMB.	26950071	RID01759	expression association
Pancreatic cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	fenofibrate	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of LncRNA MEG3.Fenofibrate significantly inhibited proliferation of pancreatic cancer cells, increased MEG3 expression and p53 levels. Moreover, knockdown of MEG3 attenuated cytotoxicity induced by fenofibrate. Furthermore, overexpression of MEG3 induced cells death and increased p53 expression. Our results indicated fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of MEG3.	26850851	RID01760	expression association
Malignant glioma	MALAT1	MMP2	negatively-E	IHC	downregulation	qPCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.	26938295	RID01761	expression association
Gastric cancer	CCAT1	HNRNPA1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(+)	ceRNA(miR-490)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000135486	NA	100507056	3178	CARLO5|CARLo-5|onco-lncRNA-40	ALS19|ALS20|HNRPA1|HNRPA1L3|IBMPFD3|UP 1|hnRNP A1|hnRNP-A1	The long noncoding RNA colon cancer-associated transcript-1/miR-490 axis regulates gastric cancer cell migration by targeting hnRNPA1.In this study, we provide the first evidence that CCAT1 regulates miR-490 in gastric cancer (GC) cells. Interestingly, miR-490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR-490 expression was downregulated in GC. The negative correlation between miR-490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR-490-binding site, and deletion of this binding site abolishes their miR-490 responsiveness. Post-transcriptional CCAT1 silencing by miR-490 significantly suppressed GC cell migration. Furthermore, miR-490 directly bound to the hnRNPA1 mRNA 3'-UTR to repress its translation.	26825578	RID01762	ceRNA or sponge
Cervical cancer	MALAT1	TJP1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104067	NA	378938	7082	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ZO-1	Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	26798987	RID01763	expression association
Cervical cancer	MALAT1	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers beta-catenin and Vimentin.	26798987	RID01764	expression association
Gastric cancer	CYTOR	CDKN2B	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000147883	NA	112597	1030	C2orf59|LINC00152|NCRNA00152	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID01765	epigenetic regulation
Gastric cancer	CYTOR	CDKN2A	negatively-E	RIP;ChIP;IHC;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000147889	NA	112597	1029	C2orf59|LINC00152|NCRNA00152	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID01766	epigenetic regulation
Breast cancer	PANDAR	CDKN2A	negatively-E	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle phase transition (G1/S)(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000147889	NA	101154753	1029	PANDA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression.In this study, we investigated the role of lncRNA PANDAR in the progression of breast cancer and found that PANDAR was up-regulated in breast cancer tissues and cell lines. The knockdown of PANDAR suppresses G1/S transition of breast cancer cells. We demonstrated mechanistically that the regulation of G1/S transition by PANDAR was partly due to the transcriptional modulation of p16(INK4A).	26927017	RID01767	transcriptional regulation
Non-small cell lung cancer	PVT1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000147883	NA	5820	1030	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer.Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines.In conclusion, our study demonstrated that PVT1 might serve as a promising biomarker for diagnosis and prognosis of NSCLC, and it could promote the proliferation of NSCLC cells by downregulating p15 and p21 expression.	26490983	RID01768	expression association
Non-small cell lung cancer	PVT1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124762	NA	5820	1026	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer.Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines.In conclusion, our study demonstrated that PVT1 might serve as a promising biomarker for diagnosis and prognosis of NSCLC, and it could promote the proliferation of NSCLC cells by downregulating p15 and p21 expression.	26490983	RID01769	expression association
Osteosarcoma	SNHG12	AMOT	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000126016	NA	85028	154796	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	NA	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes cell proliferation and migration by upregulating angiomotin gene expression in human osteosarcoma cells.SNHG12 and AMOT messenger RNA (mRNA) expression was upregulated in osteosarcoma tissues and cell lines when compared with normal tissues and cells. Upregulation of AMOT mRNA was associated with upregulation of SNHG12.This preliminary study has shown that the lncRNA SNHG12 promotes cell proliferation and migration by upregulating AMOT gene expression in osteosarcoma cells in vivo and in vitro.	26486328	RID01770	expression association
Pancreatic ductal adenocarcinoma	HOTAIR	WIF1	negatively-E	RNAi	upregulation	qPCR	NA	NA	radiosensitivity(-)	NA	association	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000156076	NA	100124700	11197	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	WIF-1	The long non-coding RNA HOTAIR affects the radiosensitivity of pancreatic ductal adenocarcinoma by regulating the expression of Wnt inhibitory factor 1. HOX transcript antisense intergenic RNA (HOTAIR) is overexpressed in PDAC.And HOTAIR silencing increased the expression of WIF-1. Furthermore, the overexpression of WIF-1 revealed that HOTAIR modulated the radiosensitivity of PDAC cells by regulating the expression of WIF-1.	26482614	RID01771	expression association
Breast cancer	MALAT1	KDM5B	positively-E	IHC	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117139	NA	378938	10765	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CT31|JARID1B|MRT65|PLU-1|PLU1|PPP1R98|PUT1|RBBP2H1A|RBP2-H1	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.Compared with other breast cancer types, the highly metastatic MDA-MB-231 cells concurrently exhibited increased expression levels of Lysine-specific demethylase 5B protein (KDM5B) and long non-coding RNA (lncRNA), MALAT1, suggesting their functional association.KDM5B-silencing in the TNBC cells correlated with the upregulation of hsa-miR-448 and led to suppression of MALAT1 expression with decreased migration, invasion and clonogenic capacity in vitro.	26917489	RID01772	expression association
Breast cancer	MALAT1	miR-448	negatively-E	IHC	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.Compared with other breast cancer types, the highly metastatic MDA-MB-231 cells concurrently exhibited increased expression levels of Lysine-specific demethylase 5B protein (KDM5B) and long non-coding RNA (lncRNA), MALAT1, suggesting their functional association.KDM5B-silencing in the TNBC cells correlated with the upregulation of hsa-miR-448 and led to suppression of MALAT1 expression with decreased migration, invasion and clonogenic capacity in vitro.	26917489	RID01773	expression association
Gastric cancer	TUG1	CDKN1C	negatively-E	RIP;ChIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000129757	NA	55000	1028	LINC00080|NCRNA00080|TI-227H	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation.	26913601	RID01774	epigenetic regulation
Neuroblastoma	MALAT1	FGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000138685	NA	378938	2247	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BFGF|FGF-2|FGFB|HBGF-2	The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.	26848616	RID01775	expression association
Colorectal cancer	CTNNB1	KCNQ1OT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000269821	GRCh38_11:2608328-2699994	1499	10984	CTNNB|EVR7|MRD19|NEDSDV|armadillo	KCNQ1-AS2|KCNQ10T1|Kncq1|KvDMR1|KvLQT1-AS|LIT1|NCRNA00012	Regulation of functional KCNQ1OT1 lncRNA by beta-catenin.Here, we show that the KCNQ1OT1 transcriptional level was significantly increased in human colorectal cancer cells in which beta-catenin was excessively accumulated in the nucleus. Additionally, overexpression of beta-catenin resulted in an increase in KCNQ1OT1 lncRNA-coated territory. On the other hand, knockdown of beta-catenin resulted in significant decrease of KCNQ1OT1 lncRNA-coated territory and an increase in the mRNA expression of the SLC22A18 and PHLDA2 genes that are regulated by KCNQ1OT1. We showed that beta-catenin can promote KCNQ1OT1 transcription through direct binding to the KCNQ1OT1 promoter. Our evidence indicates that beta-catenin signaling may contribute to development of colorectal cancer by functioning as a novel lncRNA regulatory factor via direct targeting of KCNQ1OT1.	26868975	RID01776	transcriptional regulation
Pancreatic cancer	lncRNA-NUTF2P3-001	KRAS	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-3923)	regulation	NA	NA	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENST00000448540	GRCh38_9:77580245-77580628	ENSG00000133703	NA	NA	3845	NA	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Hypoxia-induced lncRNA-NUTF2P3-001 contributes to tumorigenesis of pancreatic cancer by derepressing the miR-3923/KRAS pathway.Microarray co-assay for lncRNAs and mRNAs demonstrates that lncRNA-NUTF2P3-001 is remarkably overexpressed in pancreatic cancer and chronic pancreatitis tissues, which positively correlates with KRAS mRNA expression. The dual-luciferase reporter assay further validates that lncRNA-NUTF2P3-001 and 3'UTR of KRAS mRNA competitively bind with miR-3923.	26755660	RID01777	ceRNA or sponge
Hepatocellular carcinoma	MALAT1	EPAS1	positively-E	RNAi;IHC;luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	transcriptional regulation	association	protein-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116016	NA	378938	2034	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ECYT4|HIF2A|HLF|MOP2|PASD2|bHLHe73	A MALAT1/HIF-2alpha feedback loop contributes to arsenite carcinogenesis.We have found that MALAT1, a non-coding RNA, is over-expressed in the sera of people exposed to arsenite and in hepatocellular carcinomas (HCCs). In addition, hypoxia-inducible factor (HIF)-2alpha is up-regulated in HCCs, and MALAT1 and HIF-2alpha have a positive correlation in HCC tissues. In turn, HIF-2alpha transcriptionally regulates MALAT1, thus forming a positive feedback loop to ensure expression of arsenite-induced MALAT1 and HIF-2alpha, which are involved in malignant transformation.	26735578	RID01778	transcriptional regulation
Colon cancer	AOC4P	UHRF1	positively-F	RIP;RNA pull-down assay;ChIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000260105	GRCh38_17:42865922-42874369	ENSG00000276043	NA	90586	29128	NA	ICBP90|Np95|RNF106|TDRD22|hNP95|hUHRF1|huNp95	Long noncoding RNA UPAT promotes colon tumorigenesis by inhibiting degradation of UHRF1.UPAT interacts with and stabilizes the epigenetic factor UHRF1 by interfering with its beta-transducin repeat-containing protein (TrCP)-mediated ubiquitination.	26768845	RID01779	interact with protein
Malignant glioma	DNMT1	MEG3	negatively-E	Methylation-specific polymerase chain reaction;5-aza-2'-deoxycytidine treatment	downregulation	qPCR	NA	NA	cell proliferation(+);apoptosis proces(-)s;p53 signaling pathway(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Genome Instability and Mutation	Cancer	Brain glioma	PCG	lncRNA	ENSG00000130816	NA	ENSG00000214548	GRCh38_14:100779410-100861031	1786	55384	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Epigenetic repression of long non-coding RNA MEG3 mediated by DNMT1 represses the p53 pathway in gliomas.In this investigation we showed that the downregulation of MEG3 expression due to hypermethylation of MEG3 was observed in gliomas tissues. In addition, DNMT1 was involved in MEG3 promoter methylation, and was inversely correlated with MEG3 expression in gliomas. The inhibition of DNMT1 repressed the proliferation, clone formation, and induced apoptosis in glioma cells.These results suggest that DNMT1-mediated MEG3 hypermethylation caused the loss of MEG3 expression, followed by the inhibition of the p53 pathways in gliomas.	26676363	RID01780	epigenetic regulation
Ovarian cancer	HOTAIR	PIK3R3	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000117461	NA	100124700	8503	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	p55|p55-GAMMA|p55PIK	HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3.The expression of HOTAIR and PIK3R3 in ovarian SKOV3 and OVCAR3 was increased compared with A2780 cells (P<0.05). The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced (p<0.05).	26826873	RID01781	expression association
Laryngeal squamous cell carcinoma	NEAT1	CDK6	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	ceRNA(miR-107)	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105810	NA	283131	1021	LINC00084|NCRNA00084|TncRNA|VINC	MCPH12|PLSTIRE	Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway.NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression.Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107.Based on two databases targetscan (www.targetscan.org) and starbase (starbase.sysu.edu.cn), we found that CDK6 is a potential target of miR-107 while NEAT1 may acts as a regulator of miR-107.	26822763	RID01782	ceRNA or sponge
Nasopharynx carcinoma	HOTAIR	VEGFA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Long noncoding RNA Hotair mediated angiogenesis in nasopharyngeal carcinoma by direct and indirect signaling pathways. In this study, we discovered that lncRNA Hotair was extremely abundant in NPC cells and clinical NPC samples.Our study also demonstrated that Hotair promoted angiogenesis through directly activating the transcription of angiogenic factor VEGFA as well as through GRP78-mediated upregulation of VEGFA and Ang2 expression.	26717040	RID01783	expression association
Nasopharynx carcinoma	HOTAIR	ANGPT2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000091879	NA	100124700	285	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AGPT2|ANG2	Long noncoding RNA Hotair mediated angiogenesis in nasopharyngeal carcinoma by direct and indirect signaling pathways. In this study, we discovered that lncRNA Hotair was extremely abundant in NPC cells and clinical NPC samples.Our study also demonstrated that Hotair promoted angiogenesis through directly activating the transcription of angiogenic factor VEGFA as well as through GRP78-mediated upregulation of VEGFA and Ang2 expression.	26717040	RID01784	expression association
Colorectal cancer	PANTR1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000110092	NA	100506421	595	LINC01158|linc-Brn1a|linc-POU3F3	BCL1|D11S287E|PRAD1|U21B31	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01785	expression association
Colorectal cancer	PANTR1	CDK4	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000135446	NA	100506421	1019	LINC01158|linc-Brn1a|linc-POU3F3	CMM3|PSK-J3	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01786	expression association
Colorectal cancer	PANTR1	CDKN2C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000123080	NA	100506421	1031	LINC01158|linc-Brn1a|linc-POU3F3	INK4C|p18|p18-INK4C	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01787	expression association
Colorectal cancer	PANTR1	RB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000139687	NA	100506421	5925	LINC01158|linc-Brn1a|linc-POU3F3	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage.Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb.	26510906	RID01788	expression association
Head and neck squamous cell carcinoma	HOTAIR	ELAVL1	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+);cell metastasis(+)	ceRNA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000066044	NA	100124700	1994	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ELAV1|HUR|Hua|MelG	A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and Neck Squamous Cell Carcinoma Progression and Metastasis. Moreover, HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. Finally, HuR and HOTAIR levels were positively correlated and significantly up-regulated in tumours samples.We demonstrated the existence of a regulatory loop in which the expression of HOTAIR and HuR is reciprocally and temporally regulated during the metastasis and progression of HNSCC.	27941336;25112469	RID01789	ceRNA or sponge
Hepatocellular carcinoma	MEG3	ILF3	interact	western blot;RNA pull-down assay	downregulation	qPCR	NA	NA	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000129351	NA	55384	3609	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CBTF|DRBF|DRBP76|MMP4|MPHOSPH4|MPP4|MPP4110|NF-AT-90|NF110|NF110b|NF90|NF90a|NF90b|NF90c|NF90ctv|NFAR|NFAR-1|NFAR-2|NFAR110|NFAR2|NFAR90|TCP110|TCP80	The mechanism of adenosine-mediated activation of lncRNA MEG3 and its antitumor effects in human hepatoma cells.The co-expression network of MEG3 was generated by GO analysis and ILF3 was identified as MEG3 binding protein by RNA pulldown and western blot analysis. Ectopic expression of MEG3 increased p53, caspase-3 mRNA and protein levels, decreased MDM2 and cyclin D1 mRNA and protein levels, as well as ILF3 protein expression in HepG2 cells. These findings are the first to identify that adenosine increases MEG3 expression by inhibition of DNA methylation and its antitumor effects is involved in MEG3 activation. ILF3 may participate in the anticancer regulation of MEG3 by interacting with MEG3.	26647875	RID01790	interact with protein
Small cell lung cancer	HOTAIR	HOXA1	negatively-E	RIP;Bisulfite Sequencing PCR	downregulation	qPCR	NA	NA	chemoresistance(-)	DNA methylation	regulation	NA	cisplatin;adriamycin;etoposide	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105991	NA	100124700	3198	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSAS|HOX1|HOX1F	Long noncoding RNA-HOTAIR affects chemoresistance by regulating HOXA1 methylation in small cell lung cancer cells.Moreover, HOXA1 methylation increased in the resistant cells using bisulfite sequencing PCR. Depletion of HOTAIR reduced HOXA1 methylation by decreasing DNMT1 and DNMT3b expression. The interaction between HOTAIR and HOXA1 was validated by RNA immunoprecipitation. Taken together, our study suggested that HOTAIR mediates chemoresistance of SCLC by regulating HOXA1 methylation and could be utilized as a potential target for new adjuvant therapies against chemoresistance.A total of three anticancer drugs (Cisplatin (CDDP; Shandong, China), Adriamycin (ADM; Jiangsu, China), and Etoposide (VP-16; Jiangsu, China)) were obtained from commercial sources and were dissolved according to the manufacturer's instructions and tested in eight concentrations.	26707824	RID01791	epigenetic regulation
Ovarian cancer	TGFB1	MALAT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01792	expression association
Ovarian cancer	MALAT1	MAP2K1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169032	NA	378938	5604	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01793	expression association
Ovarian cancer	MALAT1	MAPK3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102882	NA	378938	5595	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01794	expression association
Ovarian cancer	MALAT1	MAPK14	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112062	NA	378938	1432	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01795	expression association
Ovarian cancer	MALAT1	MAPK8	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000107643	NA	378938	5599	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1.	27565324	RID01796	expression association
Gastric cancer	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	H19 serves as a diagnostic biomarker and up-regulation of H19 expression contributes to poor prognosis in patients with gastric cancer.H19 expression was remarkably increased in GC tissues and cell lines compared with that in the normal control.Furthermore, knockdown of H19 expression by siRNA could inhibit cell migration and invasion in GC cells partly via regulating E-cadherin protein expression. H19 might serve as a promising biomarker for early detection and prognosis prediction of GC.	26774144	RID01797	expression association
Lung cancer	PCAT6	TP53	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228288	GRCh38_1:202810954-202812156	ENSG00000141510	NA	100506696	7157	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	BCC7|BMFS5|LFS1|P53|TRP53	Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells.n this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation.	27458097	RID01798	expression association
Lung cancer	PCAT6	MYC	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228288	GRCh38_1:202810954-202812156	ENSG00000136997	NA	100506696	4609	KDM5B-AS1|KDM5BAS1|PCAN-R1|ncRNA-a2|onco-lncRNA-96	MRTL|MYCC|bHLHe39|c-Myc	Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells.n this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation.	27458097	RID01799	expression association
Hepatocellular carcinoma	miR-190a	TRERNA1	negatively-F	luciferase reporter assay	downregulation	qPCR;sequencing	TCGA	LIHC.zip	epithelial to mesenchymal transition(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000231265	GRCh38_20:50040716-50041504	NA	100887755	NA	LINC00651|treRNA	miR-190a inhibits epithelial-mesenchymal transition of hepatoma cells via targeting the long non-coding RNA treRNA. In this study, we show that miR-190a can silence treRNA post-transcriptionally. Suppression of treRNA by miR-190a led to significant changes of mesenchymal-epithelial transition markers and impaired migration and invasion capability of hepatoma cells. TCGA data indicated that miR-190a exhibited lower expression in hepatoma tissues, especially from patients with vascular tumor invasion, compared to normal tissues.	26608035	RID01800	ceRNA or sponge
Gallbladder cancer	H19	TWIST1	positively-E	IHC	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000122691	NA	283120	7291	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition.The overexpression of H19 in GBC cells enhanced tumor invasion and promoted EMT by upregulated transcription factor Twist1.	27073719	RID01801	expression association
Acute promyelocytic leukemia	PVT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia.Moreover, PVT1 knockdown by RNA interference led to suppression of the MYC protein level, and cell proliferation was inhibited.	26545364	RID01802	expression association
Embryonic carcinoma	H19	POU5F1	positively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000204531	NA	283120	5460	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01803	expression association
Embryonic carcinoma	H19	NANOG	positively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111704	NA	283120	79923	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01804	expression association
Embryonic carcinoma	H19	CDH1	negatively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01805	expression association
Embryonic carcinoma	H19	FUT4	negatively-E	IHC	upregulation	qPCR	NA	NA	pluripotency(+);tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Embryonic carcinoma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000196371	NA	283120	2526	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells.H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.	26415227	RID01806	expression association
Liver cancer	miR-675	H19	positively-E	RIP;ChIP;IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	epigenetic regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer.Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1alpha expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3) , histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac).Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. Strikingly, H19 may induce and activate tumor-specific pyruvate kinase M2 (PKM2) which is essential for the Warburg effect in its dimer and for gene expression in its teramer during tumorigenesis.	26376677	RID01807	epigenetic regulation
Liver cancer	H19	PKM	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000067225	NA	283120	5315	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CTHBP|HEL-S-30|OIP3|PK3|PKM2|TCB|THBP1	miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer.Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1alpha expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3) , histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac).Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. Strikingly, H19 may induce and activate tumor-specific pyruvate kinase M2 (PKM2) which is essential for the Warburg effect in its dimer and for gene expression in its teramer during tumorigenesis.	26376677	RID01808	expression association
Non-small cell lung cancer	MYC	H19	positively-E	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-);cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000130600	GRCh38_11:1995176-2001470	4609	283120	MRTL|MYCC|bHLHe39|c-Myc	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	c-Myc-regulated long non-coding RNA H19 indicates a poor prognosis and affects cell proliferation in non-small-cell lung cancer.Multivariate analyses found that H19 expression could serve as an independent prognostic factor for overall survival of NSCLC. Moreover, chromatin immunoprecipitation (ChIP) assays revealed that H19 was a direct transcriptional target of c-Myc. And, knockdown of H19 significantly inhibited NSCLC cell proliferation both in vitro and in vivo. In conclusion, our study demonstrated that H19 is involved in the oncogenesis of NSCLC, and H19 may be a potential diagnostic and target for new therapies in patients with NSCLC.c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively.	26482621;26722426	RID01809	transcriptional regulation
Non-small cell lung cancer	H19	miR-107	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively.	26722426	RID01810	expression association
Colorectal cancer	ETS1	BANCR	negatively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	chemosensitivity(+);cell invasion(+);cell metastasis(+)	histone modification	regulation	NA	fentanyl	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000134954	NA	ENSG00000278910	GRCh38_9:69296682-69311111	2113	100885775	ETS-1|EWSR2|c-ets-1|p54	LINC00586	Fentanyl inhibits the invasion and migration of colorectal cancer cells via inhibiting the negative regulation of Ets-1 on BANCR.Fentanyl induced BANCR upregulation and Ets-1 downregulation in CRC cells. Further studies showed that Ets-1 negatively regulated BANCR expression via the deacetylation of histones H3 within BANCR promoter.	26296467	RID01811	epigenetic regulation
Malignant glioma	CRNDE	XIAP	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);tumor malignant transformation(+)	ceRNA(miR-186)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000101966	NA	NA	331	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2. In conclusion, CRNDE played an oncogenic role of GSCs through the negative regulation of miR-186. Both CRNDE and miR-186 could be regarded as potential targets in the glioma therapy.	26231038	RID01812	ceRNA or sponge
Malignant glioma	CRNDE	PAK5	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);tumor malignant transformation(+)	ceRNA(miR-186)	regulation	NA	NA	CSC	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000101349	NA	NA	57144	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2. In conclusion, CRNDE played an oncogenic role of GSCs through the negative regulation of miR-186. Both CRNDE and miR-186 could be regarded as potential targets in the glioma therapy.	26231038	RID01813	ceRNA or sponge
Malignant glioma	HOTAIR	FGF1	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	ceRNA(miR-326)	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113578	NA	100124700	2246	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AFGF|ECGF|ECGF-beta|ECGFA|ECGFB|FGF-1|FGF-alpha|FGFA|GLIO703|HBGF-1|HBGF1	Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326.Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.These results suggested that FGF1 was a direct target of miR-326.	26183397	RID01814	ceRNA or sponge
Lung cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/beta-catenin signaling pathway.The present study detected that the expression levels of Meg3 were significantly lower in cisplatin-resistant A549/DDP lung cancer cells, compared with those in parental A549 cells. The results of the present study also demonstrated that the Meg3-mediated chemosensitivity enhancement was associated with the induction of cell-cycle arrest and increased apoptosis, through regulation of p53, beta-catenin and survivin, which is a target gene of the WNT/beta-catenin signaling pathway.	26059239	RID01815	expression association
Lung cancer	MEG3	CTNNB1	positively-E	RNAi	downregulation	qPCR	NA	NA	chemosensitivity(-);WNT/beta-catenin signaling pathway(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000168036	NA	55384	1499	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/beta-catenin signaling pathway.The present study detected that the expression levels of Meg3 were significantly lower in cisplatin-resistant A549/DDP lung cancer cells, compared with those in parental A549 cells. The results of the present study also demonstrated that the Meg3-mediated chemosensitivity enhancement was associated with the induction of cell-cycle arrest and increased apoptosis, through regulation of p53, beta-catenin and survivin, which is a target gene of the WNT/beta-catenin signaling pathway.	26059239	RID01816	expression association
Brain cancer	TUG1	HSF2	positively-E	RIP;ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	blood-tumor barrier(-)	ceRNA(miR-144)	regulation	NA	NA	NA	NA	Cancer	Brain cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000025156	NA	55000	3298	LINC00080|NCRNA00080|TI-227H	HSF 2|HSTF 2	The long noncoding RNA TUG1 regulates blood-tumor barrier permeability by targeting miR-144.Both bioinformatics and luciferase reporter assays demonstrated that TUG1 influenced BTB permeability via binding to miR-144. Furthermore, Knockdown of TUG1 also down-regulated Heat shock transcription factor 2 (HSF2), a transcription factor of the heat shock transcription factor family, which was defined as a direct and functional downstream target of miR-144. HSF2 up-regulated the promoter activities and interacted with the promoters of ZO-1, occludin, and claudin-5 in GECs. In conclusion, our results indicate that knockdown of TUG1 increased BTB permeability via binding to miR-144 and then reducing EC tight junction protein expression by targeting HSF2. Thus, TUG1 may represent a useful future therapeutic target for enhancing BTB permeability.	26078353	RID01817	ceRNA or sponge
Hepatocellular carcinoma	CDKN2B-AS1	KLF2	negatively-E	RIP;IHC	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000127528	NA	100048912	10365	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	LKLF	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID01818	epigenetic regulation
Her2-receptor positive breast cancer	LNCRNA-ATB	ZEB1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	trastuzumab	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000148516	NA	114004396	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.We identified long noncoding RNA activated by TGF-beta (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients.SKBR-3 which is HER-2 overexpressed breast cancer cell line. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. lnc-ATB shares regulatory miR-200c with ZEB1 and ZNF 217 which has been proven to be the direct targets of miR-200c in TR SKBR-3 cells.	25871474	RID01819	ceRNA or sponge
Her2-receptor positive breast cancer	LNCRNA-ATB	ZNF217	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);epithelial to mesenchymal transition(+)	ceRNA(miR-200c)	regulation	NA	trastuzumab	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	NA	GRCh38_14:19126530-19128974	ENSG00000171940	NA	114004396	7764	NA	ZABC1	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.We identified long noncoding RNA activated by TGF-beta (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients.SKBR-3 which is HER-2 overexpressed breast cancer cell line. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. lnc-ATB shares regulatory miR-200c with ZEB1 and ZNF 217 which has been proven to be the direct targets of miR-200c in TR SKBR-3 cells.	25871474	RID01820	ceRNA or sponge
Her2-receptor positive breast cancer	LNCRNA-ATB	PTEN	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	ceRNA(miR-21)	regulation	NA	trastuzumab	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000171862	NA	114004396	5728	NA	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.Lapatinib upregulates GAS5 in trastuzumab-resistant breast cancer through mTOR pathway. Additionally, inhibition of mTOR by rapamycin increases the expression of GAS5.In summary, GAS5, regulated by mTOR pathway, serves as a ceRNA of miR-21 to regulate PTEN in the development of breast cancer trastuzumab resistance (Figure 5c).	25871474	RID01821	ceRNA or sponge
Prostate cancer	MTOR	GAS5	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000198793	NA	ENSG00000234741	GRCh38_1:173858559-173868882	2475	60674	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	NCRNA00030|SNHG2	Reciprocal regulation of GAS5 lncRNA levels and mTOR inhibitor action in prostate cancer cells.mTOR inhibition enhances GAS5 transcript levels in certain prostate cancer cell lines. This selectivity is likely to be related to endogenous GAS5 expression levels, since GAS5 lncRNA is itself required for mTOR inhibitor action in prostate cancer cells. This lncRNA promotes the apoptosis of prostate cancer cells and its levels decline as prostate cancer cells acquire castrate-resistance, so that enhancing GAS5 expression may improve the effectiveness of chemotherapies.	25650269	RID01822	expression association
Triple-receptor negative breast cancer	miR-148a	HOTAIR	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer. In this study, we found that HOTAIR was increased in the peripheral blood mononuclear cells and cancer tissues from breast cancer patients, and was especially higher in patients with metastatic breast cancer. In addition, we found that estrogen promoted HOTAIR through its receptor GPER and estrogen-induced breast cancer cell migration was reversed by deleting HOTAIR in TN breast cancer cells MDA-MB-231 and BT549. Furthermore, we identified that E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients.	25928008	RID01823	expression association
Pancreatic ductal adenocarcinoma	HOTTIP	HOXA13	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+)	NA	regulation	NA	gemcitabine	NA	NA	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106031	NA	100316868	3209	HOXA-AS6|HOXA13-AS1|NCRNA00213	HOX1|HOX1J	The long non-coding RNA HOTTIP promotes progression and gemcitabine resistance by regulating HOXA13 in pancreatic cancer.Microarray analyses revealed that HOTTIP was one of the most significantly upregulated lncRNAs in PDAC tissues compared with pancreatic tissues.Furthermore, knockdown of HOXA13 by RNA interference (siHOXA13) revealed that HOTTIP promoted PDAC cell proliferation, invasion, and chemoresistance, at least partly through regulating HOXA13. As a crucial tumor promoter, HOTTIP promotes cell proliferation, invasion, and chemoresistance by modulating HOXA13. Therefore, the HOTTIP/HOXA13 axis is a potential therapeutic target and molecular biomarker for PDAC.	25889214	RID01824	expression association
Prostate cancer	AR	PCGEM1	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000227418	GRCh38_2:192749845-192776899	367	64002	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LINC00071|NCRNA00071|PCAT9	The long non-coding RNA PCGEM1 is regulated by androgen receptor activity in vivo.PCGEM1 was sharply down-regulated following castration and up-regulated upon AR activation in vivo. PCGEM1 and PRNCR1 were implicated in progression of prostate cancer (PCa) as transcriptional co-regulators of the androgen receptor (AR).	25744782	RID01825	expression association
Osteosarcoma	miR-9	MALAT1	negatively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);cell proliferation(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	17beta-estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner. Here we found that the high dose of E2 treatment upregulated miR-9 thus posttranscriptionally regulated MALAT-1 RNA level in OS cells, and then the downregulation of MALAT-1 inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) processes in the E2-dose dependent and ER-independent ways.	25592968	RID01826	expression association
Hepatocellular carcinoma	CCAT1	HMGA2	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(let-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000149948	NA	100507056	8091	CARLO5|CARLo-5|onco-lncRNA-40	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.CCAT1 levels are markedly increased in HCC tissues compared with pair-matched noncancerous hepatic tissues. CCAT1 promotes the proliferation and migration of HCC cells. CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7.	25884472	RID01827	ceRNA or sponge
Hepatocellular carcinoma	CCAT1	MYC	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(let-7)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.CCAT1 levels are markedly increased in HCC tissues compared with pair-matched noncancerous hepatic tissues. CCAT1 promotes the proliferation and migration of HCC cells. CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7.	25884472	RID01828	ceRNA or sponge
Neuroblastoma	NBAT1	REST	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Neuroblastoma	lncRNA	TF	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000084093	NA	729177	5978	CASC14|NBAT-1	DFNA27|GINGF5|HGF5|NRSF|WT6|XBR	The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation. CpG methylation and a high-risk neuroblastoma associated SNP on chromosome 6p22 functionally contribute to NBAT-1 differential expression. Loss of NBAT-1 increases cellular proliferation and invasion. It controls these processes via epigenetic silencing of target genes. NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST.	25517750	RID01829	expression association
Breast cancer	HOTAIR	miR-7	negatively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	CSC	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway.In addition, the downregulation of miR-7 in BCSCs may be indirectly attributed to lincRNA HOTAIR by modulating the expression of HoxD10 that promotes the expression of miR-7.	25070049	RID01830	expression association
Hepatocellular carcinoma	SPP1	HOTAIR	positively-E	luciferase reporter assay;IHC	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	PCG	lncRNA	ENSG00000118785	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6696	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Osteopontin enhances the expression of HOTAIR in cancer cells via IRF1.Interestingly, our data demonstrated that OPN could regulate PI3K/AKT and IRF1 expression and signaling, thereby influencing the expression of HOTAIR. We therefore conclude that OPN, as an extracellular matrix protein, can stimulate the expression of HOTAIR by attenuating the inhibitory effect of IRF1, and this results in promotion of the invasion and metastasis of cancer cells.	24999034	RID01831	expression association
Non-small cell lung cancer	EZH2	SPRY4-IT1	negatively-E	IHC;RNAi;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+);epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000106462	NA	NA	GRCh38_5:142317636-142318322	2146	100642175	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	SPRIGHTLY	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01832	epigenetic regulation
Non-small cell lung cancer	SPRY4-IT1	CDH1	positively-E	IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000039068	NA	100642175	999	SPRIGHTLY	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01833	expression association
Non-small cell lung cancer	SPRY4-IT1	VIM	positively-E	IHC	downregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000026025	NA	100642175	7431	SPRIGHTLY	NA	EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2). Moreover, overexpression of SPRY4-IT1 was found to have a key role in the epithelial-mesenchymal transition through the regulation of E-cadherin and vimentin expression.	24967960	RID01834	expression association
Endometrial cancer	LINC-ROR	miR-145	negatively-F	RNAi;site-directed mutagenesis kit	upregulation	qPCR;FISH	NA	NA	cell differentiation(-)	sponge	binding/interaction	RNA-RNA	NA	CSC	NA	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000258609	GRCh38_18:57054558-57072119	NA	NA	100885779	NA	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	24589415	RID01835	ceRNA or sponge
Cancer	TGFB1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell stemness(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7040	100124700	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines. We found that treatment with TGF-beta1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-beta1, and also the colony-forming capacity of colon and breast cancer cells.	24022994	RID01836	expression association
Cancer	miR-21	GAS5	negatively-F	RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Cancer	miRNA	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Negative regulation of lncRNA GAS5 by miR-21.This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Importantly, there is a putative miR-21-binding site in exon 4 of GAS5; deletion of the miR-21-binding site abolishes this activity.We further show that the biotin-labeled GAS5-RNA probe is able to pull down the key component (AGO2) of the RNA-induced silencing complex (RISC) and we subsequently identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs. Together, these results suggest that miR-21 targets not only tumor-suppressive protein-coding genes but also lncRNA GAS5.	23933812	RID01837	ceRNA or sponge
Osteosarcoma	E2F3	ERICD	positively-E	ChIP	downregulation	qPCR	NA	NA	apoptosis process(-);DNA damage(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Evading Apoptosis;Genome Instability and Mutation	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000112242	NA	ENSG00000280303	GRCh38_8:140636281-140638283	1871	104355217	E2F-3	ERIC|LINC01130|TCONS_00014875	The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage.Here, we report that lncRNA XLOC 006942, which we named ERIC, is regulated by E2F1 and, most probably, also E2F3. We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Our data identify ERIC as a novel lncRNA that is transcriptionally regulated by E2Fs, and restricts apoptosis induced by E2F1, as well as by DNA damage.	24168400	RID01838	transcriptional regulation
Osteosarcoma	E2F1	ERICD	positively-E	ChIP	downregulation	qPCR	NA	NA	apoptosis process(-);DNA damage(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	Evading Apoptosis;Genome Instability and Mutation	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000101412	NA	ENSG00000280303	GRCh38_8:140636281-140638283	1869	104355217	E2F-1|RBAP1|RBBP3|RBP3	ERIC|LINC01130|TCONS_00014875	The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage.Here, we report that lncRNA XLOC 006942, which we named ERIC, is regulated by E2F1 and, most probably, also E2F3. We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Our data identify ERIC as a novel lncRNA that is transcriptionally regulated by E2Fs, and restricts apoptosis induced by E2F1, as well as by DNA damage.	24168400	RID01839	transcriptional regulation
Osteosarcoma	loc285194	miR-211	negatively-F	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709788-116717040	NA	NA	NA	NA	NA	NA	LncRNA loc285194 is a p53-regulated tumor suppressor.In this study, we show that loc285194 is a p53 transcription target; ectopic expression of loc285194 inhibits tumor cell growth both in vitro and in vivo. Through deletion analysis, we identify an active region responsible for tumor cell growth inhibition within exon 4, which harbors two miR-211 binding sites. Importantly, this loc285194-mediated growth inhibition is in part due to specific suppression of miR-211. Together, these results suggest that loc285194 is a p53-regulated tumor suppressor, which acts in part through repression of miR-211.	23558749	RID01840	ceRNA or sponge
Cancer	RASSF1-AS1	RASSF1	negatively-E	RIP;ChIP	upregulation	qPCR;microarray	GSE5823;GSE11118;GSE10879;GSE12056;GSE13471	GSE5823.zip;GSE11118.zip;GSE10879.zip;GSE12056.zip;GSE13471.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000281358	GRCh38_3:50337511-50338300	ENSG00000068028	NA	102060282	11186	ANRASSF1	NA	The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation.ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region.	23990798	RID01841	epigenetic regulation
Hepatocellular carcinoma	RAB4B-EGLN2	EGLN2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000171570	GRCh38_19:40778242-40808418	ENSG00000269858	NA	100529264	112398	EGLN2|EIT-6|EIT6|HIF-PH1|HPH-1|HPH-3|PHD1|RERT-lncRNA	EIT-6|EIT6|HIF-PH1|HIFPH1|HPH-1|HPH-3|PHD1	An insertion/deletion polymorphism within RERT-lncRNA modulates hepatocellular carcinoma risk.Genotype-phenotype correlation studies showed that the deletion allele was significantly correlated with higher expression of both EGLN2 and RERT-lncRNA [a long noncoding RNA whose sequence overlaps with Ras-related GTP-binding protein 4b (RAB4B) and EGLN2)] in vivo and in vitro. Furthermore, RERT-lncRNA expression was also significantly correlated with EGLN2 expression in vivo, consistent with in vitro gain-of-function study that showed overexpressing RERT-lncRNA upregulated EGLN2.Taken together, rs10680577 contributes to hepatocarcinogenesis, possibly by affecting RERT-lncRNA structure and subsequently EGLN2 expression, making it a promising biomarker for early diagnosis of HCC.	23026137	RID01842	expression association
Cancer	MEG3	GDF15	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Activation of p53 by MEG3 non-coding RNA.We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter.Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways.	17569660	RID01843	transcriptional regulation
Cancer	MEG3	TP53	positively-E	ChIP;luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-)	transcriptional regulation	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Activation of p53 by MEG3 non-coding RNA.We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter.Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways.	17569660	RID01844	transcriptional regulation
Hepatocellular carcinoma	H19	ABCB1	negatively-E	western blot;RNAi;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	chemoresistance(+)	DNA methylation	regulation	NA	doxorubicin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000085563	NA	283120	5243	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells.In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells.H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Antisense H19 oligonucleotides transfection induced a marked increase in the percentage of MDR1 promoter methylation and decrease in MDR1 expression in R-HepG2 cells. Thus, the H19 gene is believed to induce P-glycoprotein expression and MDR1-associated drug resistance at least in liver cancer cells through regulation of MDR1 promoter methylation.	17297456	RID01845	epigenetic regulation
Breast cancer	E2F1	H19	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	TF	lncRNA	ENSG00000101412	NA	ENSG00000130600	GRCh38_11:1995176-2001470	1869	283120	E2F-1|RBAP1|RBBP3|RBP3	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	H19 mRNA-like noncoding RNA promotes breast cancer cell proliferation through positive control by E2F1. We show here that H19 transcription is up-regulated during the S-phase of growth-stimulated cells and that the H19 promoter is activated by E2F1 in breast cancer cells. Consistently, we demonstrate by chromatin immunoprecipitation assays that endogenous E2F1 is recruited to the H19 promoter in vivo. we conclude that the H19 RNA is actively linked to E2F1 to promote cell cycle progression of breast cancer cells.	15985428	RID01846	transcriptional regulation
Triple-receptor negative breast cancer	MYC	SNHG12	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Breast cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000197989	GRCh38_1:28578538-28583132	4609	85028	MRTL|MYCC|bHLHe39|c-Myc	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer.SNHG12 is upregulated in TNBC. Mechanistic investigations show that SNHG12 is a direct transcriptional target of c-MYC. Silencing SNHG12 expression inhibits TNBC cells proliferation and apoptosis promotion, whereas SNHG12 overexpression has the opposite effect. In addition, we reveal that SNHG12 may promote cells migration by regulating MMP13 expression.	28337281	RID01847	transcriptional regulation
Triple-receptor negative breast cancer	SNHG12	MMP13	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000197989	GRCh38_1:28578538-28583132	ENSG00000137745	NA	85028	4322	ASLNC04080|C1orf79|LINC00100|NCRNA00100|PNAS-123	CLG3|MANDP1|MDST|MMP-13	C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer.SNHG12 is upregulated in TNBC. Mechanistic investigations show that SNHG12 is a direct transcriptional target of c-MYC. Silencing SNHG12 expression inhibits TNBC cells proliferation and apoptosis promotion, whereas SNHG12 overexpression has the opposite effect. In addition, we reveal that SNHG12 may promote cells migration by regulating MMP13 expression.	28337281	RID01848	expression association
Cervical cancer	HOTAIR	MTOR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(+);apoptosis process(-)	NA	regulation	NA	propofol	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000198793	NA	100124700	2475	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer	26523512	RID01849	expression association
Oral squamous cell carcinoma	MALAT1	CTNNB1	positively-E	IHC	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of beta-catenin and NF-kB were attenuated, while elevated MALAT1 level triggered the expression of beta-catenin and NF-kB. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo.	26522444	RID01850	expression association
Oral squamous cell carcinoma	MALAT1	NFKB1	positively-E	IHC	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109320	NA	378938	4790	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of beta-catenin and NF-kB were attenuated, while elevated MALAT1 level triggered the expression of beta-catenin and NF-kB. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo.	26522444	RID01851	expression association
Hepatocellular carcinoma	LNCRNA-ATB	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000039068	NA	114004396	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA-ATB mediated E-cadherin repression promotes the progression of colon cancer and predicts poor prognosis.Long non-coding RNA-activated by TGF-beta (lncRNA-ATB) promotes the invasion-metastasis cascade in hepatocellular carcinoma via downregulating E-cadherin (E-cad) and inducing epithelial-to- mesenchymal transition (EMT) and is clinically significant in human colon cancer.	26487301	RID01852	expression association
Colon cancer	LNCRNA-ATB	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	NA	GRCh38_14:19126530-19128974	ENSG00000039068	NA	114004396	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	LncRNA-ATB mediated E-cadherin repression promotes the progression of colon cancer and predicts poor prognosis.Reduction of lncRNA-ATB increased expression of epithelial markers E-cad, ZO-1, and decreased expression of mesenchymal markers ZEB1 and N-cadherin (N-cad), and significantly influenced colon cancer cell progression. Long non-coding RNA-activated by TGF-beta may act on colon tumorigenesis by suppressing E-cad expression and promoting EMT process, and lncRNA-ATB inhibition may provide a promising therapeutic option for suppressing colon cancer progression.	26487301	RID01853	expression association
Neuroblastoma	MIR100HG	miR-125b-1	positively-E	ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	host	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	miRNA	ENSG00000255248	GRCh38_11:122028325-122556721	NA	NA	399959	NA	AGD1|linc-NeD125|lncRNA-N2	NA	Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. We also demonstrate that linc-NeD125 functions independently of the hosted microRNA, by reducing cell proliferation and activating the antiapoptotic factor BCL-2.	26480000	RID01854	expression association
Neuroblastoma	MIR100HG	BCL2	positively-E	RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroblastoma	lncRNA	PCG	ENSG00000255248	GRCh38_11:122028325-122556721	ENSG00000171791	NA	399959	596	AGD1|linc-NeD125|lncRNA-N2	Bcl-2|PPP1R50	Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. We also demonstrate that linc-NeD125 functions independently of the hosted microRNA, by reducing cell proliferation and activating the antiapoptotic factor BCL-2.	26480000	RID01855	expression association
Osteosarcoma	PACERR	PTGS2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000273129	GRCh38_1:186680622-186681446	ENSG00000073756	NA	103752588	5743	PACER|PTGS2-AS1|PTGS2AS1	COX-2|COX2|GRIPGHS|PGG/HS|PGHS-2|PHS-2|hCox-2	P50-associated COX-2 extragenic RNA (PACER) overexpression promotes proliferation and metastasis of osteosarcoma cells by activating COX-2 gene.Downregulation of PACER significantly suppressed the expression of COX-2, and the effects of PACER on cell proliferation and invasion were rescued by COX-2 overexpression.Taken together, these findings suggest that PACER promotes proliferation and metastasis of osteosarcoma cells by activating the COX-2 gene and its own expression was influenced by DNA methylation.	26476537	RID01856	expression association
Diffuse large B-cell lymphoma	TP53COR1	CCND1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000110092	NA	102800311	595	TRP53COR1|linc-p21|lincRNA-p21	BCL1|D11S287E|PRAD1|U21B31	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01857	expression association
Diffuse large B-cell lymphoma	TP53COR1	CDK4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000135446	NA	102800311	1019	TRP53COR1|linc-p21|lincRNA-p21	CMM3|PSK-J3	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01858	expression association
Diffuse large B-cell lymphoma	TP53COR1	CDKN1A	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000124762	NA	102800311	1026	TRP53COR1|linc-p21|lincRNA-p21	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy. We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal.Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines.	26475621	RID01859	expression association
Hepatocellular carcinoma	WT1-AS	WT1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(-);apoptosis process(+);JAK/STAT signaling pathway(-)	transcriptional regulation	binding/interaction	RNA-DNA	doxorubicin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000183242	GRCh38_11:32435518-32458769	ENSG00000184937	NA	51352	7490	WIT-1|WIT1|WT1-AS1|WT1AS	AWT1|GUD|NPHS4|WAGR|WIT-2|WT33	WT1-AS promotes cell apoptosis in hepatocellular carcinoma through down-regulating of WT1.WT1-AS expression correlated negatively with WT1 expression in HCC tumor tissue. Kaplan-Meier curve analysis revealed that WT1-AS expression is a reliable indicator of HCC prognosis. The downregulation of WT1 expression by WT1-AS promoted cell apoptosis by suppressing the JAK/STAT3 signaling pathway. Bioinformatics analysis showed that WT1-AS downregulates WT1 by binding to the TATA region of the WT1 promotor. WT1-AS was also able to reverse WT1-mediated resistance to Dox based chemotherapy in HCC cells.	26462627	RID01860	transcriptional regulation
Clear cell renal cell carcinoma	MALAT1	ZEB2	positively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma.Together these data indicated that by binding miR-200s family, especially miR-200c, MALAT1 acts as a ceRNA for the target ZEB2 mRNA thereby modulating the derepression of ZEB2 and imposing an additional level of post-transcriptional regulation. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC.	26461224	RID01861	ceRNA or sponge
Urinary bladder cancer	EZH2	HOTAIR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cancer progression(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000106462	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2146	100124700	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Analysis of the Polycomb-related lncRNAs HOTAIR and ANRIL in bladder cancer.We also observed a significant correlation between EZH2 and HOTAIR expression levels. Using overexpression, knockdown, and pharmacological approaches in bladder cancer cell lines, we also observed that EZH2 regulates HOTAIR expression.The observed HOTAIR regulation by EZH2 and the possibility of modulating EZH2 activity with specific inhibitors open new possible paths to be explored in bladder cancer therapy.	26457124	RID01862	expression association
Hepatocellular carcinoma	STAT3	WSPAR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000249073	GRCh38_5:133913677-133917269	6774	105664404	ADMIO|ADMIO1|APRF|HIES	LncTCF7|TCONS_00009511	Long noncoding RNA lncTCF7, induced by IL-6/STAT3 transactivation, promotes hepatocellular carcinoma aggressiveness through epithelial-mesenchymal transition. we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HCC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HCC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies.	26452542	RID01863	transcriptional regulation
Gastric cancer	WT1-AS	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000183242	GRCh38_11:32435518-32458769	ENSG00000100030	NA	51352	5594	WIT-1|WIT1|WT1-AS1|WT1AS	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Decreased expression of long non-coding RNA WT1-AS promotes cell proliferation and invasion in gastric cancer.Finally, we found that WT1-AS overexpression could decrease ERK protein phosphorylation. Our study indicates that WT1-AS is significantly down-regulated in gastric cancers and may be correlated with tumor progression.	26449525	RID01864	expression association
Gallbladder cancer	FAM30A	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000226777	GRCh38_14:105917979-105932642	ENSG00000168036	NA	9834	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Noncoding RNA KIAA0125 Potentiates Cell Migration and Invasion in Gallbladder Cancer. Moreover, the expression of beta-Catenin was increased and the expression of Vimentin was decreased in GBC-SD/M cells after KIAA0125 knockdown.	26448925	RID01865	expression association
Gallbladder cancer	FAM30A	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000226777	GRCh38_14:105917979-105932642	ENSG00000026025	NA	9834	7431	NA	NA	Long Noncoding RNA KIAA0125 Potentiates Cell Migration and Invasion in Gallbladder Cancer. Moreover, the expression of beta-Catenin was increased and the expression of Vimentin was decreased in GBC-SD/M cells after KIAA0125 knockdown.	26448925	RID01866	expression association
Liver fibrosis	TP53COR1	CDKN1A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000124762	NA	102800311	1026	TRP53COR1|linc-p21|lincRNA-p21	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	lincRNA-p21 inhibits hepatic stellate cell activation and liver fibrogenesis via p21.Our results show that over-expression of lincRNA-p21 promotes up-regulation of p21 at both the mRNA and protein levels. Furthermore, lincRNA-p21 inhibited cell-cycle progression and proliferation of primary HSCs through enhancement of p21 expression.	26433205	RID01867	expression association
Thyroid cancer	PVT1	TSHR	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000165409	NA	5820	7253	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	CHNG1|LGR3|hTSHR-I	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID01868	transcriptional regulation
Thyroid cancer	PVT1	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000110092	NA	5820	595	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	BCL1|D11S287E|PRAD1|U21B31	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID01869	expression association
Breast cancer	GAS1RR	GAS1	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000180447	NA	100506834	2619	LncRNA-Hh	NA	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01870	transcriptional regulation
Breast cancer	TWIST1	GAS1RR	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	Hedgehog signaling pathway(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	CSC	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000122691	NA	ENSG00000226237	GRCh38_9:86948666-87002033	7291	100506834	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	LncRNA-Hh	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01871	transcriptional regulation
Breast cancer	GAS1RR	SOX2	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000181449	NA	100506834	6657	LncRNA-Hh	ANOP3|MCOPS3	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01872	expression association
Breast cancer	GAS1RR	POU5F1	negatively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	CSC	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000226237	GRCh38_9:86948666-87002033	ENSG00000204531	NA	100506834	5460	LncRNA-Hh	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway. Especially, the Shh-GLI1 pathway associated lncRNA-Hh, transcriptionally regulated by Twist, directly targets GAS1 to stimulate the activation of hedgehog signaling (Hh). The activated Hh increases GLI1 expression, and enhances the expression of SOX2 and OCT4 to play a regulatory role in CSC maintenance.lncRNA-Hh silence in Twist-positive breast cells attenuates the activated Shh-GLI1 signaling and decreases the CSC-associated SOX and OCT4 levels, thus reduces the MFE and tumorigenesis of transplanted tumor.	26418365	RID01873	expression association
Colon cancer	YAP1	RMRP	positively-E	ChIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);Hippo/YAP signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Colon cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000269900	GRCh38_9:35657751-35658018	10413	6023	COB1|YAP|YAP2|YAP65|YKI	CHH|NME1|RMRPR|RRP2	Wnt activated beta-catenin and YAP proteins enhance the expression of non-coding RNA component of RNase MRP in colon cancer cells.As expected, Wnt signal activation significantly induced the RMRP transcription thru beta-catenin and YAP transcription factors. More importantly, YAP protein was critical for RMRP transcription by association to the proximal site near the transcription start site of the RMRP gene, a Pol III promoter, along with beta-catenin and TBX5 proteins. We propose that the interplay of Wnt and Hippo signaling pathways could regulate target genes, coding or non-coding, by the beta-catenin/YAP/TBX5 transcription complex in cancer cells.Association of beta-catenin and YAP to the RMRP promoter in conjunction with DNA binding proteins, TCF and TBX5, lead to the enhanced expression of RMRP.	26415221	RID01874	transcriptional regulation
Colon cancer	CTNNB1	RMRP	positively-E	ChIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);Hippo/YAP signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Colon cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000269900	GRCh38_9:35657751-35658018	1499	6023	CTNNB|EVR7|MRD19|NEDSDV|armadillo	CHH|NME1|RMRPR|RRP2	Wnt activated beta-catenin and YAP proteins enhance the expression of non-coding RNA component of RNase MRP in colon cancer cells	26415221	RID01875	transcriptional regulation
Osteosarcoma	FOXC2-AS1	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	doxorubicin	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000260944	GRCh38_16:86565145-86567761	ENSG00000085563	NA	103752587	5243	ODRUL	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	A long non-coding RNA contributes to doxorubicin resistance of osteosarcoma.LncRNA microarray revealed that lncRNA ODRUL was the most up-regulated expressed in the doxorubicin-resistant OS cell line.In addition, we found that the expression of classical drug resistance-related ATP-binding cassette, subfamily B, member 1 (ABCB1) gene was decreased after the lncRNA ODRUL knockdown. Thus, we concluded that lncRNA ODRUL may act as a pro-doxorubicin-resistant molecule through inducing the expression of the classical multidrug resistance-related ABCB1 gene in osteosarcoma cells.	26408180	RID01876	expression association
Gastric cancer	HOXA-AS2	CDKN1A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124762	NA	285943	1026	HOXA3as	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01877	epigenetic regulation
Gastric cancer	HOXA-AS2	PLK3	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000173846	NA	285943	1263	HOXA3as	CNK|FNK|PLK-3|PRK	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01878	epigenetic regulation
Gastric cancer	HOXA-AS2	DDIT3	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000175197	NA	285943	1649	HOXA3as	AltDDIT3|C/EBPzeta|CEBPZ|CHOP|CHOP-10|CHOP10|GADD153	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated	26384350	RID01879	epigenetic regulation
Hepatocellular carcinoma	SP1	MALAT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6667	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1 cooperates with Sp3 to upregulate MALAT1 expression in human hepatocellular carcinoma. The results showed a high expression of Sp1, Sp3 and MALAT1 in HCC vs. paired non-tumor liver tissues, which was associated with the AFP level (Sp1, r=7.44, P=0.0064; MALAT1, r=12.37, P=0.0004). Co-silencing of Sp1 and Sp3 synergistically repressed MALAT1 expression. Sp1 binding inhibitor, mithramycin A (MIT), also inhibited MALAT1 expression in HCC cells. In conclusion, the upstream of MALAT1 contains five Sp1/3 binding sites, which may be responsible for MALAT1 transcription. Inhibitors, such as MIT, provide a potential therapeutic strategy for HCC patients with MALAT1 overexpression.	26352013	RID01880	transcriptional regulation
Hepatocellular carcinoma	SP3	MALAT1	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000172845	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6670	378938	SPR2	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1 cooperates with Sp3 to upregulate MALAT1 expression in human hepatocellular carcinoma. The results showed a high expression of Sp1, Sp3 and MALAT1 in HCC vs. paired non-tumor liver tissues, which was associated with the AFP level (Sp1, r=7.44, P=0.0064; MALAT1, r=12.37, P=0.0004). Co-silencing of Sp1 and Sp3 synergistically repressed MALAT1 expression. Sp1 binding inhibitor, mithramycin A (MIT), also inhibited MALAT1 expression in HCC cells. In conclusion, the upstream of MALAT1 contains five Sp1/3 binding sites, which may be responsible for MALAT1 transcription. Inhibitors, such as MIT, provide a potential therapeutic strategy for HCC patients with MALAT1 overexpression.	26352013	RID01881	transcriptional regulation
Burkitt lymphoma	MYC	MINCR	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	cell cycle(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Lymphoma	TF	lncRNA	ENSG00000136997	NA	ENSG00000253716	GRCh38_8:143280161-143281690	4609	100507316	MRTL|MYCC|bHLHe39|c-Myc	LINC01604	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01882	transcriptional regulation
Burkitt lymphoma	MINCR	AURKA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000087586	NA	100507316	6790	LINC01604	AIK|ARK1|AURA|BTAK|PPP1R47|STK15|STK6|STK7	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01883	expression association
Burkitt lymphoma	MINCR	AURKB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000178999	NA	100507316	9212	LINC01604	AIK2|AIM-1|AIM1|ARK-2|ARK2|AurB|IPL1|PPP1R48|STK-1|STK12|STK5|aurkb-sv1|aurkb-sv2	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01884	expression association
Burkitt lymphoma	MINCR	CDT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lymphoma	lncRNA	PCG	ENSG00000253716	GRCh38_8:143280161-143281690	ENSG00000167513	NA	100507316	81620	LINC01604	DUP|RIS2	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A (AURKA) and B and chromatin licensing and DNA replication factor 1 (CDT1) may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.	26351698	RID01885	expression association
Liver cancer	UCA1	HULC	positively-E	ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	DNA methylation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	lncRNA	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000285219	GRCh38_6:8435568-9294133	652995	728655	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HCCAT1|LINC00078|NCRNA00078	Long Noncoding RNA CUDR Regulates HULC and beta-Catenin to Govern Human Liver Stem Cell Malignant Differentiation. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like cells by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On the other hand, excessive CUDR triggers hepatocyte-like cells malignant transformation. Mechanistically, we identify CUDR causes highly upregulated in liver cancer (HULC) and beta-catenin abnormal expression by inhibiting HULC promoter methylation and promoting beta-catenin promoter-enhancer chromatin looping formation mediated by CUDR-ccctc-binding factor (CTCF) complex, which recruits more RNA polII and P300. Strikingly, HULC and beta-catenin activity are crucial for CUDR oncogenic function.	26347501	RID01886	epigenetic regulation
Liver cancer	UCA1	CTNNB1	positively-E	ChIP	upregulation	qPCR	NA	NA	tumor malignant transformation(+)	chromatin looping;enhancer	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168036	NA	652995	1499	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Noncoding RNA CUDR Regulates HULC and beta-Catenin to Govern Human Liver Stem Cell Malignant Differentiation. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like cells by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On the other hand, excessive CUDR triggers hepatocyte-like cells malignant transformation. Mechanistically, we identify CUDR causes highly upregulated in liver cancer (HULC) and beta-catenin abnormal expression by inhibiting HULC promoter methylation and promoting beta-catenin promoter-enhancer chromatin looping formation mediated by CUDR-ccctc-binding factor (CTCF) complex, which recruits more RNA polII and P300. Strikingly, HULC and beta-catenin activity are crucial for CUDR oncogenic function.	26347501	RID01887	chromatin looping
Osteoarthritis	PCGEM1	miR-770-5p	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell autophagy(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000227418	GRCh38_2:192749845-192776899	NA	NA	64002	NA	LINC00071|NCRNA00071|PCAT9	NA	PCGEM1 stimulates proliferation of osteoarthritic synoviocytes by acting as a sponge for miR-770.the results revealed that prostate cancer gene expression marker 1 (PCGEM1) was significantly overexpressed in osteoarthritic synoviocytes. We demonstrate that PCGEM1 act as sponge lncRNA for miR-770 that regulates proliferation/apoptosis and autophagy, and suggest PCGEM1 as possible target for OA therapy.	26340084	RID01888	ceRNA or sponge
Cancer	MALINC1	PURA	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemosensitivity(+);cell cycle(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Cancer	lncRNA	PCG	ENSG00000245146	GRCh38_5:140071312-140109274	ENSG00000185129	NA	100505636	5813	LINC01024|MA-linc1	MRD31|PUR-ALPHA|PUR1|PURALPHA	A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel.We further demonstrate that MA-linc1 predominantly functions in cis to repress expression of its neighboring gene, Puralpha, which is often deleted in human cancers and whose ectopic expression inhibits cell cycle progression.In agreement with its suggested role in M phase, inhibition of MA-linc1 enhances apoptotic cell death induced by the antimitotic drug, Paclitaxel and this enhancement of apoptosis is rescued by Puralpha knockdown.	26337085	RID01889	expression association
Gastric cancer	PRDM16-DT	CDKN2B	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177133	GRCh38_1:3059615-3068437	ENSG00000147883	NA	440556	1030	NA	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Upregulated expression of long non-coding RNA LINC00982 regulates cell proliferation and its clinical relevance in patients with gastric cancer.n this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Kaplan-Meier analysis demonstrated that decreased LINC00982 expression contributed to poor overall survival and disease-free survival of patients. A multivariate survival analysis also indicated that LINC00982 could be an independent prognostic marker. Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions.	26334618	RID01890	expression association
Gastric cancer	PRDM16-DT	CDKN2A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);cell cycle(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177133	GRCh38_1:3059615-3068437	ENSG00000147889	NA	440556	1029	NA	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Upregulated expression of long non-coding RNA LINC00982 regulates cell proliferation and its clinical relevance in patients with gastric cancer.n this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Kaplan-Meier analysis demonstrated that decreased LINC00982 expression contributed to poor overall survival and disease-free survival of patients. A multivariate survival analysis also indicated that LINC00982 could be an independent prognostic marker. Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions.	26334618	RID01891	expression association
T-cell acute lymphocytic leukemia	NALT1	NOTCH1	positively-F	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000237886	GRCh38_9:136546212-136549893	ENSG00000148400	NA	101928483	4851	LINC01573|MIR4674HG|NALT|TCONS_l2_00029132	AOS5|AOVD1|TAN1|hN1	LncRNA NALT interaction with NOTCH1 promoted cell proliferation in pediatric T cell acute lymphoblastic leukemia. In this study, we reported that lncRNA named NALT which was located near NOTCH1 within 100 bp away. We confirmed that up-regulation of NALT associating with NOTCH1 in human samples. Taken together, we found a neighbor of NOTCH1, Lnc-RP11-611D20.2 (named NALT) which could regulate the NOTCH1 signal pathway through cis-regulation. the NALT might interact with NOTCH1 or influence the function of NICD induced cell proliferation.	26330272	RID01892	interact with protein
Hepatitis C	STAT3	IGF2-AS	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	TF	lncRNA	ENSG00000168610	NA	ENSG00000099869	GRCh38_11:2140501-2148666	6774	51214	ADMIO|ADMIO1|APRF|HIES	IGF2-AS1|IGF2AS|PEG8	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01893	expression association
Hepatitis C	STAT3	RN7SK	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	TF	lncRNA	ENSG00000168610	NA	ENSG00000283293	GRCh38_6:52995621-52995948	6774	125050	ADMIO|ADMIO1|APRF|HIES	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01894	expression association
Hepatitis C	RN7SK	PI4P	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000283293	GRCh38_6:52995621-52995948	NA	NA	125050	NA	NA	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01895	expression association
Hepatitis C	IGF2-AS	PI4P	positively-E	RNAi	upregulation	qPCR	NA	NA	HCV replication(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Hepatitis	lncRNA	PCG	ENSG00000099869	GRCh38_11:2140501-2148666	NA	NA	51214	NA	IGF2-AS1|IGF2AS|PEG8	NA	STAT3-regulated long non-coding RNAs lnc-7SK and lnc-IGF2-AS promote hepatitis C virus replication.Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C virus (HCV) and in turn increases the replication of HCV. it was identified that lnc-IGF2-AS, lnc-7SK, lnc-SChLAP1 and lnc-SRA1 are upregulated by STAT3. In addition, among these four lncRNAs, only lnc-IGF2-AS and lnc-7SK were involved in HCV replication. Transfection of siRNA lnc-7SK and siRNA lnc-IGF2-AS partially inhibited the replication of HCV in Huh7 cells.Data also indicated that when transfected with siRNA lnc-7SK and siRNA lnc-IGF2-AS, the expression of phosphatidylinositol 4-phosphate (PI4P), which was identified to be associated with HCV replication, was reduced. Thus, the present study identified two new types of lncRNAs, lnc-IGF2-AS and lnc-7SK, which can be upregulated by STAT3 and are involved in HCV replication by regulating PI4P.	26328522	RID01896	expression association
Breast cancer	BCAR4	ERBB2	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	lapatinib	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000141736	NA	400500	2064	NA	CD340|HER-2|HER-2/neu|HER2|MLN 19|NEU|NGL|TKR1	Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. A similar effect was observed upon knockdown of ERBB2/3 and exposure to lapatinib, implying that BCAR4 acts in an ERBB2/3-dependent manner.BCAR4 encodes a functional protein, which drives proliferation of endocrine-resistant breast cancer cells. Lapatinib, a clinically approved EGFR/ERBB2 inhibitor, counteracts BCAR4-driven tumor cell growth, a clinical relevant observation.	26317614	RID01897	expression association
Breast cancer	BCAR4	ERBB3	positively-E	IHC	upregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(+)	NA	association	NA	lapatinib	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000065361	NA	400500	2065	NA	ErbB-3|FERLK|HER3|LCCS2|MDA-BF-1|c-erbB-3|c-erbB3|erbB3-S|p180-ErbB3|p45-sErbB3|p85-sErbB3	Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. A similar effect was observed upon knockdown of ERBB2/3 and exposure to lapatinib, implying that BCAR4 acts in an ERBB2/3-dependent manner.BCAR4 encodes a functional protein, which drives proliferation of endocrine-resistant breast cancer cells. Lapatinib, a clinically approved EGFR/ERBB2 inhibitor, counteracts BCAR4-driven tumor cell growth, a clinical relevant observation.	26317614	RID01898	expression association
Lung cancer	SPRY4-IT1	MMP2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000087245	NA	100642175	4313	SPRIGHTLY	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Effect of Long Non-coding RNA SPRY4-IT1 on Invasion and Migration of A549 Cells.Transwell assays showed that the numbers of transmembrane A549 cells were significantly higher in SPRY4-IT1 over expression group than that in control group (P<0.05). Meanwhile, over expression of SPRY4-IT1 reduced the expression of MMP-2 and MMP-9. Over expression of SPRY4-IT1 enhanced the invasion and migration of A549 cells. MMP-2 and MMP-9 might play an important role in this regulation.	26302345	RID01899	expression association
Lung cancer	SPRY4-IT1	MMP9	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000100985	NA	100642175	4318	SPRIGHTLY	CLG4B|GELB|MANDP2|MMP-9	Effect of Long Non-coding RNA SPRY4-IT1 on Invasion and Migration of A549 Cells.Transwell assays showed that the numbers of transmembrane A549 cells were significantly higher in SPRY4-IT1 over expression group than that in control group (P<0.05). Meanwhile, over expression of SPRY4-IT1 reduced the expression of MMP-2 and MMP-9. Over expression of SPRY4-IT1 enhanced the invasion and migration of A549 cells. MMP-2 and MMP-9 might play an important role in this regulation.	26302345	RID01900	expression association
Pituitary adenoma	MEG3	TP53	positively-E	RNAi;northern blot	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	NA	association	NA	NA	NA	NA	Endocrine system disease	Pituitary adenoma	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Tumor suppression by MEG3 lncRNA in a human pituitary tumor derived cell line.Human clinically non-functioning pituitary adenomas (NFAs) account for approximately 40% of diagnosed pituitary tumors. When induced in culture, MEG3 caused cell cycle arrest at the G1 phase. In addition, inactivation of p53 completely abolished tumor suppression by MEG3, indicating that MEG3 tumor suppression is mediated by p53.	26284494	RID01901	expression association
Gastric cancer	GAS5	CDK6	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	GAS5 Inhibits Gastric Cancer Cell Proliferation Partly by Modulating CDK6. GAS5 expression was significantly lower in GC tissues relative to normal tissues, and its lower expression was correlated with larger tumor size and a more advanced clinical stage of GC. GAS5 induced growth arrest of GC cells through inhibition of G1-S phase translation. The action of GAS5 may be mediated by upregulation of P21 and suppression of CDK6.	26278580	RID01902	expression association
Gastric cancer	GAS5	CDKN1A	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000124762	NA	60674	1026	NCRNA00030|SNHG2	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	GAS5 Inhibits Gastric Cancer Cell Proliferation Partly by Modulating CDK6. GAS5 expression was significantly lower in GC tissues relative to normal tissues, and its lower expression was correlated with larger tumor size and a more advanced clinical stage of GC. GAS5 induced growth arrest of GC cells through inhibition of G1-S phase translation. The action of GAS5 may be mediated by upregulation of P21 and suppression of CDK6.Decreased expression of long noncoding RNA GAS5 indicates a poor prognosis and promotes cell proliferation in gastric cancer. we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression. lncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer. In this study, we found that lncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. lncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and lncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. lncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of lncRNA GAS5 in suppressing stomach carcinogenesis, and the lncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing lncRNA-based therapies for stomach cancer.	26278580;25959498;24884417	RID01903	expression association
Lung cancer	HOTTIP	CDC25C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000158402	NA	100316868	995	HOXA-AS6|HOXA13-AS1|NCRNA00213	CDC25|PPP1R60	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01904	expression association
Lung cancer	HOTTIP	CCNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000134057	NA	100316868	891	HOXA-AS6|HOXA13-AS1|NCRNA00213	CCNB	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01905	expression association
Lung cancer	HOTTIP	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000110092	NA	100316868	595	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01906	expression association
Lung cancer	HOTTIP	BAD	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000002330	NA	100316868	572	HOXA-AS6|HOXA13-AS1|NCRNA00213	BBC2|BCL2L8	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01907	expression association
Lung cancer	HOTTIP	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000171791	NA	100316868	596	HOXA-AS6|HOXA13-AS1|NCRNA00213	Bcl-2|PPP1R50	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01908	expression association
Lung cancer	HOTTIP	BCL2L1	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000171552	NA	100316868	598	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long non-coding RNA HOTTIP promotes tumor growth and inhibits cell apoptosis in lung cancer. Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. Cell cycle regulators Cdc25C, Cyclin B1 and Cyclin D1 were decreased upon depletion of HOTTIP. Pro-apoptotic factor Bad was up-regulated, whereas anti-apoptotic factors Bcl-2 and Bcl-xL were down-regulated after HOTTIP ablation. These data suggest that lncRNA HOTTIP contributes to tumor growth in vivo and in vitro and inhibits cell apoptosis in lung cancer.	26265284	RID01909	expression association
Non-small cell lung cancer	TARDBP	MALAT1	positively-F	RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell growth(+)	interact with protein	binding/interaction	protein-RNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000120948	NA	ENSG00000251562	GRCh38_11:65497688-65506516	23435	378938	ALS10|TDP-43	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Regulation of MALAT1 expression by TDP43 controls the migration and invasion of non-small cell lung cancer cells in vitro.We also confirm that TDP-43 directly bound to MALAT1 RNA by a RNA immunoprecipitation (RIP) assay and by luciferase reporter activity assay. In a RT-PCR assay, silencing TDP-43 expression effectively decreased MALAT1 RNA transcript level. In contrast, TDP-43 overexpression markedly increased MALAT1 transcript level. In summary, these findings demonstrated that MALAT1 expression by regulation of TDP-43 controls cellular growth, migration, and invasion of NSCLCs.	26265046	RID01910	interact with protein
Nasopharynx carcinoma	EZH2	NPTN-IT1	negatively-E	western blot;ChIP	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Nasopharynx carcinoma	PCG	lncRNA	ENSG00000106462	NA	ENSG00000281183	GRCh38_15:73567012-73569294	2146	101241892	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	lncRNA-LET	Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell.lncRNA-LET was significantly downregulated in nasopharyngeal carcinoma (NPC) tissues compared with corresponding normal tissues. Importantly, we found lncRNA-LET is transcriptional repressed by EZH2-mediated H3K27 histone methylation on the LET promoter. The expressions of EZH2 and lncRNA-LET are significantly inversely correlated in NPC tissues. Collectively, these findings indicate a pivotal role for lncRNA-LET in NPC cell proliferation and apoptosis, and reveal an epigenetic mechanism for lncRNA-LET dysregulation.	26243049	RID01911	epigenetic regulation
Colorectal cancer	ETS2	UCA1	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+);prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	TF	lncRNA	ENSG00000157557	NA	ENSG00000214049	GRCh38_19:15828206-15836328	2114	652995	ETS2IT1	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Increased urothelial cancer associated 1 is associated with tumor proliferation and metastasis and predicts poor prognosis in colorectal cancer. qPCR analysis confirmed that UCA1 was upregulated in CRC (p<0.001) and the expression of UCA1 was statistically correlated with lymph node metastasis (P=0.040), distant metastasis (P=0.043) and tumor stage (P=0.010). To further investigate the regulatory mechanisms of UCA1, we identified that Ets-2 bound to the UCA1 core promoter using luciferase assays.	26238511	RID01912	transcriptional regulation
Renal cell carcinoma	MEG3	BCL2	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+);mitochondrial signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171791	NA	55384	596	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Bcl-2|PPP1R50	Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway. The results showed that MEG3 was evidently downregulated in RCC tissues (P<0.05) and RCC cell lines (P<0.05). The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h (P<0.05). Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h (P<0.05). Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm (P<0.05). Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression (P<0.05).	26223924	RID01913	expression association
Renal cell carcinoma	MEG3	CASP9	negatively-E	RNAi	downregulation	qPCR	NA	NA	apoptosis process(+);mitochondrial signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000132906	NA	55384	842	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway. The results showed that MEG3 was evidently downregulated in RCC tissues (P<0.05) and RCC cell lines (P<0.05). The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h (P<0.05). Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h (P<0.05). Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm (P<0.05). Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression (P<0.05).	26223924	RID01914	expression association
Cancer	LINC-ROR	TESC	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	tumorigenesis(+);cell growth(+);cell metastasis(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000088992	NA	100885779	54997	ROR|lincRNA-RoR|lincRNA-ST8SIA3	CHP3|TSC	Long non-coding RNA ROR decoys gene-specific histone methylation to promote tumorigenesis. Here, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis.	26169368	RID01915	epigenetic regulation
Urinary bladder cancer	TGFB1	ZEB2-AS1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000238057	GRCh38_2:144517978-144521477	7040	100303491	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	ZEB2-AS|ZEB2AS|ZEB2NAT	TGFbeta1 secreted by cancer-associated fibroblasts induces epithelial-mesenchymal transition of bladder cancer cells through lncRNA-ZEB2NAT.Interestingly, a long non-coding RNA, ZEB2NAT, was demonstrated to be essential for this TGFbeta1-dependent process. ZEB2NAT depletion reversed CAF-CM-induced EMT and invasion of cancer cells, as well as reduced the ZEB2 protein level. Consistently, TGFbeta1 mRNA expression is positively correlated with ZEB2NAT transcript and ZEB2 protein levels in human bladder cancer specimens. Our data revealed a novel mechanism that CAFs induces EMT and invasion of human UBC cells through the TGFbeta1-ZEB2NAT-ZEB2 axis.	26152796	RID01916	expression association
Urinary bladder cancer	ZEB2-AS1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000238057	GRCh38_2:144517978-144521477	ENSG00000169554	NA	100303491	9839	ZEB2-AS|ZEB2AS|ZEB2NAT	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	TGFbeta1 secreted by cancer-associated fibroblasts induces epithelial-mesenchymal transition of bladder cancer cells through lncRNA-ZEB2NAT.Interestingly, a long non-coding RNA, ZEB2NAT, was demonstrated to be essential for this TGFbeta1-dependent process. ZEB2NAT depletion reversed CAF-CM-induced EMT and invasion of cancer cells, as well as reduced the ZEB2 protein level. Consistently, TGFbeta1 mRNA expression is positively correlated with ZEB2NAT transcript and ZEB2 protein levels in human bladder cancer specimens. Our data revealed a novel mechanism that CAFs induces EMT and invasion of human UBC cells through the TGFbeta1-ZEB2NAT-ZEB2 axis.	26152796	RID01917	expression association
Breast cancer	AK058003	SNCG	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_10:86948677-87023220	ENSG00000173267	NA	NA	6623	NA	BCSG1|SR	Unregulated long non-coding RNA-AK058003 promotes the proliferation, invasion and metastasis of breast cancer by regulating the expression levels of the gamma-synuclein gene. The expression levels of lncRNA-AK058003 were increased significantly in the breast cancer tissues and were found to strongly correlate with the severity of the breast cancer clinical stage. Bioinformatics analysis revealed that the gamma-synuclein gene (SNCG) may be a target gene regulated by lncRNA-AK058003. Furthermore, the proliferation, invasion and migration rates of the MCF-7 breast cancer cells were significantly reduced. Therefore, the results demonstrated that unregulated lncRNA-AK058003 in breast cancer cells promotes cancer cell proliferation, invasion and metastasis via the regulation of SNCG expression.	26136884	RID01918	expression association
Ovarian cancer	HOTAIR	MAPK1	interact	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100030	NA	100124700	5594	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion. The expression of HOTAIR and MAPK1 in ovarian SKOV3, ES-2, and OVCAR3 increased compared with A2780 and COC1 cells (P<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05). The proliferation, migration, and invasion was inhibited in ovarian SKOV3 after silencing HOTAIR or MAPK1 (p<0.05).	26117268	RID01919	interact with protein
Glioblastoma	BRD4	HOTAIR	positively-E	RNAi;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	I-BET151	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000141867	NA	ENSG00000228630	GRCh38_12:53962308-53974956	23476	100124700	CAP|HUNK1|HUNKI|MCAP	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	The Bromodomain protein BRD4 controls HOTAIR, a long noncoding RNA essential for glioblastoma proliferation. Treatment of GBM cells with the BET bromdomain inhibitor I-BET151 reduced levels of the tumor-promoting lncRNA HOX transcript antisense RNA (HOTAIR) and restored the expression of several other GBM down-regulated lncRNAs. Conversely, overexpression of HOTAIR in conjunction with I-BET151 treatment abrogates the antiproliferative activity of the BET bromodomain inhibitor. Moreover, chromatin immunoprecipitation analysis demonstrated binding of Bromodomain Containing 4 (BRD4) to the HOTAIR promoter, suggesting that BET proteins can directly regulate lncRNA expression. Our data unravel a previously unappreciated mechanism through which BET proteins control tumor growth of glioblastoma cells and suggest that modulation of lncRNA networks may, in part, mediate the antiproliferative effects of many epigenetic inhibitors currently in clinical trials for cancer and other diseases.	26111795	RID01920	transcriptional regulation
Hepatocellular carcinoma	ZEB1-AS1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000237036	GRCh38_10:31206278-31320447	ENSG00000148516	NA	220930	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulation of long noncoding RNA ZEB1-AS1 promotes tumor metastasis and predicts poor prognosis in hepatocellular carcinoma. We found that ZEB1-AS1 is frequently upregulated in HCC samples, especially in metastatic tumor tissues. DNA methylation analysis shows a tumor-specific ZEB1-AS1 promoter hypomethylation. Aberrant methylation is tightly correlated with overexpression of ZEB1-AS1 in HCC. Patients with ZEB1-AS1 hypomethylation or with high ZEB1-AS1 expression have poor recurrence-free survival. Functionally, ZEB1-AS1 promotes tumor growth and metastasis, acts as an oncogene in HCC. The ZEB1-AS1 gene is located in physical contiguity with ZEB1 and positively regulates the ZEB1 expression. ZEB1 inhibition partially abrogates ZEB1-AS1-induced epithelial to mesenchymal transition (EMT) and cancer metastasis. Our results provide novel insights into the function of lncRNA-driven hepatocarcinogenesis, highlight the important role of ZEB1-AS1 and ZEB1 in HCC progression, and indicate that ZEB1-AS1 may be served as a valuable prognostic biomarker for HCC.	26073087	RID01921	expression association
Hepatocellular carcinoma	ZFAS1	ZEB1	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000148516	NA	441951	6935	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01922	ceRNA or sponge
Hepatocellular carcinoma	ZFAS1	MMP14	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000157227	NA	441951	4323	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01923	ceRNA or sponge
Hepatocellular carcinoma	ZFAS1	MMP16	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+);cell invasion(+)	ceRNA(miR-150);amplification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000177410	GRCh38_20:49278178-49299600	ENSG00000156103	NA	441951	4325	C20orf199|HSUP1|HSUP2|NCRNA00275|ZNFX1-AS1	C8orf57|MMP-X2|MT-MMP2|MT-MMP3|MT3-MMP	Amplification of Long Noncoding RNA ZFAS1 Promotes Metastasis in Hepatocellular Carcinoma.Here, we report that ZFAS1, encoding a lncRNA that is frequently amplified in HCC, is associated with intrahepatic and extrahepatic metastasis and poor prognosis of HCC. ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor-suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14, and MMP16 expression, inhibiting these effects of miR-150. miR-150 inhibits cell invasion by targeting ZEB1, MMP14, and MMP16.	26069248	RID01924	ceRNA or sponge
Aortic aneurysm	HIF1A-AS1	CASP3	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01925	expression association
Aortic aneurysm	HIF1A-AS1	CASP8	positively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000064012	NA	100750246	841	5'aHIF-1A|5'aHIF1alpha	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01926	expression association
Aortic aneurysm	HIF1A-AS1	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000171791	NA	100750246	596	5'aHIF-1A|5'aHIF1alpha	Bcl-2|PPP1R50	Long noncoding RNA HIF1A-AS1A reduces apoptosis of vascular smooth muscle cells: implications for the pathogenesis of thoracoabdominal aorta aneurysm.We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase-3 and caspase-8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. HIF1a-AS1 was overexpressed in the TAAA and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of TAAA.	26062299	RID01927	expression association
Non-small cell lung cancer	RGMB-AS1	RGMB	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell differentiation(-);cell metastasis(-);TNM stage(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246763	GRCh38_5:98769618-98773469	ENSG00000174136	NA	503569	285704	NA	DRAGON	Study on expression of lncRNA RGMB-AS1 and repulsive guidance molecule b in non-small cell lung cancer.The results of qRT-PCR showed that lncRNA RGMB-AS1 expression was significantly higher in NSCLC tissues than in adjacent normal tissues, while RGMB mRNA showed an opposite trend. Correlation analysis indicated that the expression of lncRNA RGMB-AS1and RGMB mRNA were inversely correlated. We identified lncRNA RGMB-AS1 was upregulated and RGMB was downregulated in NSCLC patients. Both were related to differentiation status, lymph node metastases and TNM stage. Studies also indicated that lncRNA RGMB-AS1 and RGMB were inversely correlated.	26055877	RID01928	expression association
Myocardial infarction	H19	FADD	positively-E	RNAi;RNA pull-down assay	upregulation	qPCR	NA	NA	myocardial necrosis(-)	ceRNA(miR-103a-3p;miR-107)	regulation	NA	NA	NA	NA	Cardiovascular system disease	Myocardial infarction	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000168040	NA	283120	8772	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GIG3|MORT1	MicroRNA-103/107 Regulate Programmed Necrosis and Myocardial Ischemia/Reperfusion Injury Through Targeting FADD.Our results show that FADD participates in H2O2-induced necrosis by influencing the formation of RIPK1 and RIPK3 complexes in H9c2 cells. We further demonstrate that miR-103/107 target FADD directly. Knockdown of miR-103/107 antagonizes necrosis in the cellular model and also myocardial infarction in a mouse ischemia/reperfusion model. The miR-103/107-FADD pathway does not participate in tumor necrosis factor-alpha-induced necrosis. In exploring the molecular mechanism by which miR-103/107 are regulated, we show that long noncoding RNA H19 directly binds to miR-103/107 and regulates FADD expression and necrosis.Our results reveal a novel myocardial necrosis regulation model, which is composed of H19, miR-103/107, and FADD. Modulation of their levels may provide a new approach for preventing myocardial necrosis.	26038570	RID01930	ceRNA or sponge
Hepatocellular carcinoma	HOTAIR	miR-218-5p	negatively-E	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01931	epigenetic regulation
Hepatocellular carcinoma	HOTAIR	BMI1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168283	NA	100124700	648	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01932	expression association
Hepatocellular carcinoma	HOTAIR	CDKN2A	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(-)	NA	association	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000147889	NA	100124700	1029	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis.Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.Hotair silence activates P16(Ink4a) and P14(ARF) signaling by enhancing miR-218 expression and suppressing Bmi-1 expression, resulting in the suppression of tumorigenesis in HCC.	26024833;27168727;29843138	RID01933	expression association
Gastric cancer	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+);prognosis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	A Long Non-coding RNA Activated by Transforming Growth Factor-beta is an Independent Prognostic Marker of Gastric Cancer.The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor (hazard ratio 3.50; 95 % CI 1.73-7.44; p = 0.0004). miR-200c levels were lower and ZEB1 levels were higher in the high lncRNA-ATB group than in the low lncRNA-ATB group. Treatment with TGF-beta in GC cell lines resulted in morphological EMT changes, upregulation of lncRNA-ATB and ZEB1, and downregulation of miR-200c and CDH1. SB431542 reduced lncRNA-ATB expression.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGF-beta/miR-200s/ZEB axis, resulting in a poor prognosis in GC. LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients.	25986864	RID01934	expression association
Acute myeloid leukemia	HOTAIR	KIT	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000157404	NA	100124700	3815	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C-Kit|CD117|MASTC|PBT|SCFR	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID01935	ceRNA or sponge
Gastric cancer	GAS5	YBX1	positively-F	western blot;RIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell cycle(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000065978	NA	60674	4904	NCRNA00030|SNHG2	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	lncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer. In this study, we found that lncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. lncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and lncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. lncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of lncRNA GAS5 in suppressing stomach carcinogenesis, and the lncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing lncRNA-based therapies for stomach cancer.	25959498	RID01936	interact with protein
Gastric cancer	PVT1	ABCB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000085563	NA	5820	5243	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01937	expression association
Gastric cancer	PVT1	ABCC1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000103222	NA	5820	4363	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ABC29|ABCC|GS-X|MRP|MRP1	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01938	expression association
Gastric cancer	PVT1	MTOR	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000198793	NA	5820	2475	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance.PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells. While, PVT1 overexpression exhibit the anti-apoptotic property in BGC823 and SGC7901 cells transfected with LV-PVT1-GFP and treated with cisplatin. Moreover, qRT-PCR and western blotting revealed that PVT1 up-regulation increased the expression of MDR1, MRP, mTOR and HIF-1alpha. Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR, suggesting an efficacious target for reversing MDR in gastric cancer therapy.	25956062	RID01939	expression association
Oral squamous cell carcinoma	HOTAIR	CDH1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	histone modification	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long non-coding RNA HOTAIR promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in oral squamous cell carcinoma. Furthermore, significant negative correlation between HOTAIR levels and E-cadherin levels was found in OSCC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 and H3K27me3 with the E-cadherin promoter.	25901533	RID01940	epigenetic regulation
Lung adenocarcinoma	ZXF2	MYC	negatively-F	western blot;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF		GRCh38_8:134211865-134320447	ENSG00000136997	NA	NA	4609	NA	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of Long Non-Coding RNA ZXF2 Promotes Lung Adenocarcinoma Progression Through c-Myc Pathway. The expression of ZXF2 was 2 fold or higher in 27 out of 40 (67.5%) cases of lung adenocarcinoma specimens than that in non-cancerous tissues (P<0.05). ZXF2 was overexpressed in lung adenocarcinoma tissues and the high expression of ZXF was closely related to tumor progression through c-Myc related pathway. Given the fact that both ZXF2 and c-Myc are located in the same chromosome 8q24.2 loci, the potential interaction between ZXF2 and c-Myc might be a novel target for treatment of lung adenocarcinoma.	25896422	RID01941	interact with protein
Gallbladder cancer	IATPR	CTNNB1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000168036	NA	101929447	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines. Moreover, cell migration and invasion were reduced by over twofold in linc-ITGB1 knockdown cells probably due to upregulation of beta-catenin and downregulation of vimentin, slug, and TCF8.	25893892	RID01942	expression association
Gallbladder cancer	IATPR	VIM	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000026025	NA	101929447	7431	NA	NA	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01943	expression association
Gallbladder cancer	IATPR	SNAI2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000019549	NA	101929447	6591	NA	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01944	expression association
Gallbladder cancer	IATPR	ZEB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000233387	GRCh38_10:33096257-33116672	ENSG00000148516	NA	101929447	6935	NA	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Long non-coding RNA Linc-ITGB1 knockdown inhibits cell migration and invasion in GBC-SD/M and GBC-SD gallbladder cancer cell lines	25893892	RID01945	expression association
Gastric cancer	PVT1	MRPL28	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000086504	NA	5820	10573	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MAAT1|p15	Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16. Moreover, we further confirmed that PVT1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of p15 and p16.	25890171	RID01946	epigenetic regulation
Gastric cancer	PVT1	CDKN2A	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000147889	NA	5820	1029	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16	25890171	RID01947	epigenetic regulation
Triple-receptor negative breast cancer	EGFR	HOTAIR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(+)	NA	association	NA	lapatinib	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000146648	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1956	100124700	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01948	expression association
Triple-receptor negative breast cancer	ABL1	HOTAIR	positively-E	western blot	upregulation	qPCR	NA	NA	chemosensitivity(-);cell growth(+)	NA	association	NA	imatinib	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000097007	NA	ENSG00000228630	GRCh38_12:53962308-53974956	25	100124700	ABL|CHDSKM|JTK7|bcr/abl|c-ABL|c-ABL1|p150|v-abl	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01949	expression association
Triple-receptor negative breast cancer	CTNNB1	HOTAIR	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	cell growth(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	PCG	lncRNA	ENSG00000168036	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1499	100124700	CTNNB|EVR7|MRD19|NEDSDV|armadillo	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells. The dual treatment leads to synergistic repression of the long non-coding RNA (lncRNA) HOTAIR (HOX Antisense Intergenic RNA). HOTAIR has been known to induce tumor growth and metastasis in breast cancer. We show that expression of HOTAIR is regulated by beta-catenin through a LEF1/TCF4-binding site.The dual treatment blocks nuclear expression of beta-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of beta-catenin rescued HOTAIR expression and cell viability in the presence of both drugs.	25883211	RID01950	transcriptional regulation
Lung cancer	lnc-bc060912	PARP1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_22:46330875-46333698	ENSG00000143799	NA	NA	142	NA	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Functional Characterization of Long Noncoding RNA Lnc_bc060912 in Human Lung Carcinoma Cells.Here we have identified a lncRNA termed Lnc_bc060912 whose expression is increased in human lung and other tumors. we found that Lnc_bc060912 interacted with the two DNA damage repair proteins PARP1 and NPM1. Together, these results suggest that Lnc_bc060912, via PARP1 and NPM1, affects cell apoptosis and may play important roles in tumorigenesis and cancer progression.	25848691	RID01951	interact with protein
Lung cancer	lnc-bc060912	NPM1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_22:46330875-46333698	ENSG00000181163	NA	NA	4869	NA	B23|NPM	Functional Characterization of Long Noncoding RNA Lnc_bc060912 in Human Lung Carcinoma Cells.Here we have identified a lncRNA termed Lnc_bc060912 whose expression is increased in human lung and other tumors. we found that Lnc_bc060912 interacted with the two DNA damage repair proteins PARP1 and NPM1. Together, these results suggest that Lnc_bc060912, via PARP1 and NPM1, affects cell apoptosis and may play important roles in tumorigenesis and cancer progression.	25848691	RID01952	interact with protein
Pancreatic cancer	MALAT1	SOX2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(-);self-renewal(+);cell stemness(+)	NA	regulation	NA	gemcitabine	CSC	Self Sufficiency in Growth Signals;Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000181449	NA	378938	6657	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ANOP3|MCOPS3	Long noncoding RNA MALAT-1 enhances stem cell-like phenotypes in pancreatic cancer cells.In this study, our data showed that MALAT-1 was Upregulated in CSCs and could increase the proportion of pancreatic CSCs, maintain self-renewing capacity, decrease the chemosensitivity to anticancer drugs, and accelerate tumor angiogenesis in vitro. The underlying mechanisms may involve in increased expression of self-renewal related factors Sox2. Collectively, we for the first time found the potential effects of MALAT-1 on the stem cell-like phenotypes in pancreatic cancer cells, suggesting a novel role of MALAT-1 in tumor stemness, which remains to be fully elucidated.	25811929	RID01953	expression association
Pre-eclampsia	HOTAIR	CASP3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	Long noncoding RNA HOTAIR modulates the function of trophoblast cells in pre-eclampsia. The level of HOTAIR in severe pre-eclampsia groups was significantly increased compared to normal pregnant placentas (P<0.05). Western blot assay showed that the apoptotic proteins Caspase-3 showed an obvious increase in HOTAIR overexpression group while decreased in si-HOTAIR group. And BCL-2 presented an opposite trend.	25807808	RID01954	expression association
Pre-eclampsia	HOTAIR	BCL2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	Long noncoding RNA HOTAIR modulates the function of trophoblast cells in pre-eclampsia. The level of HOTAIR in severe pre-eclampsia groups was significantly increased compared to normal pregnant placentas (P<0.05). Western blot assay showed that the apoptotic proteins Caspase-3 showed an obvious increase in HOTAIR overexpression group while decreased in si-HOTAIR group. And BCL-2 presented an opposite trend.	25807808	RID01955	expression association
Varicosity	GAS5	ANXA2	interact	RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Varicosity	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000182718	NA	60674	302	NCRNA00030|SNHG2	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Low expression of lncRNA-GAS5 is implicated in human primary varicose great saphenous veins. we selected the lower expressed lncRNA-GAS5 (growth arrest specific transcript 5) for functional assessments. RNA pull-down experiment revealed a direct bind of lncRNA-GAS5 to a Ca2+-dependent RNA-binding protein, Annexin A2. Further experiments showed that silencing of Annexin A2 reduced the HSVSMCs proliferation and vice versa. In the context of lncRNA-GAS5 knockdown, silencing of Annexin A2 reduced the proliferation of HSVSMCs while overexpression of Annexin A2 increased the proliferation. Thus, the low expression of lncRNA-GAS5 may facilitate HSVSMCs proliferation and migration through Annexin A2 and thereby the pathogenesis of GSV varicosities.	25806802	RID01956	interact with protein
Lung cancer	SP1	MALAT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6667	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Sp1-mediated transcriptional regulation of MALAT1 plays a critical role in tumor. Sp1 knockdown also decreased the MALAT1 and inhibited A549 lung cancer cells' growth and invasion in vitro. Furthermore, knockdown of Sp1 also mimicked the inhibition of MALAT1 in A549 lung cancer cells' growth and metastasis in vivo.	25773124	RID01957	expression association
Glioblastoma	WIF1	MALAT1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell migration(-);WNT signaling pathway(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	PCG	lncRNA	ENSG00000156076	NA	ENSG00000251562	GRCh38_11:65497688-65506516	11197	378938	WIF-1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WIF1 re-expression in glioblastoma inhibits migration through attenuation of non-canonical WNT signaling by downregulating the lncRNA MALAT1.The aim of this study was the dissection of WIF1-associated tumor-suppressing effects mediated by canonical and non-canonical WNT signaling. Hence, loss of WIF1 enhances the migratory potential of glioblastoma through WNT5A that activates the WNT/Ca(2+) pathway and MALAT1.	25772239	RID01958	expression association
Hepatocellular carcinoma	UCA1	FGFR1	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-216b)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000077782	NA	652995	2260	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BFGFR|CD331|CEK|ECCL|FGFBR|FGFR-1|FLG|FLT-2|FLT2|HBGFR|HH2|HRTFDS|KAL2|N-SAM|OGD|bFGF-R-1	Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway.UCA1 could act as an endogenous sponge by directly binding to miR-216b and downregulation miR-216b expression. In addition, UCA1 could reverse the inhibitory effect of miR-216b on the growth and metastasis of HCC cells, which might be involved in the derepression of fibroblast growth factor receptor 1 (FGFR1) expression, a target gene of miR-216b, and the activation of ERK signaling pathway.	25760077	RID01959	ceRNA or sponge
Breast cancer	NKILA	NFKB1	interact	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01960	interact with protein
Breast cancer	NKILA	NFKBIA	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000100906	NA	105416157	4792	NA	EDAID2|IKBA|MAD-3|NFKBI	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01961	interact with protein
Breast cancer	NKILA	NFKBIB	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	phosphorylation	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000104825	NA	105416157	4793	NA	IKBB|TRIP9	A cytoplasmic NF-kB interacting long noncoding RNA blocks IkB phosphorylation and suppresses breast cancer metastasis. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kB modulators to suppress cancer metastasis.	25759022	RID01962	interact with protein
Multiple myeloma	MEG3	BMP4	negatively-E	western blot;RIP	downregulation	qPCR	NA	NA	cell differentiation(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000125378	NA	55384	652	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BMP2B|BMP2B1|MCOPS6|OFC11|ZYME	Upregulation of lncRNA MEG3 Promotes Osteogenic Differentiation of Mesenchymal Stem Cells From Multiple Myeloma Patients By Targeting BMP4 Transcription.Here we showed that MEG3 was critical for SOX2 transcriptional repression of the BMP4. MEG3, which is located near the BMP4 gene, could dissociate the transcription factor SOX2 from the BMP4 promoter.	25753650	RID01963	transcriptional regulation
Breast cancer	SPRY4-IT1	ZNF703	positively-E	qPCR;RNAi	upregulation	qPCR;microarray	GSE62507	GSE62507.zip	cell proliferation(+);apoptosis process(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000183779	NA	100642175	80139	SPRIGHTLY	NLZ1|ZEPPO1|ZNF503L|ZPO1	The long noncoding RNA SPRY4-IT1 increases the proliferation of human breast cancer cells by upregulating ZNF703 expression.The knockdown of SPRY4-IT1 significantly suppressed proliferation and caused apoptosis of breast cancer cells in vitro. Furthermore, we discovered that ZNF703 was a target of SPRY4-IT1 and was downregulated by SPRY4-IT1 knockdown.	25742952	RID01964	transcriptional regulation
Osteosarcoma	HOTAIR	MMP2	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087245	NA	100124700	4313	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Overexpression of Long Non-Coding RNA HOTAIR Promotes Tumor Growth and Metastasis in Human Osteosarcoma.experiments demonstrated that knockdown of HOTAIR could notably suppress cellular proliferation, inhibit invasion and decrease the secretion of MMP2 and MMP9 in osteosarcoma.	25728753	RID01965	expression association
Osteosarcoma	HOTAIR	MMP9	positively-E	IHC	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Overexpression of Long Non-Coding RNA HOTAIR Promotes Tumor Growth and Metastasis in Human Osteosarcoma.experiments demonstrated that knockdown of HOTAIR could notably suppress cellular proliferation, inhibit invasion and decrease the secretion of MMP2 and MMP9 in osteosarcoma.	25728753	RID01966	expression association
Osteoporosis	DANCR	IL6	positively-E	RNAi	upregulation	qPCR	NA	NA	biomarker(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000136244	NA	57291	3569	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Long non-coding RNA-DANCR in human circulating monocytes: a potential biomarker associated with postmenopausal osteoporosis. we found significant upregulation of DANCR in the blood mononuclear cells (MNCs) from low-BMD patients with the qRT-PCR analyses. We further found that DANCR promoted the expression of IL6 and TNF-alpha at both mRNA level and protein level in MNCs. Furthermore, we found that DANCR-induced IL6 and TNF-alpha in MNCs had bone-resorbing activity. These results indicate that DANCR is involved in the pathology of osteoporosis and may be as a biomarker for postmenopausal osteoporosis.	25660720	RID01967	expression association
Osteoporosis	DANCR	TNF	positively-E	RNAi	upregulation	qPCR	NA	NA	biomarker(+)	NA	association	NA	NA	NA	NA	Musculoskeletal system disease	Bone disease	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000232810	NA	57291	7124	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	Long non-coding RNA-DANCR in human circulating monocytes: a potential biomarker associated with postmenopausal osteoporosis. we found significant upregulation of DANCR in the blood mononuclear cells (MNCs) from low-BMD patients with the qRT-PCR analyses. We further found that DANCR promoted the expression of IL6 and TNF-alpha at both mRNA level and protein level in MNCs.	25660720	RID01968	expression association
Malignant glioma	LINC-ROR	PROM1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);self-renewal(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000007062	NA	100885779	8842	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	Expression and Functional Role of Reprogramming-Related Long Noncoding RNA (lincRNA-ROR) in Glioma. To explore its functional role, gain- and loss-of-function studies were performed to assess the effect of lincRNA-ROR on cell proliferation, expression rate of GSCs marker CD133, and glioma stem sphere-forming ability in vitro. We found that the lincRNA-ROR expression was significantly lower in glioma tissues than in adjacent normal tissues. Knockdown of lincRNA-ROR expression by small hairpin RNA (shRNA) significantly elevated the cell proliferation and enhanced the CD133 expression rate and glioma stem sphere-forming ability in U87 cells, while overexpression of lincRNA-ROR in U87 cells showed the opposite effect.	25651893	RID01969	expression association
Malignant glioma	LINC-ROR	KLF4	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);self-renewal(-)	NA	association	NA	NA	CSC	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136826	NA	100885779	9314	ROR|lincRNA-RoR|lincRNA-ST8SIA3	EZF|GKLF	Expression and Functional Role of Reprogramming-Related Long Noncoding RNA (lincRNA-ROR) in Glioma. Moreover, we found that the expression of lincRNA-ROR was negatively correlated with stem cell factor KLF4 and the up- and down-regulation of lincRNA-ROR resulted in inverse modulation of KLF4 messenger RNA (mRNA) expression. Our results suggest that the reprogramming-related lincRNA-ROR may serve as a novel tumor suppressor gene in glioma, which can inhibit the proliferation of cancer cell and self-renewal of GSCs, partly by inhibiting the KLF4 expression.	25651893	RID01970	expression association
Esophagus squamous cell carcinoma	CDKN2B-AS1	TERT	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+);cell proliferation(-)	NA	regulation	NA	beta-Elemene	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164362	NA	100048912	7015	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	beta-Elemene inhibits the proliferation of esophageal squamous cell carcinoma by regulating long noncoding RNA-mediated inhibition of hTERT expression. It was also shown by flow cytometry that, compared with the scramble-treated group (negative control), the proliferation index value of ECA-109 cells in the si-CDKN2B-AS1 treatment group was notably increased (25.7 vs. 51.7%) and the TERT protein level was increased by 67.25% after the cells were treated with si-CDKN2B-AS1. The chemotherapeutic drug beta-elemene suppressed the proliferation of esophageal carcinoma ECA-109 cells by regulating the inhibition of hTERT expression by lncRNA CDKN2B-AS1.	25646744;30223861	RID01971	expression association
Liver cancer	HULC	CLOCK	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000134852	NA	728655	9575	HCCAT1|LINC00078|NCRNA00078	KAT13D|bHLHe8	A long noncoding RNA perturbs the circadian rhythm of hepatoma cells to facilitate hepatocarcinogenesis. our data show that an lncRNA, HULC, is responsible for the perturbations in circadian rhythm through upregulating circadian oscillator CLOCK in hepatoma cells, resulting in the promotion of hepatocarcinogenesis. our data exhibited that CLOCK was implicated in the HULC-accelerated proliferation of hepatoma cells in vitro and in vivo.	25622901	RID01972	expression association
Hepatocellular carcinoma	HULC	PPARA	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000186951	NA	728655	5465	HCCAT1|LINC00078|NCRNA00078	NR1C1|PPAR|PPARalpha|hPPAR	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01973	expression association
Hepatocellular carcinoma	HULC	ACSL1	positively-E	RNAi	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	transcriptional regulation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000151726	NA	728655	2180	HCCAT1|LINC00078|NCRNA00078	ACS1|FACL1|FACL2|LACS|LACS1|LACS2	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01974	transcriptional regulation
Hepatocellular carcinoma	HULC	miR-9	negatively-E	luciferase reporter assay;5-aza-2'-deoxycytidine treatment	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells.HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01975	epigenetic regulation
Hepatocellular carcinoma	RXRA	HULC	positively-E	western blot;luciferase reporter assay;mutant in binding site	upregulation	qPCR	NA	NA	lipid metabolic process(-);RXRA signaling pathway(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000186350	NA	ENSG00000285219	GRCh38_6:8435568-9294133	6256	728655	NR2B1	HCCAT1|LINC00078|NCRNA00078	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. cholesterol addition was sufficient to upregulate HULC expression through a positive feedback loop involving the retinoid receptor RXRA, which activated the HULC promoter.Overall, we concluded that HULC functions as an oncogene in hepatoma cells, acting mechanistically by deregulating lipid metabolism through a signaling pathway involving miR-9, PPARA, and ACSL1 that is reinforced by a feed-forward pathway involving cholesterol and RXRA to drive HULC signaling.	25592151	RID01976	transcriptional regulation
Diabetes mellitus	MIAT	VEGFA	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	angiogenesis(+)	ceRNA(miR-150-5p)	regulation	NA	NA	NA	Sustained Angiogenesis	Disease of metabolism	Diabetes mellitus	lncRNA	PCG	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000112715	NA	440823	7422	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	MVCD1|VEGF|VPF	lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA. RNA immunoprecipitation, and in vitro studies revealed that MIAT functioned as a competing endogenous RNA, and formed a feedback loop with vascular endothelial growth factor and miR-150-5p to regulate endothelial cell function.studies revealed that MIAT knockdown obviously ameliorated diabetes mellitus-induced retinal microvascular dysfunction in vivo, and inhibited endothelial cell proliferation, migration, and tube formation in vitro. MIAT Regulates the Expression of miR-150-5p Target Gene, VEGF.This study highlights the involvement of lncRNA-MIAT in pathological angiogenesis and facilitates the development of lncRNA-directed diagnostics and therapeutics against neovascular diseases.	25587098	RID01977	ceRNA or sponge
Pancreatic neuroendocrine tumor	MEG3	MET	negatively-E	western blot;ChIP	downregulation	qPCR;microarray	NA	NA	cell proliferation(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Neuroendocrine tumor	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000105976	NA	55384	4233	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors. Therefore, a tumor-suppressor long noncoding RNA (MEG3) and suppressed protooncogene (c-MET) combination could elicit menin's tumor-suppressor activity. Interestingly, MEG3 and c-MET expression was also altered in human sporadic insulinomas (insulin secreting PNETs) with hypermethylation at the MEG3 promoter CRE-site coinciding with reduced MEG3 expression.Furthermore, in MIN6 mouse insulinoma cells, DNA-demethylating drugs blocked cell proliferation and activated Meg3 expression. Our data suggest that the epigenetic activation of lncRNA MEG3 and/or inactivation of c-MET could be therapeutic for treating PNETs and insulinomas.	25565142	RID01978	transcriptional regulation
Liver fibrosis	TET3	HIF1A-AS1	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Gastrointestinal system disease	Fibrosis	PCG	lncRNA	ENSG00000187605	NA	ENSG00000258777	GRCh38_14:61681041-61695823	200424	100750246	hCG_40738	5'aHIF-1A|5'aHIF1alpha	TET3 mediates the activation of human hepatic stellate cells via modulating the expression of long non-coding RNA HIF1A-AS1. The result hinted that TET3 activate HSCs through modulating the expression of HIF1A-AS1. To confirm this hypothesis, RNA interference was performed to silence the HIF1A-AS1. Results showed that HIF1A-AS1 silencing lead to enhancing in cell proliferation and declining apoptosis. Taken together, TET3 can mediate the activation of HSCs via modulating the expression of the long non-coding RNA HIF1A-AS1.	25550811	RID01979	expression association
Thoracoabdominal aorta aneurysm	HIF1A-AS1	CASP3	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000164305	NA	100750246	836	5'aHIF-1A|5'aHIF1alpha	CPP32|CPP32B|SCA-1	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01980	expression association
Thoracoabdominal aorta aneurysm	HIF1A-AS1	CASP8	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000064012	NA	100750246	841	5'aHIF-1A|5'aHIF1alpha	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01981	expression association
Thoracoabdominal aorta aneurysm	HIF1A-AS1	BCL2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Aortic aneurysm	lncRNA	PCG	ENSG00000258777	GRCh38_14:61681041-61695823	ENSG00000171791	NA	100750246	596	5'aHIF-1A|5'aHIF1alpha	Bcl-2|PPP1R50	Regulation of apoptosis by long non-coding RNA HIF1A-AS1 in VSMCs: implications for TAA pathogenesis. In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs.	25550800	RID01982	expression association
Esophagus squamous cell carcinoma	miR-101-3p	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01983	ceRNA or sponge
Esophagus squamous cell carcinoma	miR-217	MALAT1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01984	ceRNA or sponge
Esophagus squamous cell carcinoma	MALAT1	CDKN1A	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01985	expression association
Esophagus squamous cell carcinoma	MALAT1	DCTN6	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000104671	NA	378938	10671	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WS-3|WS3|p27	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01986	expression association
Esophagus squamous cell carcinoma	MALAT1	MYBL2	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101057	NA	378938	4605	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	B-MYB|BMYB	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217 inhibits proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. In this study we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated up-regulation of p21 and p27 expression and the inhibition of B-MYB expression.	25538231	RID01987	expression association
Urinary bladder cancer	MDC1-AS1	MDC1	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	tumor-suppressive function(+)	NA	regulation	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000224328	GRCh38_6:30703067-30713184	ENSG00000137337	NA	106478956	9656	MDC1-AS	NFBD1	A novel antisense long noncoding RNA regulates the expression of MDC1 in bladder cancer. we found that the expression levels of MDC1-AS and MDC1 was down-regulated in bladder cancer. After over-expression of MDC1-AS, increased levels of MDC1 were observed in bladder cancer cells. We also found a remarkably inhibitory role of antisense lncRNA MDC1-AS on malignant cell behaviors in bladder cancer cells EJ and T24. Subsequently, knockdown of MDC1 revealed that suppressing role of MDC1-AS was attributed to up-regulation of MDC1. In summary, we have identified a novel antisense lncRNA MDC1-AS, which may participate in bladder cancer through up-regulation of its antisense tumor-suppressing gene MDC1.	25514464	RID01988	expression association
Prostate cancer	PCGEM1	AR	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);metabolic process(+)	NA	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000169083	NA	64002	367	LINC00071|NCRNA00071|PCAT9	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	A long noncoding RNA connects c-Myc to tumor metabolism. In prostate cancer, prostate cancer gene expression marker 1 (PCGEM1) is an androgen-induced prostate-specific lncRNA whose overexpression is highly associated with prostate tumors. PCGEM1's tumorigenic potential has been recently shown to be in part due to its ability to activate androgen receptor (AR).Together, our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells. By being a coactivator for both c-Myc and AR, PCGEM1 reprograms the androgen network and the central metabolism in a tumor-specific way, making it a promising target for therapeutic intervention.	25512540	RID01989	expression association
Prostate cancer	PCGEM1	MYC	positively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);metabolic process(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000227418	GRCh38_2:192749845-192776899	ENSG00000136997	NA	64002	4609	LINC00071|NCRNA00071|PCAT9	MRTL|MYCC|bHLHe39|c-Myc	A long noncoding RNA connects c-Myc to tumor metabolism. we report a novel function of PCGEM1 that provides growth advantages for cancer cells by regulating tumor metabolism via c-Myc activation. PCGEM1 binds directly to target promoters, physically interacts with c-Myc, promotes chromatin recruitment of c-Myc, and enhances its transactivation activity.our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells.Together, our data uncover PCGEM1 as a key transcriptional regulator of central metabolic pathways in prostate cancer cells. By being a coactivator for both c-Myc and AR, PCGEM1 reprograms the androgen network and the central metabolism in a tumor-specific way, making it a promising target for therapeutic intervention.	25512540	RID01990	transcriptional regulation
Hepatocellular carcinoma	LINC00974	KRT19	positively-E	western blot;RIP	upregulation	qPCR	NA	NA	cell growth(-);cell metastasis(-)	ceRNA(miR-642a-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226629	GRCh38_17:41549606-41554495	ENSG00000171345	NA	147093	3880	NA	CK19|K19|K1CS	A novel biomarker Linc00974 interacting with KRT19 promotes proliferation and metastasis in hepatocellular carcinoma.We further investigated the interaction pattern of Linc00974 and KRT19. MiR-642 was identified, by acting as the competing endogenous RNA in regulating Linc00974 and KRT19. Linc00974 was increased owing to an abnormal hypomethylation promoter, which induced the upregulation of KRT19 via ceRNA interaction, resulting in the activation of the Notch and TGF-beta pathways as detected by cDNA microarray.	25476897	RID01991	ceRNA or sponge
Osteosarcoma	MALAT1	PCNA	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132646	NA	378938	5111	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ATLD2	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01992	expression association
Osteosarcoma	MALAT1	MMP9	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01993	expression association
Osteosarcoma	MALAT1	PI3K	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01994	expression association
Osteosarcoma	MALAT1	AKT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. In our research, the MALAT1 messenger RNA (mRNA) was highly expressed in human osteosarcoma tissues, and its expression level was closely correlated with pulmonary metastasis. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. Knockdown of MALAT1 inhibited the proliferation and invasion of human osteosarcoma cell and suppressed its metastasis in vitro and vivo. At the same time, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), phosphorylated PI3Kp85alpha, and Akt expressions were significantly inhibited in MALAT1-deleted cells. These findings indicated that MALAT1 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway.	25431257	RID01995	expression association
Glioblastoma	HOTAIR	EZH2	interact	RIP	downregulation	sequencing	TCGA	GBM.zip	cell cycle(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTAIR promotes glioblastoma cell cycle progression in an EZH2 dependent manner. In this study, we found that EZH2 (predominant PRC2 complex component) inhibition blocked cell cycle progression in glioma cells, consistent with the effects elicited by HOTAIR siRNA. However, the inhibition of LSD1 did not affect cell cycle progression in glioma cells. These results suggest that HOTAIR might regulate cell cycle progression through EZH2.In conclusion, HOTAIR promotes cell cycle progression in glioma as a result of the binding of its 5' domain to the PRC2 complex.Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	25428914;27277755	RID01996	interact with protein
Prostate cancer	PCAT1	miR-3667-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	miRNA	ENSG00000253438	GRCh38_8:126556323-127419050	NA	NA	100750225	NA	PCA1|PCAT-1	NA	The long non-coding RNA PCAT-1 promotes prostate cancer cell proliferation through cMyc. The PCAT-1-cMyc relationship is mediated through the post-transcriptional activity of the MYC 3' untranslated region, and we characterize a role for PCAT-1 in the disruption of MYC-targeting microRNAs. To further elucidate a role for post-transcriptional regulation, we demonstrate that targeting PCAT-1 with miR-3667-3p, which does not target MYC, is able to reverse the stabilization of cMyc by PCAT-1. This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer.	25425964	RID01997	ceRNA or sponge
Prostate cancer	PCAT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	post-transcriptional level	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	TF	ENSG00000253438	GRCh38_8:126556323-127419050	ENSG00000136997	NA	100750225	4609	PCA1|PCAT-1	MRTL|MYCC|bHLHe39|c-Myc	The long non-coding RNA PCAT-1 promotes prostate cancer cell proliferation through cMyc. The PCAT-1-cMyc relationship is mediated through the post-transcriptional activity of the MYC 3' untranslated region, and we characterize a role for PCAT-1 in the disruption of MYC-targeting microRNAs. To further elucidate a role for post-transcriptional regulation, we demonstrate that targeting PCAT-1 with miR-3667-3p, which does not target MYC, is able to reverse the stabilization of cMyc by PCAT-1. This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer.	25425964	RID01998	expression association
Hepatocellular carcinoma	miR-125b-5p	HOTTIP	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	miRNA	lncRNA	NA	NA	ENSG00000243766	GRCh38_7:27198575-27207259	NA	100316868	NA	HOXA-AS6|HOXA13-AS1|NCRNA00213	Long non-coding RNA HOTTIP is frequently up-regulated in hepatocellular carcinoma and is targeted by tumour suppressive miR-125b. In our profiling study, HOTTIP was identified as the most significantly up-regulated lncRNA in human HCCs, even in early stage of HCC formation. Functionally, knock-down of HOTTIP attenuated HCC cell proliferation in vitro and markedly abrogated tumourigenicity in vivo. HOTTIP is an antisense lncRNA mapped to the distal end of the HOXA gene cluster. Knock-down of HOTTIP significantly suppressed the expression of a number of HOXA genes.Furthermore, we identified miR-125b as a post-transcriptional regulator of HOTTIP. Ectopic expression of miR-125b reduced HOTTIP-coupled luciferase activity and suppressed the endogenous level of HOTTIP. Moreover, in human HCCs, HOTTIP expression negatively correlated with that of miR-125b.HOTTIP is a novel oncogenic lncRNA, which negatively regulated by miR-125b. Overexpression of HOTTIP contributes to hepatocarcinogenesis by regulating the expression of its neighbouring protein-coding genes.	25424744	RID01999	ceRNA or sponge
Nasopharynx carcinoma	TP53	LOC401317	positively-E	luciferase reporter assay	downregulation	qPCR;microarray	GSE60379	GSE60379.zip	cell cycle(-);apoptosis process(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	TF	lncRNA	ENSG00000141510	NA	NA	GRCh38_7:28449124-28451460	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	NA	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Further studies indicated that LOC401317 is directly regulated by p53 and that ectopic expression of LOC401317 inhibits HNE2 cell proliferation in vitro and in vivo by inducing cell cycle arrest and apoptosis.	25422887	RID02000	transcriptional regulation
Nasopharynx carcinoma	LOC401317	CDKN1A	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000124762	NA	NA	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID02001	expression association
Nasopharynx carcinoma	LOC401317	CCND1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60381	GSE60381.zip	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000110092	NA	NA	595	NA	BCL1|D11S287E|PRAD1|U21B31	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID02002	expression association
Nasopharynx carcinoma	LOC401317	CCNE1	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60382	GSE60382.zip	cell cycle(-)	NA	regulation	NA	NA	NA	NA	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000105173	NA	NA	898	NA	CCNE|pCCNE1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID02003	expression association
Nasopharynx carcinoma	LOC401317	CASP3	negatively-E	RNAi	downregulation	qPCR;microarray	GSE60383	GSE60383.zip	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000164305	NA	NA	836	NA	CPP32|CPP32B|SCA-1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID02004	expression association
Nasopharynx carcinoma	LOC401317	PARP1	negatively-E	RNAi	downregulation	qPCR;microarray	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	NA	GRCh38_7:28449124-28451460	ENSG00000143799	NA	NA	142	NA	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	LOC401317, a p53-regulated long non-coding RNA, inhibits cell proliferation and induces apoptosis in the nasopharyngeal carcinoma cell line HNE2. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage.	25422887	RID02005	expression association
Prostate cancer	ESR1	NEAT1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Prostate cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000245532	GRCh38_11:65422774-65445540	2099	283131	ER|ESR|ESRA|ESTRR|Era|NR3A1	LINC00084|NCRNA00084|TncRNA|VINC	The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer. Among putatively ERalpha-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Analysis of two large clinical cohorts also revealed that NEAT1 expression is associated with prostate cancer progression. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists.	25415230	RID02006	transcriptional regulation
Neuroblastoma	POU3F3	DALIR	positively-E	ChIP	downregulation	qPCR	NA	NA	cell differentiation(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Neuroblastoma	TF	lncRNA	ENSG00000198914	NA	NA	GRCh38_2:104860077-104861124	5455	104940698	BRN1|OTF8|brain-1|oct-8	DALI	The long non-coding RNA Dali is an epigenetic regulator of neural differentiation. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans.	25415054	RID02007	transcriptional regulation
Neuroblastoma	DALIR	DNMT1	interact	ChIP	downregulation	qPCR	NA	NA	cell differentiation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Neuroblastoma	lncRNA	PCG	NA	GRCh38_2:104860077-104861124	ENSG00000130816	NA	104940698	1786	DALI	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The long non-coding RNA Dali is an epigenetic regulator of neural differentiation. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans.	25415054	RID02008	interact with protein
Cervical cancer	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	Long non-coding RNA HOTAIR is associated with human cervical cancer progression. The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues.Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. Therefore, HOTAIR may promote tumor aggressiveness through the upregulation of VEGF and MMP-9 and EMT-related genes.	25405331	RID02009	expression association
Cervical cancer	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA HOTAIR is associated with human cervical cancer progression. The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues.Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. Therefore, HOTAIR may promote tumor aggressiveness through the upregulation of VEGF and MMP-9 and EMT-related genes.	25405331	RID02010	expression association
Triple-receptor negative breast cancer	LINC-ROR	ARF6	positively-E	Targetscan;RNAi;MS2 binding assay	upregulation	qPCR;sequencing	TCGA	BRCA.zip	cell invasion(-)	ceRNA(miR-145-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000165527	NA	100885779	382	ROR|lincRNA-RoR|lincRNA-ST8SIA3	NA	lincRNA-RoR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6. Interestingly, lincRNA-RoR is dramatically upregulated in TNBC and in metastatic disease and knockdown restores miR-145 expression.Investigation of miR-145-regulated pathways involved in tumor invasion revealed a novel target, the small GTPase ADP-ribosylation factor 6 (Arf6).lincRNA-RoR is overexpressed in TNBC where it serves as competitive endogenous RNA for miR-145. miR-145 directly targets the 3'UTR of ARF6 mRNA. Subsequent analysis demonstrated that ARF6, a known regulator of breast tumor cell invasion, is dramatically upregulated in TNBC and in breast tumor metastasis. Mechanistically, ARF6 regulates E-cadherin localization and affects cell-cell adhesion. These results reveal a lincRNA-RoR/miR-145/ARF6 pathway that regulates invasion in TNBCs.	25253741	RID02011	ceRNA or sponge
Acute promyelocytic leukemia	PRAM1	NEAT1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell differentiation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	PCG	lncRNA	ENSG00000133246	NA	ENSG00000245532	GRCh38_11:65422774-65445540	84106	283131	PML-RAR|PRAM-1	LINC00084|NCRNA00084|TncRNA|VINC	Inhibition of long non-coding RNA NEAT1 impairs myeloid differentiation in acute promyelocytic leukemia cells. we found that nuclear enriched abundant transcript 1 (NEAT1), a lncRNA essential for the formation of nuclear body paraspeckles, is significantly repressed in de novo APL samples compared with those of healthy donors. We further provide evidence that NEAT1 expression was repressed by PML-RARalpha.	25245097	RID02012	expression association
Ovarian cancer	FALEC	BMI1	interact	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000168283	NA	100874054	648	FAL1|LINC00568|ncRNA-a1	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer. we identified an oncogene, focally amplified lncRNA on chromosome 1 (FAL1), whose copy number and expression are correlated with outcomes in ovarian cancer. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.The high degree of similarity between FAL1- and BMI1-mediated transcriptional repression strongly indicates a functional interaction between FAL1 and BMI1.	25203321	RID02013	interact with protein
Ovarian cancer	FALEC	CDKN1A	negatively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(-)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000124762	NA	100874054	1026	FAL1|LINC00568|ncRNA-a1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.	25203321;25367941	RID02014	epigenetic regulation
Multiple myeloma	MALAT1	LTBP3	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	biomarker(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168056	NA	378938	4054	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DASS|GPHYSD3|LTBP-3|LTBP2|STHAG6|pp6425	Activation of LTBP3 gene by a long noncoding RNA (lncRNA) MALAT1 transcript in mesenchymal stem cells from multiple myeloma. Our data suggested that lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1, and recruitment of Sp1 to the promoter.Our knowledge of the role of MALAT1 in cellular transformation is pointing toward its potential use as a biomarker and a target for novel therapeutic approaches in multiple myeloma	25187517	RID02015	transcriptional regulation
Endometrial fibrosis	miR-29b-3p	MEG3	positively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Reproductive system disease	Fibrosis	miRNA	lncRNA	NA	NA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MicroRNA-29b inhibits TGF-beta1-induced fibrosis via regulation of the TGF-beta1/Smad pathway in primary human endometrial stromal cells. ectopic overexpression of miR-29b increased the expression levels of MEG3, inhibited myofibroblast-like cell proliferation and induced apoptosis.	27035110	RID02016	expression association
Malignant glioma	GAS5	miR-222	negatively-F	western blot;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	Gas5 Exerts Tumor-suppressive Functions in Human Glioma Cells by Targeting miR-222. We showed that the introduction of Gas5 by plasmid transfection increased the expression of tumor suppressor Bcl-2-modifying factor (bmf) and Plexin C1 via directly targeting and reducing the expression of miR-222.knockdown of miR-222 attenuated U87 and U251 cell migration and invasion by upregulating Plexin C1, and cofilin was a crucial regulator targeted by Plexin C1.In summary, we show that Gas5 suppresses tumor malignancy by downregulating miR-222, which may serve as a promising therapy for glioma.	26370254	RID02017	ceRNA or sponge
Nasopharynx carcinoma	EWSAT1	CCND1	positively-E	western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-326-5p;miR-330-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000110092	NA	283673	595	LINC00277|NCRNA00277|TMEM84	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p. mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters.Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	27816050	RID02018	ceRNA or sponge
Malignant glioma	MEG3	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-)	ceRNA(miR-19a-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000171862	NA	55384	5728	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion by Acting as a Competing Endogenous RNA of miR-19a. miR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration, and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis.Bioinformatics analyses (TargetScan, miRanda, and starBase V2.0) showed that phosphatase and tensin homolog (PTEN) is a target of miR-19a with complementary binding sites in the 3'-UTR.	28276316	RID02019	ceRNA or sponge
Non-small cell lung cancer	XIST	BCL2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-449a)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000171791	NA	7503	596	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	Bcl-2|PPP1R50	The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer.the expression levels of XIST were significantly elevated. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2.knockdown of XIST by siRNA significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis.Hence, by competing with Bcl-2 to bind miR-449a, XIST influences the regulation of tumor progression in NSCLC.	28248928	RID02020	ceRNA or sponge
Osteonecrosis	HOTAIR	SMAD7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell differentiation(-);cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000101665	NA	100124700	4092	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CRCS3|MADH7|MADH8	Long non-coding RNA HOTAIR inhibits miR-17-5p to regulate osteogenic differentiation and proliferation in non-traumatic osteonecrosis of femoral head.HOTAIR downregulation induced by si-HOTAIR led to the increase of miR-17-5p expression and the decrease of miR-17-5p target gene SMAD7 expression.The following experiments showed that downregulation of HOTAIR contributed to the reduced DNA methylation level of miR-17-5p promotor.	28207735	RID02021	expression association
Osteonecrosis	HOTAIR	miR-17-5p	negatively-E	5-Aza-CdR	upregulation	qPCR	NA	NA	cell differentiation(-);cell proliferation(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR inhibits miR-17-5p to regulate osteogenic differentiation and proliferation in non-traumatic osteonecrosis of femoral head.HOTAIR downregulation induced by si-HOTAIR led to the increase of miR-17-5p expression and the decrease of miR-17-5p target gene SMAD7 expression.The following experiments showed that downregulation of HOTAIR contributed to the reduced DNA methylation level of miR-17-5p promotor	28207735	RID02022	epigenetic regulation
Chronic myeloid leukemia	MEG3	miR-21-5p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	sponge	binding/interaction	RNA-RNA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	miRNA	ENSG00000214548	GRCh38_14:100779410-100861031	NA	NA	55384	NA	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	NA	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02023	ceRNA or sponge
Chronic myeloid leukemia	MEG3	ABCC1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000103222	NA	55384	4363	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC29|ABCC|GS-X|MRP|MRP1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02024	expression association
Chronic myeloid leukemia	MEG3	ABCB1	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000085563	NA	55384	5243	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02025	expression association
Chronic myeloid leukemia	MEG3	ABCG2	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);cell proliferation(-);apoptosis process(+)	NA	association	NA	imatinib	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000118777	NA	55384	9429	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ABC15|ABCP|BCRP|BCRP1|BMDP|CD338|CDw338|EST157481|GOUT1|MRX|MXR|MXR-1|MXR1|UAQTL1	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	28190319	RID02026	expression association
Gallbladder cancer	TUG1	miR-300	negatively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 promotes cell proliferation and metastasis by negatively regulating miR-300 in gallbladder carcinoma.TUG1 expression was significantly overexpressed in GBC tissues. Mechanically, we found that TUG1 is upregulated by TGF-beta1, and knockdown of TUG1 inhibited GBC cell EMT. Furthermore, we identified that miR-300, which has been reported as a suppressor in other types of cancer, is negatively regulated by TUG1.	28178615	RID02027	expression association
Hepatocellular carcinoma	HULC	SIRT1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell autophagy(+)	NA	regulation	NA	oxaliplatin;5-fluorouracil;pirarubicin	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000096717	NA	728655	23411	HCCAT1|LINC00078|NCRNA00078	SIR2|SIR2L1|SIR2alpha	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells. In this study, we for the first time demonstrated that treatment with antitumor reagents such as oxaliplatin, 5-fluorouracil and pirarubicin (THP) dramatically induced HULC expression and protective autophagy. Silencing of HULC sensitized HCC cells to the three antitumor reagents via inhibiting protective autophagy.Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1.	28166203	RID02028	expression association
Hepatocellular carcinoma	HULC	USP22	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	chemosensitivity(-);cell autophagy(+)	NA	regulation	NA	oxaliplatin;5-fluorouracil;pirarubicin	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124422	NA	728655	23326	HCCAT1|LINC00078|NCRNA00078	USP3L	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells. we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.HULC does not act as a miRNA sponge to suppress the expression and activity of the threemiRNAs. Furthermore, we found that HULC didn't affect thestability of the three miRNAs using actinomycin D (Supplementary Figure 4D), suggesting that HULC may downregulate the thre emiRNAs through transcription inhibition or epigenetic regulation.	28166203	RID02029	expression association
Colorectal cancer	miR-200a-3p	H19	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	miRNA	lncRNA	NA	NA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing beta-Catenin Expression in Colorectal Cancer. H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues. H19 overexpression facilitated colon cancer cell proliferation, whereas H19 knockdown inhibited cell proliferation. miR-200a bound to H19 and inhibited its expression, thereby decreasing CRC cell proliferation.	28164117	RID02030	ceRNA or sponge
Non-small cell lung cancer	DUXAP8	EGR1	negatively-E	RIP;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000120738	NA	503637	1958	NA	AT225|G0S30|KROX-24|NGFI-A|TIS8|ZIF-268|ZNF225	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB. We identified a transcribed pseudogene named DUXAP8 that is upregulated in tumor tissues. DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02031	epigenetic regulation
Non-small cell lung cancer	DUXAP8	RHOB	negatively-E	RIP;western blot;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000143878	NA	503637	388	NA	ARH6|ARHB|MST081|MSTP081|RHOH6	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02032	epigenetic regulation
Liver fibrosis	HOTAIR	MEG3	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	histone modification	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	lncRNA	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000214548	GRCh38_14:100779410-100861031	100124700	55384	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.	27979710	RID02033	epigenetic regulation
Liver fibrosis	HOTAIR	miR-148b	negatively-F	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.	27979710	RID02034	ceRNA or sponge
Colorectal cancer	BLACAT1	MRPL28	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);prognosis(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000086504	NA	101669762	10573	LINC00912|linc-UBC1|onco-lncRNA-30	MAAT1|p15	Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation.	28277544	RID02035	epigenetic regulation
Multiple myeloma	CRNDE	miR-451a	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Myeloma	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	Long Noncoding RNA CRNDE Promotes Multiple Myeloma Cell Growth by Suppressing miR-451. In this study, we found that the CRNDE expression level, in MM samples and cell lines, is higher than that in the control detected by real-time qPCR, which is also closely related to tumor progression and poor survival in MM patients. Bioinformatics analysis and luciferase assay reveal the interaction by complementary bonding between CRNDE and miR-451. Pearson's correlation shows that CRNDE is negatively correlated to miR-451 expression in human MM samples. Our study illustrates that lncRNA CRNDE induces the proliferation and antiapoptosis capability of MM by acting as a ceRNA or molecular sponge via negatively targeting miR-451, which could act as a novel diagnostic marker and therapeutic target for MM.	28276319	RID02036	ceRNA or sponge
Gastric cancer	MALAT1	CDH5	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000179776	NA	378938	1003	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	7B4|CD144	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02037	expression association
Gastric cancer	MALAT1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168036	NA	378938	1499	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02038	expression association
Gastric cancer	MALAT1	MMP14	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000157227	NA	378938	4323	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MMP-14|MMP-X1|MT-MMP|MT-MMP 1|MT1-MMP|MT1MMP|MTMMP1|WNCHRS	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02039	expression association
Gastric cancer	MALAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000087245	NA	378938	4313	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02040	expression association
Gastric cancer	MALAT1	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02041	expression association
Gastric cancer	MALAT1	MAPK1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100030	NA	378938	5594	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02042	expression association
Gastric cancer	MALAT1	PTK2	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169398	NA	378938	5747	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FADK|FAK|FAK1|FRNK|PPP1R71|p125FAK|pp125FAK	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02043	expression association
Gastric cancer	MALAT1	PXN	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);angiogenesis(+);cell metastasis(+);vasculogenic mimicry(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000089159	NA	378938	5829	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes gastric cancer tumorigenicity and metastasis by regulating vasculogenic mimicry and angiogenesis. MALAT1 knockdown markedly reduced GC cell migration, invasion, tumorigenicity, metastasis, and VM, while restricting HUVEC angiogenesis and increasing vascular permeability. Moreover, MALAT1 was found to regulate expression of VE-cadherin, beta-catenin, MMPs 2 and 9, MT1-MMP, p-ERK, p-FAK, and p-paxillin, which have been established as classical markers of VM and angiogenesis and components of associated signaling pathways. MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/beta-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.	28268166	RID02044	expression association
Tongue cancer	MALAT1	JAG1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-124-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101384	NA	378938	182	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AGS|AGS1|AHD|AWS|CD339|DCHE|HJ1|JAGL1	Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1.lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo.In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.	28260102	RID02045	ceRNA or sponge
Gastric adenocarcinoma	SRF	HOTAIR	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell proliferation(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000112658	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6722	100124700	MCM1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells. miR-101-3p could directly target and suppress the expression of the serum response factor (SRF) gene, which is a transcription factor of HOTAIR, a well-characterized tumor promoter lncRNA. silencing of either SRF or HOTAIR could counteract the promotion of gastric adenocarcinoma cell proliferation and invasion by miR-101-3p inhibition. Our findings indicate that miR-101-3p suppresses HOTAIR-induced proliferation and invasion through directly targeting SRF in gastric carcinoma cells.	28251884	RID02046	transcriptional regulation
Gastric cancer	SP1	LINC00673	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000227036	GRCh38_17:72403322-72592804	6667	100499467	NA	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02047	transcriptional regulation
Gastric cancer	LINC00673	KLF2	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000127528	NA	100499467	10365	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	LKLF	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02048	epigenetic regulation
Gastric cancer	LINC00673	LATS2	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000150457	NA	100499467	26524	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	KPM	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02049	epigenetic regulation
Gastric cancer	SP1	AGAP2-AS1	positively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000255737	GRCh38_12:57726271-57728356	6667	100130776	NA	PUNISHER	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02050	transcriptional regulation
Gastric cancer	AGAP2-AS1	CDKN1A	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000124762	NA	100130776	1026	PUNISHER	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02051	epigenetic regulation
Gastric cancer	AGAP2-AS1	CDH1	negatively-E	RIP;western blot;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000039068	NA	100130776	999	PUNISHER	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02052	epigenetic regulation
Gastric cancer	FEZF1-AS1	CDKN1A	negatively-E	RIP;western blot;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000124762	NA	154860	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. ChIP assays demonstrated that LSD1 could directly bind to the promoter of P21, inducing H3K4me2 demethylation. knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis.	28209170	RID02053	epigenetic regulation
Malignant glioma	PTCSC3	LRP6	negatively-E	RNAi	downregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cell proliferation(-);cell migration(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000070018	NA	100886964	4040	NA	ADCAD2|STHAG7	Long noncoding RNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) inhibits proliferation and invasion of glioma cells by suppressing the Wnt/beta-catenin signaling pathway. LncRNA PTCSC3 was significantly downregulated in glioma cell lines. The study also demonstrated that LRP6, as a receptor of the Wnt/beta-catenin pathway, was a target of lncRNA PTCSC3. By evaluating the expression levels of Axin1, active beta-catenin, c-myc, and cyclin D1, the study indicated that lncRNA PTCSC3 inhibited the activation of the Wnt/beta-cateninpathway through targeting LRP6.In western blot analysis, lncRNA PTCSC3 overexpression downregulated LRP6 expression, subsequently suppressing the expression of active beta-catenin, C-myc and cyclin D1, while increasing Axin1 expression, and vice versa. LncRNA PTCSC3 inhibits the proliferation and migration of glioma cells and suppresses Wnt/beta-catenin signaling pathway by targeting LRP6. LncRNA PTCSC3 is a potential therapeutic target for treatment of glioma.	28187755	RID02054	expression association
Chondrosarcoma	HOTAIR	miR-454-3p	negatively-E	Bisulfite sequencing analysis;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(-)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02055	epigenetic regulation
Renal cell carcinoma	HOTAIR	KDM6B	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132510	NA	100124700	23135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	JMJD3	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.In the present study, HOTAIR expression was elevated in tissues of renal cell carcinoma compared to adjacent normal tissues, and positively correlated with metastasis (P<0.05). Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05).	28177890	RID02056	expression association
Renal cell carcinoma	HOTAIR	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05). Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.	28177890	RID02057	expression association
Renal cell carcinoma	HOTAIR	PCDHB5	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113209	NA	100124700	26167	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-BETA5	Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3. Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression (P<0.05). Meanwhile, the level of histone methytransferase EZH2 target gene PCDHB5 was increased (P<0.05). Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3.	28177890	RID02058	expression association
Breast cancer	PTCSC1	DHX9	interact	RIP;Co-immunoprecipitation	upregulation	qPCR	NA	NA	AKT signaling pathway(+);cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENST00000664551.1	GRCh38.p13:133054959-133057767	ENSG00000135829	NA	100302522	1660	NA	DDX9|LKP|NDH2|NDHII|RHA	LncRNA AK023948 is a positive regulator of AKT. Among lncRNAs identified from this screen, we demonstrate that AK023948 is a positive regulator for AKT. Knockout of AK023948 suppresses, whereas rescue with AK023948 restores the AKT activity. Mechanistically, AK023948 functionally interacts with DHX9 and p85. Importantly, AK023948 is required for the interaction between DHX9 and p85 to hence the p85 stability and promote AKT activity. AK023948 is upregulated in breast cancer; interrogation of TCGA data set indicates that upregulation of DHX9 in breast cancer is associated with poor survival. Together, this study demonstrates two previously uncharacterized factors AK023948 and DHX9 as important players in the AKT pathway, and that their upregulation may contribute to breast tumour progression.	28176758	RID02059	interact with protein
Inflammatory bowel disease	CBR3-AS1	TJP1	positively-E	RNAi	downregulation	qPCR	NA	NA	intestinal epithelial barrier(+)	NA	regulation	NA	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	lncRNA	PCG	ENSG00000236830	GRCh38_21:36131767-36175815	ENSG00000104067	NA	100506428	7082	PlncRNA-1|PlncRNA1	ZO-1	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease. DSS induced injury of intestinal epithelial barrier, while overexpression of PlncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.	28153728	RID02060	expression association
Inflammatory bowel disease	miR-34c-5p	CBR3-AS1	negatively-F	RNA pull-down assay;luciferase reporter assay	downregulation	qPCR	NA	NA	intestinal epithelial barrier(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Gastrointestinal system disease	Inflammatory bowel disease	miRNA	lncRNA	NA	NA	ENSG00000236830	GRCh38_21:36131767-36175815	NA	100506428	NA	PlncRNA-1|PlncRNA1	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease. DSS induced injury of intestinal epithelial barrier, while overexpression of PlncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.	28153728	RID02061	ceRNA or sponge
Oral squamous cell carcinoma	TLR3	lnc-IL7R	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	chemosensitivity(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Oral cavity cancer	PCG	lncRNA	ENSG00000164342	NA	ENSG00000168685	GRCh38_5:35852695-35879603	7098	NA	CD283|IIAE2	NA	The TLR3 Agonist Inhibit Drug Efflux and Sequentially Consolidates Low-Dose Cisplatin-Based Chemoimmunotherapy while Reducing Side Effects. TLR3 negatively manipulated the inflammation-related long noncoding RNA lnc-IL7R, which was upregulated during this chemotherapy. Knockdown of lnc-IL7R improved the chemotherapy sensitivity. Knockdown of lnc-IL7R improved the chemotherapy sensitivity. Overall, this study provided preclinically new instructions for the PIC/cisplatin utilization to target tumor microenvironment and strengthen the low-dose cisplatin-based chemotherapy with reduced side effects.	28138030	RID02062	expression association
Malignant glioma	UCA1	PPP1R13L	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	ceRNA(miR-182-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000104881	NA	652995	10848	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	IASPP|NKIP1|RAI|RAI4	The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP. In this study, we firstly found that UCA1 was upregulated in glioma tumor samples and negatively correlated with survival time. Our results showed that upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation. MiR-182 directly binds to the iASPP 3'UTR and inhibits iASPP expression	28137422	RID02063	ceRNA or sponge
Retinoblastoma	BDNF-AS	CDC42	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000070831	NA	497258	998	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CDC42Hs|G25K|TKS	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02064	expression association
Retinoblastoma	BDNF-AS	CCNE1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000105173	NA	497258	898	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	CCNE|pCCNE1	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02065	expression association
Retinoblastoma	BDNF-AS	BDNF	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell cycle(-)	NA	association	NA	NA	NA	NA	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000245573	GRCh38_11:27506830-27698231	ENSG00000176697	NA	497258	627	ANTI-BDNF|BDNF|BDNF-AS1|BDNFAS|BDNFOS|NCRNA00049	ANON2|BULN2	Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS is downregulated in RB tumors and cell lines. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF.DNF-AS is lowly expressed, and may be used as a prognostic biomarker in RB. Upregulating BDNF-AS has inhibitory effect on RB development, probably through the suppression of cell-cycle transition.	28131827	RID02066	expression association
Non-small cell lung cancer	LINC00511	CDKN1C	negatively-E	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	oncogenic role(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000129757	NA	400619	1028	LCAL5|onco-lncRNA-12	BWCR|BWS|KIP2|WBS|p57|p57Kip2	Long Intergenic Noncoding RNA 00511 Acts as an Oncogene in Non-small-cell Lung Cancer by Binding to EZH2 and Suppressing p57. We found LINC00511 was upregulated and associated with oncogenesis, tumor size, metastasis, and poor prognosis in NSCLC. LINC00511 affected cell proliferation, invasiveness, metastasis, and apoptosis in multiple NSCLC cell lines. Mechanistically, LINC00511 bound histone methyltransferase enhancer of zeste homolog 2 ((EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), a highly conserved protein complex that regulates gene expression by methylating lysine 27 on histone H3), and acted as a modular scaffold of EZH2/PRC2 complexes, coordinated their localization, and specified the histone modification pattern on the target genes, including p57, and consequently altered NSCLC cell biology.	27845772	RID02067	epigenetic regulation
Melanoma	NKILA	NFKB1	negatively-E	western blot;RNAi	downregulation	qPCR	NA	NA	cell growth(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	TF	ENSG00000278709	GRCh38_20:57710156-57712780	ENSG00000109320	NA	105416157	4790	NA	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	The long non-coding RNA NKILA inhibits the invasion-metastasis cascade of malignant melanoma via the regulation of NF-kB. Real-time PCR (qRT-PCR) showed that NKILA was expressed at low levels in human melanoma tissues. Furthermore, qRT-PCR showed that NF-kB, which was negatively correlated with NKILA, was highly expressed in human melanoma tissues. Moreover, our results indicated that NKILA inhibited the carcinogenesis of melanoma cells through the inhibition of NF-kB in vitro. More importantly, we found that NKILA suppressed the growth of melanoma tumors via NF-kB in vivo. In conclusion, NKILA suppressed the development of malignant melanoma via the regulation of NF-kB and may be a potential therapeutic target in patients with melanoma.	28123845	RID02068	expression association
Osteosarcoma	POU5F1	AK055347	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Osteosarcoma	TF	lncRNA	ENSG00000204531	NA	NA	GRCh38_1:166057426-166166969	5460	NA	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	NA	Transcription factor Oct4 promotes osteosarcoma by regulating lncRNA AK055347. The present study observed Oct4 was markedly increased in osteosarcoma cell lines and in human osteosarcoma tissue samples. Notably, downregulation of Oct4 decreased the expression of AK055347, a newly identified long noncoding RNA (lncRNA) in human tissues. The downregulation of AK055347 by siRNA resulted in a significant suppressive effect on proliferative and invasive ability, and promotion of cell apoptosis in osteosarcoma cells.	28123573	RID02069	expression association
Oral squamous cell carcinoma	TUG1	CTNNB1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000168036	NA	55000	1499	LINC00080|NCRNA00080|TI-227H	CTNNB|EVR7|MRD19|NEDSDV|armadillo	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02070	expression association
Oral squamous cell carcinoma	TUG1	CCND1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000110092	NA	55000	595	LINC00080|NCRNA00080|TI-227H	BCL1|D11S287E|PRAD1|U21B31	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02071	expression association
Oral squamous cell carcinoma	TUG1	MYC	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(-);cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Oral cavity cancer	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000136997	NA	55000	4609	LINC00080|NCRNA00080|TI-227H	MRTL|MYCC|bHLHe39|c-Myc	LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.qRT-PCR results showed that TUG1 was up-regulated in both OSCC tissues and cell lines. knock-down of TUG1 in Tca8113 and TSCCA cells significantly suppressed the mRNA and protein expression levels of beta-catenin, cyclin D1, and c-myc. Wnt/beta-catenin pathway activator (LiCl) reversed the TUG1 knock-down effect on cell proliferation, cell invasion and cell apoptosis in Tca8113 and TSCCA cells. LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/beta-catenin signaling.	28119088	RID02072	expression association
Gastric cancer	LNCRNA-ATB	miR-141-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	NA	GRCh38_14:19126530-19128974	NA	NA	114004396	NA	NA	NA	Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFbeta2 feedback loop. We found that lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-beta actives lnc-ATB and TGF-beta2 directly binds mir-141-3p. Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner.	28115163	RID02073	ceRNA or sponge
Gastric cancer	TGFB2	LNCRNA-ATB	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000092969	NA	NA	GRCh38_14:19126530-19128974	7042	114004396	G-TSF|LDS4|TGF-beta2	NA	Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFbeta2 feedback loop. We found that lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-beta actives lnc-ATB and TGF-beta2 directly binds mir-141-3p. Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner.	28115163	RID02074	expression association
Colorectal cancer	HOXA-AS2	CDKN1A	negatively-E	RIP;western blot;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000124762	NA	285943	1026	HOXA3as	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02075	epigenetic regulation
Colorectal cancer	HOXA-AS2	KLF2	negatively-E	RIP;western blot;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000127528	NA	285943	10365	HOXA3as	LKLF	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02076	epigenetic regulation
Malignant glioma	UCA1	CCND1	positively-E	western blot;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000110092	NA	652995	595	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	BCL1|D11S287E|PRAD1|U21B31	A long noncoding RNA UCA1 promotes proliferation and predicts poor prognosis in glioma.LncRNA UCA1 expression in the glioma samples was obviously higher as compared with the normal brain samples (P < 0.001), and the expression was correlated significantly with grading of the tumors (P < 0.05). LncRNA UCA1 can promote the proliferation and cell cycle progression of glioma cells by upregulating cyclin D1 transcription.	28105536	RID02077	expression association
Colorectal cancer	GAS5	IL10	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);ERK1/1 signaling pathway(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000136634	NA	60674	3586	NCRNA00030|SNHG2	CSIF|GVHDS|IL-10|IL10A|TGIF	Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression. In this study, we found that GAS5 was commonly downregulated in CRC tissues, serum of CRC patients and CRC cell lines. We further demonstrated that knockdown of GAS5 increased the expression and secretion of interleukin-10 (IL-10) and vascular endothelial growth factor (VEGF-A) via NF-kB and Erk1/2 pathways. The cytokines IL-10 and VEGF-A inhibited by GAS5 may provide targets for lncRNA-based therapies for CRC.	28099146	RID02078	expression association
Colorectal cancer	GAS5	VEGFA	negatively-E	RNAi	downregulation	qPCR	NA	NA	NF-kB signaling pathway(-);ERK1/2 signaling pathway(-);tumorigenesis(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000112715	NA	60674	7422	NCRNA00030|SNHG2	MVCD1|VEGF|VPF	Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression.We further demonstrated that knockdown of GAS5 increased the expression and secretion of interleukin-10 (IL-10) and vascular endothelial growth factor (VEGF-A) via NF-kB and Erk1/2 pathways.	28099146	RID02079	expression association
Cervical cancer	TUG1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000171791	NA	55000	596	LINC00080|NCRNA00080|TI-227H	Bcl-2|PPP1R50	Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl-2 and caspase-3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial-mesenchymal transition (EMT).	28088836	RID02080	expression association
Cervical cancer	TUG1	CASP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000164305	NA	55000	836	LINC00080|NCRNA00080|TI-227H	CPP32|CPP32B|SCA-1	Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl-2 and caspase-3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial-mesenchymal transition (EMT).	28088836	RID02081	expression association
Non-small cell lung cancer	CCAT2	ZBTB7A	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000178951	NA	101805488	51341	LINC00873|NCCP1	FBI-1|FBI1|LRF|TIP21|ZBTB7|ZNF857A|pokemon	LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer. CCAT2 and Pokemon were over-expressed in NSCLC tissue and cells. CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21; The results indicated that CCAT2 promotes tumorigenesis by over-expression of Pokemon, and the potential mechanism might relate to the Pokemon related gene p21.	28088736	RID02082	expression association
Non-small cell lung cancer	CCAT2	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000124762	NA	101805488	1026	LINC00873|NCCP1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer.CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21;	28088736	RID02083	expression association
Retinoblastoma	CCAT1	miR-218-5p	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Retinoblastoma	lncRNA	miRNA	NA	GRCh38_8:127207382-127219268	NA	NA	100507056	NA	CARLO5|CARLo-5|onco-lncRNA-40	NA	Long non-coding RNA CCAT1 promotes human retinoblastoma SO-RB50 and Y79 cells through negative regulation of miR-218-5p. LncRNA CCAT1 promotes the proliferation migration and invasion, and reduces cell apoptosis of SO-RB50 and Y79 cells, probably through negative modulation of miR-218-5p.	28088735	RID02084	expression association
Hepatocellular carcinoma	ACTA2-AS1	ACTA2	positively-E	RNAi	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000180139	GRCh38_10:88932390-88940820	ENSG00000107796	NA	100132116	59	UC001kfo|ZXF1|uc001kfo.1	ACTSA	Long non-coding RNA UC001kfo promotes hepatocellular carcinoma proliferation and metastasis by targeting alpha-SMA. The present study found that the expression of UC001kfo was upregulated in HCC tissues and cell lines in comparison with tumour-adjacent tissues and normal hepatocytes, respectively. UC001kfo was verified to promote the proliferation, metastasis and epithelial-mesenchymal transition (EMT) in HCC cells in both in vitro and in vivo assays. Mechanistically, alpha-SMA was indicated as a potential target gene of UC001kfo in mediating HCC metastasis.	28088733	RID02085	expression association
Gastric cancer	TGFB1	UCA1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000214049	GRCh38_19:15828206-15836328	7040	652995	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02086	expression association
Gastric cancer	UCA1	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000124216	NA	652995	6615	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02087	expression association
Gastric cancer	UCA1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000026025	NA	652995	7431	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02088	expression association
Gastric cancer	UCA1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000039068	NA	652995	999	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02089	expression association
Gastric cancer	UCA1	TJP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000104067	NA	652995	7082	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ZO-1	TGFbeta1-Induced LncRNA UCA1 Upregulation Promotes Gastric Cancer Invasion and Migration.lncRNA-UCA1 was specifically upregulated in GC tissues and cell lines, and augmented GC cell proliferation, and invasive and migratory capabilities. UCA1 silence reduced the protein levels of EMT-related factors, vimentin and snail, while promoted E-cadherin and zonula occludens-1 protein levels in GC cells; the effect of UCA1 could be partly restored by TGFbeta1 treatment. Taken together, UCA1 might regulate the tumor proliferation, invasion, and metastasis under TGFbeta1 induction.	28075173	RID02090	expression association
Chronic myeloid leukemia	HULC	MYC	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	imatinib	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000136997	NA	728655	4609	HCCAT1|LINC00078|NCRNA00078	MRTL|MYCC|bHLHe39|c-Myc	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548	RID02091	expression association
Chronic myeloid leukemia	HULC	BCL2	negatively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000171791	NA	728655	596	HCCAT1|LINC00078|NCRNA00078	Bcl-2|PPP1R50	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548	RID02092	expression association
Klatskin's tumor	MALAT1	CXCR4	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000121966	NA	378938	7852	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD184|D2S201E|FB22|HM89|HSY3RR|LAP-3|LAP3|LCR1|LESTR|NPY3R|NPYR|NPYRL|NPYY3R|WHIM|WHIMS	Long Non-Coding RNA MALAT1 Interacts With miR-204 to Modulate Human Hilar Cholangiocarcinoma Proliferation, Migration, and Invasion by Targeting CXCR4. In our research, lncRNA-MALAT1 was specifically upregulated in HCCA tissues and cell lines, and was associated with pathological T stage, a larger tumor size, and perineural invasion.In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration, and invasion. By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion. Taken together, our data indicated that MALAT1 might play an oncogenic role in HCCA through miR-204-dependent CXCR4 regulation, and could be regarded as a therapeutic target in HCCA.	28059437	RID02093	ceRNA or sponge
Breast cancer	LINC00052	ERBB3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000259527	GRCh38_15:87576929-87579866	ENSG00000065361	NA	145978	2065	NCRNA00052|TMEM83	ErbB-3|FERLK|HER3|LCCS2|MDA-BF-1|c-erbB-3|c-erbB3|erbB3-S|p180-ErbB3|p45-sErbB3|p85-sErbB3	HER3 and LINC00052 interplay promotes tumor growth in breast cancer.Here we report that the lncRNA LINC00052 expression correlates positively with HER3/ErbB3 levels in breast cancer cells. Gene silencing of LINC00052 diminished both LINC00052 and HER3 expression and reduced cancer cell growth in vitro and in vivo. LINC00052 overexpression promoted cancer cell growth in vitro and in vivo and increased HER3-mediated downstream signaling.Taken together, our results indicate that high LINC00052 levels predict activation of HER3-mediated signaling, and LINC00052 expression level may serve as a potential biomarker for HER3 targeted antibody cancer therapies.	28036286	RID02094	expression association
Osteosarcoma	PANDAR	CDKN2C	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000281450	GRCh38_6:36673621-36675126	ENSG00000123080	NA	101154753	1031	PANDA	INK4C|p18|p18-INK4C	Long Noncoding RNA PANDA Positively Regulates Proliferation of Osteosarcoma Cells. PANDA was highly expressed in U2OS cells, and its expression was induced by DNA damage. Silencing PANDA caused arrest at the G1 phase of the cell cycle, leading to inhibition of cell proliferation. Quantitative RT-PCR showed that silencing PANDA increased mRNA levels of the cyclin-dependent kinase inhibitor p18, which caused G1 phase arrest.	28011477	RID02095	expression association
Malignant glioma	H19	miR-675-5p	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	host	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	LncRNA H19 is overexpressed in glioma tissue, is negatively associated with patient survival, and promotes tumor growth through its derivative miR-675. These effects of lncRNA H19 appeared to be intermediated by miR-675. The latter was overexpressed in glioma tissue and was negatively associated with patient survival. Supporting the involvement of miR-675, its antagomir decreased proliferation of glioma cell lines, whereas its mimic increased proliferation of NHA cells.	27981546	RID02096	expression association
Retinoblastoma	HOTAIR	RB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000139687	NA	100124700	5925	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Long non-coding RNA regulates proliferation and invasion via activating Notch signalling pathway in retinoblastoma. HOTAIR expression was found to be significantly upregulated in human retinoblastomas tissues as compared with that in paracancerous tissues. Knockdown of HOTAIR restricted the proliferation and invasion of the more invasive retinoblastoma Y79 cells, and led to G0/G1 arrest, possibly through inhibiting phospho-RB1, RB1 and CCNE.	27966488	RID02097	expression association
Retinoblastoma	HOTAIR	CCNE1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);Notch signaling pathway(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Retinoblastoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105173	NA	100124700	898	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCNE|pCCNE1	Long non-coding RNA regulates proliferation and invasion via activating Notch signalling pathway in retinoblastoma.Knockdown of HOTAIR restricted the proliferation and invasion of the more invasive retinoblastoma Y79 cells, and led to G0/G1 arrest, possibly through inhibiting phospho-RB1, RB1 and CCNE.	27966488	RID02098	expression association
Choriocarcinoma	LINC00261	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000164305	NA	140828	836	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	CPP32|CPP32B|SCA-1	Long Noncoding RNA LINC00261 Suppresses Cell Proliferation and Invasion and Promotes Cell Apoptosis in Human Choriocarcinoma. The transcription level of LINC00261 was significantly lower in choriocarcinoma tissues and in choriocarcinoma cell lines. Meanwhile, it promoted cell apoptosis and the relative activities of caspase 3 and caspase 9 in choriocarcinoma JEG-3 and JAR cells.	27983929	RID02099	expression association
Choriocarcinoma	LINC00261	CASP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Choriocarcinoma	lncRNA	PCG	ENSG00000259974	GRCh38_20:22547671-22578642	ENSG00000132906	NA	140828	842	ALIEN|C20orf56|DEANR1|HCCDR1|NCRNA00261|TCONS_00027846|onco-lncRNA-17	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long Noncoding RNA LINC00261 Suppresses Cell Proliferation and Invasion and Promotes Cell Apoptosis in Human Choriocarcinoma. The transcription level of LINC00261 was significantly lower in choriocarcinoma tissues and in choriocarcinoma cell lines. Meanwhile, it promoted cell apoptosis and the relative activities of caspase 3 and caspase 9 in choriocarcinoma JEG-3 and JAR cells.	27983929	RID02100	expression association
Malignant glioma	TUG1	miR-145-5p	negatively-F	western blot;ChIP	upregulation	qPCR	NA	NA	self-renewal(+)	sponge	binding/interaction	RNA-RNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment. In this study, we find that Notch1 activation in GSCs specifically induces expression of the lncRNA, TUG1. TUG1 coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by locus-specific methylation of histone H3K27 via YY1-binding activity in the nucleus. Our results highlight the importance of the Notch-lncRNA axis in regulating self-renewal of glioma cells and provide a strong rationale for targeting TUG1 as a specific and potent therapeutic approach to eliminate the GSC population.	27922002	RID02101	ceRNA or sponge
Malignant glioma	NOTCH1	TUG1	positively-E	western blot;ChIP	upregulation	qPCR	NA	NA	self-renewal(+)	transcriptional regulation	regulation	protein-DNA	NA	CSC	Self Sufficiency in Growth Signals	Cancer	Brain glioma	PCG	lncRNA	ENSG00000148400	NA	ENSG00000253352	GRCh38_22:30969245-30979395	4851	55000	AOS5|AOVD1|TAN1|hN1	LINC00080|NCRNA00080|TI-227H	Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment. In this study, we find that Notch1 activation in GSCs specifically induces expression of the lncRNA, TUG1. TUG1 coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by locus-specific methylation of histone H3K27 via YY1-binding activity in the nucleus. Our results highlight the importance of the Notch-lncRNA axis in regulating self-renewal of glioma cells and provide a strong rationale for targeting TUG1 as a specific and potent therapeutic approach to eliminate the GSC population.	27922002	RID02102	transcriptional regulation
Malignant glioma	MALAT1	miR-155	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell viability(-)	NA	association	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. Our results showed that the expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues.The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.	27904771	RID02103	expression association
Malignant glioma	MALAT1	FBXW7	positively-E	RNAi	downregulation	qPCR	NA	NA	cancer progression(-)	NA	regulation	NA	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000109670	NA	378938	55294	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AGO|CDC4|FBW6|FBW7|FBX30|FBXO30|FBXW6|SEL-10|SEL10|hAgo|hCdc4	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. Our results showed that the expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues.The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.	27904771	RID02104	expression association
Gastric cancer	HOTAIR	miR-126-3p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP1 signaling pathway(+)	sponge	binding/interaction	RNA-RNA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02105	ceRNA or sponge
Gastric cancer	HOTAIR	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP0 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000112715	NA	100124700	7422	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MVCD1|VEGF|VPF	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02106	expression association
Gastric cancer	HOTAIR	PIK3R2	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT/MRP1 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105647	NA	100124700	5296	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MPPH|MPPH1|P85B|p85|p85-BETA	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer.	27900563	RID02107	expression association
Hepatocellular carcinoma	SPRY4-IT1	TWIST1	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	NA	GRCh38_5:142317636-142318322	ENSG00000122691	NA	100642175	7291	SPRIGHTLY	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02108	expression association
Hepatocellular carcinoma	SPRY4-IT1	VIM	positively-E	western blot	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000026025	NA	100642175	7431	SPRIGHTLY	NA	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02109	expression association
Hepatocellular carcinoma	SPRY4-IT1	CDH1	negatively-E	ChIP;western blot;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	histone modification	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000039068	NA	100642175	999	SPRIGHTLY	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02110	epigenetic regulation
Endometrial cancer	BANCR	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000087245	NA	100885775	4313	LINC00586	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway. qRT-PCR revealed that the expression of lncRNA BANCR was higher in type 1 EC (P<0.01). knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression. BANCR is highly expressed in type 1 EC tissue and promotes EC-cell proliferation, migration, and invasion by activating ERK/MAPK signaling pathway that regulates MMP2/MMP1 expression. BANCR is expected to become a prognostic marker and therapeutic target in type 1 EC.	27898420	RID02111	expression association
Endometrial cancer	BANCR	MMP1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000196611	NA	100885775	4312	LINC00586	CLG|CLGN	Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway.knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression.	27898420	RID02112	expression association
Osteosarcoma	EWSAT1	MEG3	positively-E	RNAi	NA	NA	NA	NA	cell growth(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	lncRNA	ENSG00000212766	GRCh38_15:69072926-69095820	ENSG00000214548	GRCh38_14:100779410-100861031	283673	55384	LINC00277|NCRNA00277|TMEM84	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Long Noncoding RNA EWSAT1 Promotes Osteosarcoma Cell Growth and Metastasis Through Suppression of MEG3 Expression. In the present study, gain- and loss-of-function assays demonstrated that EWSAT1 enhanced OS cell proliferation, migration, and invasion. Further mechanistic studies found that EWSAT1 positively regulated lncRNA MEG3 expression in the transcriptional level. Finally, we observed that EWSAT1 facilitates OS cell growth and metastasis through regulation of MEG3, suggesting that EWSAT1-MEG3 axis might be a promising target for OS treatment.	27860482	RID02113	expression association
Pre-eclampsia	SPRY4-IT1	ELAVL1	interact	RIP	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000066044	NA	100642175	1994	SPRIGHTLY	ELAV1|HUR|Hua|MelG	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02114	interact with protein
Pre-eclampsia	SPRY4-IT1	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000168036	NA	100642175	1499	SPRIGHTLY	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02115	expression association
Pre-eclampsia	SPRY4-IT1	WNT3	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000108379	NA	100642175	7473	SPRIGHTLY	INT4|TETAMS	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02116	expression association
Pre-eclampsia	SPRY4-IT1	WNT5B	positively-E	RNAi	upregulation	qPCR	NA	NA	WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000111186	NA	100642175	81029	SPRIGHTLY	NA	The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition. The long noncoding RNA SPRY4-IT1 is more highly expressed in preeclamptic human placentas than in normal placentas. SPRY4-IT1 bound directly to HuR and mediated the beta-catenin expression associated with EMT in HTR-8/SVneo cells. Moreover, the expression levels of genes in the WNT family, such as WNT3 and WNT5B, were changed after transfection of HTR-8/SVneo with SPRY4-IT1. our results highlight the roles of SPRY4-IT1 in causing trophoblast cell dysfunction by acting through the Wnt/beta-catenin pathway.	27853262	RID02117	expression association
Estrogen-receptor positive breast cancer	H19	PMAIP1	negatively-E	ChIP;western blot;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	histone modification	regulation	NA	paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141682	NA	283120	5366	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	APR|NOXA	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02118	epigenetic regulation
Estrogen-receptor positive breast cancer	ESR1	H19	positively-E	western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000130600	GRCh38_11:1995176-2001470	2099	283120	ER|ESR|ESRA|ESTRR|Era|NR3A1	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02119	expression association
Gastric cancer	YAP1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000228630	GRCh38_12:53962308-53974956	10413	100124700	COB1|YAP|YAP2|YAP65|YKI	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02120	expression association
Gastric cancer	YAP1	H19	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000130600	GRCh38_11:1995176-2001470	10413	283120	COB1|YAP|YAP2|YAP65|YKI	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02121	expression association
Gastric cancer	YAP1	MALAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10413	378938	COB1|YAP|YAP2|YAP65|YKI	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02122	expression association
Gastric cancer	YAP1	LATS2-AS1-001	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000137693	NA	NA	GRCh38_13:21005157-21018122	10413	NA	COB1|YAP|YAP2|YAP65|YKI	NA	YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo. YAP1 and P62 were significantly up-regulated in GC specimens. Stable YAP1 silencing inhibited the proliferation, migration, and invasion of BGC-823 GC cells in vitro and inhibited the growth of xenograft tumor and hematogenous metastasis of BGC-823 GC cells in vivo. The mechanism was associated with inhibited extracellular signal-regulated kinases (ERK)1/2 phosphorylation, elevated E-cadherin protein expression and decreased vimentin protein expression, down-regulated beta-catenin protein expression and elevated alpha-catenin protein expression, and down-regulated long non-coding RNA (lncRNA) expressions including HOX transcript antisense RNA (HOTAIR), H19, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), human large tumor suppressor-2 (LATS2)-AS1-001, and LATS2.	27835600	RID02123	expression association
Lung cancer	RB1	MEG3	negatively-E	5-azadC;RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);RB signaling pathway(-)	DNA methylation	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	PCG	lncRNA	ENSG00000139687	NA	ENSG00000214548	GRCh38_14:100779410-100861031	5925	55384	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	Expression of the lncRNA Maternally Expressed Gene 3 (MEG3) Contributes to the Control of Lung Cancer Cell Proliferation by the Rb Pathway. Treatment of these cells with palbociclib also decreased the expression of pRb-regulated DNA methyltransferase 1 (DNMT1), while conversely, knockdown of DNMT1 resulted in increased expression of MEG3. As gene methylation has been suggested for MEG3 regulation, we found that palbociclib resulted in decreased methylation of the MEG3 locus similar to that observed with 5-aza-deoxycytidine.while analysis of the TCGA database revealed decreased MEG3 expression in human lung tumors harboring a disrupted RB pathway. Together, these data suggest that disruption of the pRb-DNMT1 pathway leads to a decrease in MEG3 expression, thereby contributing to the pro-proliferative state of certain cancer cells.	27832204	RID02124	epigenetic regulation
Hepatocellular carcinoma	CRNDE	miR-384	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	miRNA	ENSG00000245694	GRCh38_16:54845189-54929189	NA	NA	NA	NA	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	NA	LncRNA CRNDE promotes hepatic carcinoma cell proliferation, migration and invasion by suppressing miR-384. Herein, we found that the expression of CRNDE was increased in human hepatic carcinoma (HCC) tissues and cell lines. Moreover, we indicated CRNDE negatively regulated miR-384 expression in HCC. In addition, we found that CRNDE accelerated the expression levels of NF-kB and p-AKT though inhibition of miR-384.	27822419	RID02125	expression association
Cancer	TP53TG1	YBX1	interact	ChIP;western blot	downregulation	qPCR	NA	NA	chemoresistance(+);p53 signaling pathway(-)	interact with protein	binding/interaction	RNA-protein	compounds that damage DNA	NA	Genome Instability and Mutation	Cancer	Cancer	lncRNA	TF	ENSG00000182165	GRCh38_7:87322943-87345528	ENSG00000065978	NA	11257	4904	LINC00096|NCRNA00096|P53TG1|P53TG1-D|TP53AP1	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Epigenetic inactivation of the p53-induced long noncoding RNA TP53 target 1 in human cancer. we show that TP53TG1 binds to the multifaceted DNA/RNA binding protein YBX1 to prevent its nuclear localization and thus the YBX1-mediated activation of oncogenes. TP53TG1 epigenetic inactivation in cancer cells releases the transcriptional repression of YBX1-targeted growth-promoting genes and creates a chemoresistant tumor.The epigenetic loss of TP53TG1 therefore represents an altered event in an lncRNA that is linked to classical tumoral pathways, such as p53 signaling, but is also connected to regulatory networks of the cancer cell.	27821766	RID02126	interact with protein
Renal cell carcinoma	BX357664	TGFB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000105329	NA	NA	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02127	expression association
Renal cell carcinoma	BX357664	MAPK14	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000112062	NA	NA	1432	NA	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02128	expression association
Renal cell carcinoma	BX357664	HSPB1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);epithelial to mesenchymal transition(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	NA	GRCh38_8:101491168-101491817	ENSG00000106211	NA	NA	3315	NA	CMT2F|HEL-S-102|HMN2B|HS.76067|HSP27|HSP28|Hsp25|SRP27	Long noncoding RNA BX357664 regulates cell proliferation and epithelial-to-mesenchymal transition via inhibition of TGF-beta1/p38/HSP27 signaling in renal cell carcinoma. BX357664 was downregulated in RCC according to previous microarray analysis and qualitative real-time polymerase chain reaction. Furthermore, Western blot analysis was conducted to identify the influence of BX357664 on epithelial-to-mesenchymal transition, matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor-beta 1 (TGF-beta1)/p38/HSP27 signaling pathway in RCC.Therefore, we investigated a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression by blocking the TGF-beta1/p38/HSP27 pathway.	27806310	RID02129	expression association
Colon cancer	GSEC	DHX36	negatively-F	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE20916	GSE20916.zip	cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000280832	GRCh38_11:126340889-126355587	ENSG00000174953	NA	399972	170506	DCPS-AS1|ST3GAL4-AS1	DDX36|G4R1|MLEL1|RHAU	The novel G-quadruplex-containing long non-coding RNA GSEC antagonizes DHX36 and modulates colon cancer cell migration. In this study, we analyze the gene expression profiles of colon cancer tissues and identify a previously unannotated lncRNA, FLJ39051, that we term GSEC (G-quadruplex-forming sequence containing lncRNA), as a lncRNA that is upregulated in colorectal cancer.We also show that GSEC binds to the DEAH box polypeptide 36 (DHX36) RNA helicase via its G-quadruplex-forming sequence and inhibits DHX36 G-quadruplex unwinding activity.	27797375	RID02130	interact with protein
Gastric cancer	PVT1	FOXM1	positively-F	western blot;RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000111206	NA	5820	2305	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion. The lncRNA PVT1 was significantly upregulated in gastric cancer tissues compared with ANTs. PVT1 enhanced gastric cancer cell proliferation and invasion in vitro and in vivo. PVT1 directly bound FOXM1 protein and increased FOXM1 posttranslationally. Moreover, PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription.	27756785	RID02131	interact with protein
Gastric cancer	FOXM1	PVT1	positively-E	western blot;RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000111206	NA	ENSG00000249859	GRCh38_8:127794526-128187101	2305	5820	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion.PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription.	27756785	RID02132	transcriptional regulation
Aortic valve stenosis	H19	NOTCH1	negatively-E	western blot;ChIP	upregulation	qPCR	NA	NA	biomineral tissue development(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	NA	Cardiovascular system disease	Aortic valve disease	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148400	NA	283120	4851	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AOS5|AOVD1|TAN1|hN1	Altered DNA Methylation of Long Noncoding RNA H19 in Calcific Aortic Valve Disease Promotes Mineralization by Silencing NOTCH1.We documented that lncRNA H19 (H19) was increased in calcific aortic valve disease.Gene promoter analyses showed that H19 silenced NOTCH1 by preventing the recruitment of p53 to its promoter. A knockdown of H19 in valve interstitial cells (VICs) increased the expression of NOTCH1 and decreased the level of RUNX2 and BMP2, 2 downstream targets repressed by NOTCH1.In rescue experiments, the transfection of a vector encoding for the active Notch intracellular domain prevented H19-induced mineralization of valve interstitial cells.	27789555	RID02133	transcriptional regulation
Breast cancer	91H	H19	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	lncRNA	NA	GRCh38_11:1995176-1995988	ENSG00000130600	GRCh38_11:1995176-2001470	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications. We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development.	27780718	RID02134	epigenetic regulation
Breast cancer	91H	IGF2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(+);cell migration(+);cell invasion(+)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	NA	GRCh38_11:1995176-1995988	ENSG00000167244	NA	NA	3481	NA	C11orf43|GRDF|IGF-II|PP9974	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications. We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development.	27780718	RID02135	epigenetic regulation
Breast cancer	SATB1	UCA1	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell growth(-);cell survival(-)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Breast cancer	TF	lncRNA	ENSG00000182568	NA	ENSG00000214049	GRCh38_19:15828206-15836328	6304	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer. SATB1 is highly expressed in aggressive breast cancer cells and promotes growth and metastasis by reprograming gene expression. long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was upregulated by SATB1 depletion. Upregulation of UCA1 coincided with increased H3K4 trimethylation (H3K4me3) levels and decreased H3K27 trimethylation (H3K27me3) levels. Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells.	27697109	RID02136	epigenetic regulation
Uveal melanoma	HIC1	lncRNA-numb	positively-E	RNAi	downregulation	qPCR	NA	NA	tumorigenesis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Uveal cancer	TF	lncRNA	ENSG00000177374	NA	ENSG00000284930	GRCh38_14:73460935-73463642	3090	NA	ZBTB29|ZNF901|hic-1	NA	HIC1 modulates uveal melanoma progression by activating lncRNA-numb. In this study, we found that HIC1 acted as a tumor suppressor and that its expression was downregulated in UM. Moreover, through long non-coding RNA (lncRNA) microarray and real-time PCR, we found that expression of lncRNA-numb was activated by HIC1 in UM. The results provide evidence that lncRNA-numb is a newly proposed tumor suppressor that is involved in HIC1-induced phenotypes. Taken together, our studies of UM reveal a critical role of HIC1 in the regulation of tumorigenesis, at least partly through its downstream target, lncRNA-numb, and provide a potential therapeutic target for UM.	27449031	RID02137	expression association
Nasopharynx carcinoma	NEAT1	ZEB1	positively-E	western blot;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);radioresistance(-)	ceRNA(miR-204-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000148516	NA	283131	6935	LINC00084|NCRNA00084|TncRNA|VINC	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma.We found that lncRNA NEAT1 was significantly upregulated in NPC cell lines and tissues. we found that there was reciprocal repression between NEAT1 and miR-204. ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.	27020592	RID02138	ceRNA or sponge
Lung cancer	SNHG7	FAIM2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233016	GRCh38_9:136721366-136728184	ENSG00000135472	NA	84973	23017	NCRNA00061	LFG|LFG2|NGP35|NMP35|TMBIM2	lncRNA-SNHG7 promotes the proliferation, migration and invasion and inhibits apoptosis of lung cancer cells by enhancing the FAIM2 expression. In the present study, we found that the expression levels of lncRNA-SNHG7 mRNA and protein obviously increased in lung cancer tissues compared to adjacent non-cancerous tissues.In addition, lncRNA-SNHG7 was of positive relevance with FAIM2 in human lung cancer tissues.	27666964	RID02139	expression association
Malignant glioma	H19	PPP1R13L	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000104881	NA	283120	10848	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	IASPP|NKIP1|RAI|RAI4	The lncRNA H19 interacts with miR-140 to modulate glioma growth by targeting iASPP. lncRNA-H19 was specifically upregulated in glioma cell lines and promoted glioma cell growth through targeting miR-140. Knockdown of H19 inhibited the proliferation and invasion of human glioma cell and suppressed its metastasis in vitro and in vivo. In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth. IASPP mRNA is a direct target of miR-140.	27693036	RID02140	ceRNA or sponge
Stroke	MEG3	TP53	positively-F	western blot;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	neuronal death(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Long noncoding RNA MEG3 activation of p53 mediates ischemic neuronal death in stroke.MEG3 directly binds with the p53 DNA binding domain (DBD) consisting of amino acids 271-282 (p53-DBD), which stimulates p53-mediated transactivation and mediates ischemic neuronal death.	27651151	RID02141	interact with protein
Pancreatic cancer	UCA1	CDKN1B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes the tumorigenesis in pancreatic cancer. In this study, we detected the mRNA expression of UCA1 in 128 PC patients by qRT-PCR, and found that UCA1 expression was significantly, up-regulated in tumor tissues than that in matched adjacent non-tumor tissues (p<0.05). Meanwhile, UCA1 expression negative-correlated with p27 in PC tissues (r2=0.46, p<0.01), and knockdown of p27 partly abrogated the cell proliferative activities caused by UCA1 (p<0.05).	27562722	RID02142	expression association
Pancreatic cancer	CCDC26	PCNA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000132646	NA	137196	5111	RAM	ATLD2	Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. We found that the CCDC26 expression was significantly higher in PC tissues than in normal tissues. Moreover, we found that the expression of CCDC26 was positively correlated with PCNA and Bcl2. Our data suggest that CCDC26 may be identified as a novel oncogene in PC, and responsible for growth and apoptosis of cancer cell, partly by regulating the PCNA and Bcl2 expression. This work provides a novel biomarker and therapeutic target of PC for cancer clinic in future.	27470572	RID02143	expression association
Pancreatic cancer	CCDC26	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000171791	NA	137196	596	RAM	Bcl-2|PPP1R50	Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. We found that the CCDC26 expression was significantly higher in PC tissues than in normal tissues. Moreover, we found that the expression of CCDC26 was positively correlated with PCNA and Bcl2. Our data suggest that CCDC26 may be identified as a novel oncogene in PC, and responsible for growth and apoptosis of cancer cell, partly by regulating the PCNA and Bcl2 expression. This work provides a novel biomarker and therapeutic target of PC for cancer clinic in future.	27470572	RID02144	expression association
Thyroid cancer	MALAT1	IQGAP1	positively-E	western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000140575	NA	378938	8826	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HUMORFA01|SAR1|p195	MALAT1 promotes the proliferation and invasion of thyroid cancer cells via regulating the expression of IQGAP1. we discovered the higher level of MALAT-1 and expression of IQGAP1 in thyroid cancer tissues and in thyroid cancer cells compared to that in the control. MALAT-1 could upregulate the expression of IQGAP1 in thyroid cancer cells. In addition, IQGAP1 knockdown reversed the decreasing cell proliferation and invasion of thyroid cancer induced by MALAT-1 overexpression.	27470543	RID02145	expression association
Gallbladder cancer	MALAT1	ANXA2	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000182718	NA	378938	302	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ANX2|ANX2L4|CAL1H|HEL-S-270|LIP2|LPC2|LPC2D|P36|PAP-IV	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206. In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect.	27191262	RID02146	ceRNA or sponge
Gallbladder cancer	MALAT1	KRAS	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-206)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000133703	NA	378938	3845	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	C-K-RAS|CFC2|K-RAS2A|K-RAS2B|K-RAS4A|K-RAS4B|K-Ras|KI-RAS|KRAS1|KRAS2|NS|NS3|RALD|RASK2|c-Ki-ras2	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206. In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect.	27191262	RID02147	ceRNA or sponge
Non-small cell lung cancer	WSPAR	EPCAM	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	self-renewal(+)	ceRNA(miR-200c)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000119888	NA	105664404	4072	LncTCF7|TCONS_00009511	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	Long noncoding RNA TCF7 promotes invasiveness and self-renewal of human non-small cell lung cancer cells. We showed that lncTCF7 increased slug expression to promote the invasive capability of NSCLC cells and upregulated EpCAM expression to promote the self-renewal.	27766570	RID02148	ceRNA or sponge
Non-small cell lung cancer	WSPAR	SNAI2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000249073	GRCh38_5:133913677-133917269	ENSG00000019549	NA	105664404	6591	LncTCF7|TCONS_00009511	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Long noncoding RNA TCF7 promotes invasiveness and self-renewal of human non-small cell lung cancer cells. We showed that lncTCF7 increased slug expression to promote the invasive capability of NSCLC cells and upregulated EpCAM expression to promote the self-renewal.	27766570	RID02149	transcriptional regulation
Malignant glioma	miR-23b-3p	TUSC7	negatively-F	RIP;RNA pull-down assay;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	miRNA	lncRNA	NA	NA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Long Non-coding RNA TUSC7, a Target of miR-23b, Plays Tumor-Suppressing Roles in Human Gliomas. TUSC7 was poorly expressed in tissues and cell lines of glioma, and the lower expression was correlated with glioma of the worse histological grade. Bioinformatics analysis showed that TUSC7 specifically binds to miR-23b. MiR-23b was up-regulated in glioma and negatively correlated with the expression of TUSC7. The miR-23b expression was inhibited remarkably by the upregulation of TUSC7 and the reciprocal inhibition was determined between TUSC7 and miR-23b.We conclude that the lncRNA TUSC7 acted as a tumor suppressor gene negatively regulated by miR-23b, suggesting a novel therapeutic strategy against gliomas.	27766072	RID02150	ceRNA or sponge
Urinary bladder cancer	UCA1	miR-196a-5p	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin;gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells. Urothelial Cancer Associated 1 (UCA1), an lncRNA, is reportedly upregulated in human bladder carcinoma and promotes cancer cell proliferation, migration, invasion, and drug resistance. UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	27591936	RID02151	expression association
Urinary bladder cancer	UCA1	CDKN1B	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	cisplatin;gemcitabine	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000111276	NA	652995	1027	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells. Urothelial Cancer Associated 1 (UCA1), an lncRNA, is reportedly upregulated in human bladder carcinoma and promotes cancer cell proliferation, migration, invasion, and drug resistance. UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	27591936	RID02152	expression association
Colon cancer	CYTOR	ERBB4	positively-E	luciferase reporter assay;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);AKT signaling pathway(-)	ceRNA(miR-193a-3p)	regulation	NA	oxaliplatin	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000178568	NA	112597	2066	C2orf59|LINC00152|NCRNA00152	ALS19|HER4|p180erbB4	Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer.This study showed that a novel lncRNA, long intergenic noncoding RNA 152 (Linc00152 ), promoted tumor progression and conferred resistance to oxaliplatin (L-OHP)-induced apoptosis in vitro and in vivo. It antagonized chemosensitivity through acting as a competing endogenous RNA to modulate the expression of miR-193a-3p, and then erb-b2 receptor tyrosine kinase 4 (ERBB4). Consistent with above findings, the specific AKT signaling inhibitor and activator were used, respectively, which demonstrated that Linc00152 contributed to L-OHP resistance at least partly through activating AKT pathway. Collectively, our findings established Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance.Previous reports suggest that miR-193a-3p suppresses tumor proliferation, invasion, and metastasis by directly targeting and downregulating the expression of ERBB4.	27633443	RID02153	ceRNA or sponge
Malignant glioma	HOTTIP	BABAM2	negatively-F	RIP	downregulation	qPCR	NA	NA	cell growth(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000158019	NA	100316868	9577	HOXA-AS6|HOXA13-AS1|NCRNA00213	NA	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo.Furthermore, HOTTIP could directly bind to the brain and reproductive expression (BRE) gene and down-regulate BRE gene expression. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02154	interact with mRNA
Malignant glioma	HOTTIP	CDK2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000123374	NA	100316868	1017	HOXA-AS6|HOXA13-AS1|NCRNA00213	CDKN2|p33(CDK2)	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02155	expression association
Malignant glioma	HOTTIP	CCNA2	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000145386	NA	100316868	890	HOXA-AS6|HOXA13-AS1|NCRNA00213	CCN1|CCNA	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02156	expression association
Malignant glioma	HOTTIP	TP53	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(-)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	TF	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000141510	NA	100316868	7157	HOXA-AS6|HOXA13-AS1|NCRNA00213	BCC7|BMFS5|LFS1|P53|TRP53	Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE. HOTTIP was aberrantly down-regulated in glioma tissues and glioma cell lines (U87-MG, U118-MG, U251 and A172), and over-expression of HOTTIP inhibited the growth of glioma cell lines in vitro and in vivo. over-expression of HOTTIP significantly suppressed the expression of the cyclin A and CDK2 proteins and increased the expression of the P53 protein. these findings suggested that high levels of HOTTIP reduced glioma cell growth. Our studies demonstrated that over-expression of HOTTIP promotes cell apoptosis and inhibits cell growth in U118-MG and U87-MG human glioma cell lines by down-regulating BRE expression to regulate the expression of P53, CDK2 and Cyclin A proteins.	27733185	RID02157	expression association
Esophagus squamous cell carcinoma	BC032469	TERT	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249201	GRCh38_5:1173141-1178605	ENSG00000164362	NA	NA	7015	NA	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	Upregulated long non-coding RNA BC032469 enhances carcinogenesis and metastasis of esophageal squamous cell carcinoma through regulating hTERT expression. Western blot analysis revealed that BC032469 regulated the expression of human telomerase reverse transcriptase (hTERT), which is important for cell proliferation and metastasis.	27726103;30223861	RID02158	expression association
Gallbladder cancer	H19	FOXM1	positively-E	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	ceRNA(miR-342-3p)	regulation	NA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000111206	NA	283120	2305	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer. We demonstrated H19 was overexpressed and negatively correlated with miR-342-3p in GBC. Furthermore, transwell invasion assays and cell cycle assays indicated that H19 knockdown inhibited both cells invasion and proliferation, but this effects was attenuated by co-transfection of siRNA-H19 and miR-342-3p inhibitor in GBC cells. Our results suggest a potential ceRNA regulatory network involving H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in GBC. This mechanism may contribute to a better understanding of GBC pathogenesis and provides potential therapeutic strategy for GBC.	27716361	RID02159	ceRNA or sponge
Lung cancer	PCBP2-OT1	CCNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000134057	NA	102157401	891	NA	CCNB	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis. These results suggested the pro-oncogenic potential of uc.338 in lung cancer, which might provide novel clues for the diagnosis and treatment of lung cancer in the clinic.	27712590	RID02160	expression association
Lung cancer	PCBP2-OT1	CDC25C	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000158402	NA	102157401	995	NA	CDC25|PPP1R60	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02161	expression association
Lung cancer	PCBP2-OT1	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124216	NA	102157401	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02162	expression association
Lung cancer	PCBP2-OT1	CDH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000170558	NA	102157401	1000	NA	CD325|CDHN|CDw325|NCAD	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02163	expression association
Lung cancer	PCBP2-OT1	VIM	positively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000026025	NA	102157401	7431	NA	NA	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02164	expression association
Lung cancer	PCBP2-OT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell cycle(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000039068	NA	102157401	999	NA	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis.	27712590	RID02165	expression association
Keloid	H19	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Keloid	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000198793	NA	283120	2475	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long non-coding RNA H19 promotes the proliferation of fibroblasts in keloid scarring. The results confirmed that knockdown of H19 inhibited mTOR and VEGF expression.In summary, the results indicate that H19 may be associated with increased proliferative activity of keloid fibroblasts, which may be mediated by mTOR and VEGF.	27698867	RID02166	expression association
Keloid	H19	VEGFA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Other	Keloid	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000112715	NA	283120	7422	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MVCD1|VEGF|VPF	Long non-coding RNA H19 promotes the proliferation of fibroblasts in keloid scarring. The results confirmed that knockdown of H19 inhibited mTOR and VEGF expression.In summary, the results indicate that H19 may be associated with increased proliferative activity of keloid fibroblasts, which may be mediated by mTOR and VEGF.	27698867	RID02167	expression association
Gastric cancer	UCA1	miR-27b-3p	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	adriamycin;cisplatin;5-fluorouracil	NA	NA	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	Long Non-Coding RNA (LncRNA) Urothelial Carcinoma Associated 1 (UCA1) Increases Multi-Drug Resistance of Gastric Cancer via Downregulating miR-27b. UCA1 was significantly upregulated in the cancerous tissues and its expression was negatively correlated with miR-27b expression level. UCA1 knockdown and miR-27b overexpression reduced IC50 of ADR, DDP, and 5-FU in SGC-7901/ADR cells and increased ADR induced cell apoptosis.UCA1 is negatively correlated with miR-27b expression in gastric cancer tissue. Knockdown of UCA1 restored miR-27b expression in gastric cancer cells. The UCA1-miR-27b axis was involved in regulation of chemosensitivity of gastric cancer cells.	27694794	RID02168	expression association
Endometrial adenocarcinoma	NEAT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000136997	NA	283131	4609	LINC00084|NCRNA00084|TncRNA|VINC	MRTL|MYCC|bHLHe39|c-Myc	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma. The expression levels of NEAT1 were elevated in EEC tissues and cell lines, and higher expression levels of NEAT1 were positively correlated with FIGO stage and lymph node metastasis. Tumor metastasis real-time PRC array showed that six metastasis-related genes (c-myc, insulin like growth factor 1(IGF1), matrix metallopeptidase 2 (MMP-2) and matrix metallopeptidase 7(MMP-7) were up-regulated, and Cadherin 1 and TIMP metallopeptidase inhibitor 2 were down-regulated) in NEAT1-overexpressing HEC-59 cells. Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02169	expression association
Endometrial adenocarcinoma	NEAT1	EIF4G1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000114867	NA	283131	1981	LINC00084|NCRNA00084|TncRNA|VINC	EIF-4G1|EIF4F|EIF4G|EIF4GI|P220|PARK18	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02170	expression association
Endometrial adenocarcinoma	NEAT1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000087245	NA	283131	4313	LINC00084|NCRNA00084|TncRNA|VINC	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02171	expression association
Endometrial adenocarcinoma	NEAT1	MMP7	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000137673	NA	283131	4316	LINC00084|NCRNA00084|TncRNA|VINC	MMP-7|MPSL1|PUMP-1	Overexpression of long noncoding RNA, NEAT1 promotes cell proliferation, invasion and migration in endometrial endometrioid adenocarcinoma.Further qRT-PCR and western blot results confirmed that c-myc, IFG1, MMP-2 and MMP-7 were dys-regulated by NEAT1.	27664948	RID02172	expression association
Lung cancer	CPS1-IT1	CASP3	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000164305	NA	29034	836	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	CPP32|CPP32B|SCA-1	Long Noncoding RNA CPS1-IT1 Suppresses Cell Proliferation and Metastasis in Human Lung Cancer. It was found that lncRNA CPS1-IT1 was significantly lower in cancerous tissues than in noncancerous tissues. While cell apoptosis was induced, CPS1-IT1 overexpression promoted the activities of caspase 3 and caspase 9 without affecting that of caspase 8. These observations were suggestive of the tumor-suppressive role of lncRNA CPS1-IT1 in lung cancer.	27662619	RID02173	expression association
Lung cancer	CPS1-IT1	CASP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000132906	NA	29034	842	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long Noncoding RNA CPS1-IT1 Suppresses Cell Proliferation and Metastasis in Human Lung Cancer.While cell apoptosis was induced, CPS1-IT1 overexpression promoted the activities of caspase 3 and caspase 9 without affecting that of caspase 8. These observations were suggestive of the tumor-suppressive effect role of lncRNA CPS1-IT1 in lung cancer.	27662619	RID02174	expression association
Osteosarcoma	TUG1	POU2F1	negatively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	TF	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000143190	NA	55000	5451	LINC00080|NCRNA00080|TI-227H	OCT1|OTF1|oct-1B	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells, which involved the derepression of POU class 2 homeobox 1 (POU2F1) expression. In conclusion, our study elucidated a novel TUG1/miR-9-5p/POU2F1 pathway, in which TUG1 acted as a ceRNA by sponging miR-9-5p, leading to downregulation of POU2F1 and facilitating the tumorigenesis of osteosarcoma.	27658774	RID02175	expression association
Osteosarcoma	TUG1	miR-9-5p	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	miRNA	ENSG00000253352	GRCh38_22:30969245-30979395	NA	NA	55000	NA	LINC00080|NCRNA00080|TI-227H	NA	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells, which involved the derepression of POU class 2 homeobox 1 (POU2F1) expression. In conclusion, our study elucidated a novel TUG1/miR-9-5p/POU2F1 pathway, in which TUG1 acted as a ceRNA by sponging miR-9-5p, leading to downregulation of POU2F1 and facilitating the tumorigenesis of osteosarcoma.	27658774	RID02176	ceRNA or sponge
Renal cell carcinoma	MALAT1	BIRC7	positively-F	luciferase reporter assay;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000101197	NA	378938	79444	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	KIAP|LIVIN|ML-IAP|MLIAP|RNF50	Biological function and mechanism of MALAT-1 in renal cell carcinoma proliferation and apoptosis: role of the MALAT-1-Livin protein interaction.LncRNA MALAT-1 and the Livin protein were highly expressed in RCC tissues, as well as in RCC 786-O and Caki-1 cell lines. The RIP results showed that MALAT-1 promoted the expression of the Livin protein in 786-O and Caki-1 cells by enhancing the stability of the protein.	27655020	RID02177	interact with protein
Gastric cancer	CASC2	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000102882	NA	255082	5595	C10orf5	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway. Our results showed that CASC2 was significantly downregulated in human GC tissues and cell lines by quantitative RT-PCR. Overexpression of CASC2 in GC cells significantly inhibited the cell growth in vitro and in vivo. We further found that MAPK pathway especially the ERK1/2 and JNK component were involved in the CASC2 mediated GC cell proliferation. Moreover, combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro.	27648142	RID02178	expression association
Gastric cancer	CASC2	MAPK1	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000100030	NA	255082	5594	C10orf5	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway.combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro. Thus, these results indicated that CASC2 might serve as a tumor suppressor lncRNA that suppressed cell proliferation by inactivation of MAPK pathway.	27648142	RID02179	expression association
Gastric cancer	CASC2	MAPK8	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);MAPK signaling pathway(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000107643	NA	255082	5599	C10orf5	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA CASC2 suppresses the proliferation of gastric cancer cells by regulating the MAPK signaling pathway.combination treatment of CASC2 overexpression and suppression ERK1/2 or JNK produced synergistic inhibitory effects in vitro. Thus, these results indicated that CASC2 might serve as a tumor suppressor lncRNA that suppressed cell proliferation by inactivation of MAPK pathway.	27648142	RID02180	expression association
Pancreatic cancer	IRAIN	KLF2	negatively-E	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000127528	NA	104472848	10365	IGF1R-AS	LKLF	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02181	epigenetic regulation
Pancreatic cancer	IRAIN	CDKN2B	negatively-E	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	histone modification	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000147883	NA	104472848	1030	IGF1R-AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02182	epigenetic regulation
Urinary bladder cancer	LINC00312	miR-197-3p	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	miRNA	NA	GRCh38_3:8571782-8574668	NA	NA	29931	NA	ERR-10|ERR10|LMCD1DN|LOH3CR2A|NAG-7|NAG7|NCRNA00312	NA	LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p. LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion.	27631965	RID02183	ceRNA or sponge
Breast cancer	NEAT1	EZH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-101-3p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|NCRNA00084|TncRNA|VINC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2. lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation. Taken together, our data indicated that NEAT1 might be an oncogenic lncRNA that promoted proliferation of BC and could be regarded as a therapeutic target in human BC.	28034643	RID02184	ceRNA or sponge
Chronic myeloid leukemia	HOTAIR	ABCC1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+)	NA	association	NA	imatinib	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000103222	NA	100124700	4363	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC29|ABCC|GS-X|MRP|MRP1	The role of long noncoding RNA HOTAIR in the acquired multidrug resistance to imatinib in chronic myeloid leukemia cells.Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control. Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment. In addition, the activation of PI3K/Akt was greatly attenuated when HOTAIR was knocked down in K562-imatinib cells.These data suggest that the knockdown of HOTAIR may play a crucial role in improving acquired resistance to imatinib in CML K562-R cells via PI3K/Akt pathway.	27875938	RID02185	expression association
Esophagus squamous cell carcinoma	SPRY4-IT1	ZNF703	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000183779	NA	100642175	80139	SPRIGHTLY	NLZ1|ZEPPO1|ZNF503L|ZPO1	Upregulated long noncoding RNA SPRY4-IT1 contributes to increased cell viability by activating zinc finger 703 expression in esophageal squamous cell carcinoma.We validated that SPRY4-IT1 was upregulated in ESCC tissues of advanced clinical stages.In vitro function assays demonstrated that SPRY4-IT1 cause promotion of cell viability in ESCC cells. We further verified that SPRY4-IT1 could also activate the expression of ZNF703 in ESCC cells, which might contribute to the role of SPRY4-IT1 in ESCC cells.	27453415	RID02186	expression association
Gastric cancer	MALAT1	EGFL7	positively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000172889	NA	378938	51162	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NEU1|VE-STATIN|ZNEU1	Overexpressed MALAT1 promotes invasion and metastasis of gastric cancer cells via increasing EGFL7 expression. The expression of MALAT1 was up-regulated in GC tissues and three cell lines. ChIP assay showed that MALAT1 regulated EGFL7 expression by altering the level of H3 histone acetylation in EGFL7 promoter.Up-regulated MALAT1 promoted the invasion and metastasis of GC, and the increase of EGFL7 expression was a potential mechanism via altering its H3 histone acetylation level.	27259812	RID02187	epigenetic regulation
Hepatocellular carcinoma	LINC01225	EGFR	positively-F	RIP	upregulation	qPCR;microarray	NA	NA	cell proliferation(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000260386	GRCh38_1:31500085-31508566	ENSG00000146648	NA	149086	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	LINC01225 promotes occurrence and metastasis of hepatocellular carcinoma in an epidermal growth factor receptor-dependent pathway. Here, we verified that LINC01225 was upregulated in HCC. LINC01225 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR, and subsequently fine tune the EGFR/Ras/Raf-1/MEK/MAPK signaling pathway. Knockdown of LINC01225 resulted in inhibited cell proliferation and invasion with activated apoptosis and cell cycle arrest in vitro.	26938303	RID02188	interact with protein
Esophagus squamous cell carcinoma	NPTN-IT1	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	cell invasion(-);cell metastasis(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000281183	GRCh38_15:73567012-73569294	ENSG00000141510	NA	101241892	7157	lncRNA-LET	BCC7|BMFS5|LFS1|P53|TRP53	Long non-coding RNA-Low Expression in Tumor inhibits the invasion and metastasis of esophageal squamous cell carcinoma by regulating p53 expression. lncRNA-LET expression was decreased in primary ESCC tissues when compared with paired healthy tissues, and was identified to be associated with the clinical features. Overexpression of lncRNA-LET was observed to inhibit the migration and invasion of ESCC cells, and modulate p53 expression levels in human ESCC cell lines in vitro.	26935396	RID02189	expression association
Hypertrophic cardiomyopathy	CHAST	PLEKHM1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell autophagy(-);cardiac hypertrophy(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cardiovascular system disease	Cardiomyopathy	lncRNA	PCG	NA	GRCh38_11:103363213-103364651	ENSG00000225190	NA	NA	9842	NA	AP162|B2|OPTA3|OPTB6	Long noncoding RNA Chast promotes cardiac remodeling. Chast negatively regulated Pleckstrin homology domain-containing protein family M member 1 (opposite strand of Chast), impeding cardiomyocyte autophagy and driving hypertrophy. In accordance, CHAST homolog in humans was significantly up-regulated in hypertrophic heart tissue from aortic stenosis patients and in human embryonic stem cell-derived cardiomyocytes upon hypertrophic stimuli.	26888430	RID02190	expression association
Ovarian cancer	NRCP	STAT1	positively-F	RIP	upregulation	microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENST00000481169	GRCh38_3:149162410-149221827	ENSG00000115415	NA	NA	6772	NA	CANDF7|IMD31A|IMD31B|IMD31C|ISGF-3|STAT91	Long Noncoding RNA Ceruloplasmin Promotes Cancer Growth by Altering Glycolysis. NRCP was highly upregulated in ovarian tumors, and knockdown of NRCP resulted in significantly increased apoptosis, decreased cell proliferation, and decreased glycolysis compared with control cancer cells. We identified NRCP as an intermediate binding partner between STAT1 and RNA polymerase II, leading to increased expression of downstream target genes such as glucose-6-phosphate isomerase.	26686630	RID02191	interact with protein
Ovarian cancer	NRCP	GPI	positively-E	RNAi	upregulation	microarray	NA	NA	cell growth(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENST00000481169	GRCh38_3:149162410-149221827	ENSG00000105220	NA	NA	2821	NA	AMF|GNPI|NLK|PGI|PHI|SA-36|SA36	Long Noncoding RNA Ceruloplasmin Promotes Cancer Growth by Altering Glycolysis. NRCP was highly upregulated in ovarian tumors, and knockdown of NRCP resulted in significantly increased apoptosis, decreased cell proliferation, and decreased glycolysis compared with control cancer cells. We identified NRCP as an intermediate binding partner between STAT1 and RNA polymerase II, leading to increased expression of downstream target genes such as glucose-6-phosphate isomerase.	26686630	RID02192	expression association
Cancer	LINC-ROR	HNRNPD	interact	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000138668	NA	100885779	3184	ROR|lincRNA-RoR|lincRNA-ST8SIA3	AUF1|AUF1A|HNRPD|P37|hnRNPD0	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02193	interact with protein
Cancer	LINC-ROR	PTBP1	interact	RIP	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000011304	NA	100885779	5725	ROR|lincRNA-RoR|lincRNA-ST8SIA3	HNRNP-I|HNRNPI|HNRPI|PTB|PTB-1|PTB-T|PTB2|PTB3|PTB4|pPTB	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02194	interact with protein
Cancer	LINC-ROR	MYC	negatively-E	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);tumorigenesis(+)	RNA stability	regulation	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	TF	ENSG00000258609	GRCh38_18:57054558-57072119	ENSG00000136997	NA	100885779	4609	ROR|lincRNA-RoR|lincRNA-ST8SIA3	MRTL|MYCC|bHLHe39|c-Myc	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. Mechanistically, Linc-RoR interacts with heterogeneous nuclear ribonucleoprotein (hnRNP) I and AU-rich element RNA-binding protein 1 (AUF1), respectively, with an opposite consequence to their interaction with c-Myc mRNA. Together, these results support a role for Linc-RoR in c-Myc expression in part by specifically enhancing its mRNA stability, leading to cell proliferation and tumorigenesis.	26656491	RID02195	interact with mRNA
Loeys-Dietz syndrome	TGFB1	AK056155	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Genetic disease	Autosomal dominant disease	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_1:181059435-181061937	7040	NA	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	Long noncoding RNA AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway.Then we further verified that AK056155 was also overexpressed in aortic aneurysm patients by RT-PCR. Moreover, we demonstrated that the expression of AK056155 can be enhanced by TGF-beta1 in a concentration or time depended manner in HUVECs by RT-PCR. Furthermore, the expression of AK056155 was reduced with treatment of PI3K inhibitor (LY294002) or AKT inhibitor (GDC-0068) in combination with TGF-beta1. These results indicate that AK056155 involved in the development of Loeys-Dietz syndrome through AKT/PI3K signaling pathway, it may provide a promising target gene to prevent LDS develop in to aortic aneurysm.	26617788	RID02196	expression association
Lung cancer	miR-217	MALAT1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	miRNA	lncRNA	NA	NA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Posttranscriptional silencing of the lncRNA MALAT1 by miR-217 inhibits the epithelial-mesenchymal transition via enhancer of zeste homolog 2 in the malignant transformation of HBE cells induced by cigarette smoke extract.the CSE-induced increase of MALAT1 expression was blocked by an miR-217 mimic, indicating that miR-217 negatively regulates MALAT1 expression.	26415832	RID02197	expression association
Breast cancer	NBAT1	DKK1	negatively-E	ChIP;RIP	downregulation	qPCR	NA	NA	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000107984	NA	729177	22943	CASC14|NBAT-1	DKK-1|SK	NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2. ectopic NBAT1 inhibits migration and invasion of breast cancer cells. Mechanistic study shows that NBAT1 is associated with PRC2 member EZH2 and regulates global gene expression profile. Among them, DKK1 (dickkopf WNT signaling pathway inhibitor 1) is found to be regulated by NBAT1 in a PRC2 dependent manner, and is responsible for NBAT1's effects in inhibiting migration and invasion of breast cancer cells.	26378045	RID02198	epigenetic regulation
Lung adenocarcinoma	LUADT1	CDKN1B	negatively-E	ChIP	upregulation	qPCR;microarray	GSE66654	GSE66654.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000111276	NA	106182249	1027	NA	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27.Further analysis indicated that LUADT1 may regulate cell cycle progression by epigenetically inhibiting the expression of p27.RNA immunoprecipitation and chromatin immunoprecipitation assays confirmed that LUADT1 binds to SUZ12, a core component of polycomb repressive complex 2, and mediates the trimethylation of H3K27 at the promoter region of p27.	26291312	RID02199	epigenetic regulation
Malignant glioma	NEAT1	MET	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+);cell migration(+)	ceRNA(miR-449b-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000105976	NA	283131	4233	LINC00084|NCRNA00084|TncRNA|VINC	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis. By real-time PCR, we suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met. This regulation menchaism promotes glioma pathogenesis and may provide a potential target for the prognosis and treatment of glioma.	26242266	RID02200	ceRNA or sponge
Lung cancer	GPLD1	CDKN2B-AS1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	PCG	lncRNA	ENSG00000112293	NA	ENSG00000240498	GRCh38_9:21994139-22128103	2822	100048912	GPIPLD|GPIPLDM|PIGPLD|PIGPLD1|PLD	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Down-regulation of Phospholipase D Stimulates Death of Lung Cancer Cells Involving Up-regulation of the Long ncRNA ANRIL. the expression level of antisense noncoding RNA in the INK4 locus (ANRIL) was increased up to 13.6-fold by PLD inhibition in H460 human lung cancer cells. Moreover, knockdown of ANRIL using its specific small-interfering RNA significantly suppressed PLD inhibition-induced apoptosis.	25964559	RID02201	expression association
Esophagus squamous cell carcinoma	LINC01426	RUNX1	interact	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis	alternative splicing	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000234380	GRCh38_21:34745757-34784886	ENSG00000159216	NA	100506385	861	lincRNA-uc002yug.2	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	LincRNA-uc002yug.2 involves in alternative splicing of RUNX1 and serves as a predictor for esophageal cancer and prognosis. lincRNA-uc002yug.2 promoted a combination of RUNX1 and alternative splicing (AS) factors in the nucleus to produce more RUNX1a, the short isoform and inhibitor of RUNX1, and reduce CEBPalpha (CCAAT/enhancer-binding protein-alpha) gene expression, thereby promoting ESCC progression.These results indicated that lincRNA-uc002yug.2 might involve in AS of RUNX1/AML1 and serve as a predictor for esophageal cancer and prognosis.	25486427	RID02202	interact with mRNA
Liver cancer	RUNX1	MT1DP	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000159216	NA	ENSG00000205361	GRCh38_16:56643705-56644786	861	326343	AML1|AML1-EVI-1|AMLCR1|CBF2alpha|CBFA2|EVI-1|PEBP2aB|PEBP2alpha	MTM	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02203	transcriptional regulation
Liver cancer	YAP1	MT1DP	negatively-E	luciferase reporter assay;RIP	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000205361	GRCh38_16:56643705-56644786	10413	326343	COB1|YAP|YAP2|YAP65|YKI	MTM	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02204	transcriptional regulation
Liver cancer	MT1DP	FOXA1	negatively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	tumorigenesis(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	NA	Cancer	Liver cancer	lncRNA	TF	ENSG00000205361	GRCh38_16:56643705-56644786	ENSG00000129514	NA	326343	3169	MTM	HNF3A|TCF3A	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP.	25261601	RID02205	expression association
Osteoarthritis	GAS5	miR-21-5p	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	apoptosis process(+);autophagic response(-)	NA	regulation	NA	NA	NA	Evading Apoptosis;Self Sufficiency in Growth Signals	Musculoskeletal system disease	Bone disease	lncRNA	miRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	NA	NCRNA00030|SNHG2	NA	A long non-coding RNA, GAS5, plays a critical role in the regulation of miR-21 during osteoarthritis. The expression level of miR-21 was significantly reduced in OA patients, and the ectopic expression of GAS5 is capable of suppressing miR-21 induction. Consistent with GAS5 experiments, the introduction of miR-21 stimulated the apoptosis of chondrocytes and inhibited the expression levels of autophagic complexes, including LC-3B. Together, these results show that GAS5 contributes to the pathogenesis of OA by acting as a negative regulator of miR-21 and thereby regulating cell survival.	25196583	RID02206	expression association
B-cell lymphoma	FAS-AS1	FAS	negatively-F	RIP;ChIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+);autophagic response(-)	alternative splicing	binding/interaction	RNA-RNA	NA	NA	Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	NA	GRCh38_10:88991422-88992975	ENSG00000026103	NA	100302740	355	FAS-AS|FASAS|SAF	ALPS1A|APO-1|APT1|CD95|FAS1|FASTM|TNFRSF6	FAS-antisense 1 lncRNA and production of soluble versus membrane Fas in B-cell lymphoma. We found that the alternative splicing of Fas in lymphomas is tightly regulated by a long-noncoding RNA corresponding to an antisense transcript of Fas (FAS-AS1).EZH2-mediated repression of FAS-AS1 promoter can be released by DZNeP (3-Deazaneplanocin A) or overcome by ectopic expression of FAS-AS1, both of which increase levels of FAS-AS1 and correspondingly decrease expression of sFas. Treatment with Bruton's tyrosine kinase inhibitor or EZH2 knockdown decreases the levels of EZH2, RBM5 and sFas, thereby enhancing Fas-mediated apoptosis. This is the first report showing functional regulation of Fas repression by its antisense RNA.Treatment with Bruton's tyrosine kinase inhibitor or EZH2 knockdown decreases the levels of EZH2, RBM5 and sFas, thereby enhancing Fas-mediated apoptosis. This is the first report showing functional regulation of Fas repression by its antisense RNA.FAS-AS1 binds RBM5 and interferes with RBM5-mediated exon 6 skipping of Fas pre-mRNA.	24811343	RID02207	interact with mRNA
Gastric cancer	MYC	H19	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000130600	GRCh38_11:1995176-2001470	4609	283120	MRTL|MYCC|bHLHe39|c-Myc	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	c-Myc-induced, long, noncoding H19 affects cell proliferation and predicts a poor prognosis in patients with gastric cancer.The results show that lncRNA H19 is overexpressed in tumor tissues compared with adjacent normal tissues. exogenous c-Myc significantly induces H19 expression, and the expression of H19 was positively correlated with the c-Myc levels in the 80 samples used in our study. In conclusion, our study demonstrates that the altered expression of lncRNA H19, which is induced by c-Myc, is involved in the development and progression of GC by regulating cell proliferation and shows that H19 may be a potential diagnostic and prognostic target in patients with GC.	24671855	RID02208	expression association
Esophagus squamous cell carcinoma	PANTR1	POU3F3	negatively-E	RIP;ChIP	upregulation	qRT-PCR	NA	NA	cancer progression(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000198914	NA	100506421	5455	LINC01158|linc-Brn1a|linc-POU3F3	BRN1|OTF8|brain-1|oct-8	Increased levels of the long intergenic non-protein coding RNA POU3F3 promote DNA methylation in esophageal squamous cell carcinoma cells. Levels of a lincRNA encoded by a gene located next to POU3F3 (linc-POU3F3) were significantly higher in ESCC than neighboring nontumor tissues. In RNA immunoprecipitation assays, linc-POU3F3 was associated with the EZH2 messenger RNA (mRNA). Overexpression of linc-POU3F3 in cell lines increased their proliferation and ability to form colonies, and reduced the expression of POU3F3 mRNA, whereas knockdown of linc-POU3F3 increased the levels of POU3F3 mRNA. CpG islands in POU3F3 were densely hypermethylated in cell lines that overexpressed linc-POU3F3; methylation at these sites was reduced by knockdown of linc-POU3F3. Pharmacologic inhibition of EZH2 increased the levels of POU3F3 mRNA and significantly reduced binding of DNA methyltransferase (DNMT)1, DNMT3A, and DNMT3B to POU3F3. Levels of linc-POU3F3 are increased in ESCC samples from patients compared with nontumor tissues. This noncoding RNA contributes to the development of ESCC by interacting with EZH2 to promote methylation of POU3F3, which encodes a transcription factor.	24631494	RID02209	epigenetic regulation
Small cell lung cancer	HOTAIR	ASTN1	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000152092	NA	100124700	460	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ASTN	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02210	expression association
Small cell lung cancer	HOTAIR	PCDHA1	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204970	NA	100124700	56147	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-ALPHA1	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02211	expression association
Small cell lung cancer	HOTAIR	MUC5AC	negatively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000215182	NA	100124700	4586	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MUC5|TBM|leB|mucin	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02212	expression association
Small cell lung cancer	HOTAIR	NTM	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000182667	NA	100124700	50863	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CEPU-1|HNT|IGLON2|NTRI	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02213	expression association
Small cell lung cancer	HOTAIR	PTK2B	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000120899	NA	100124700	2185	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CADTK|CAKB|FADK2|FAK2|PKB|PTK|PYK2|RAFTK	Long noncoding RNA HOTAIR is relevant to cellular proliferation, invasiveness, and clinical relapse in small-cell lung cancer. The knockdown of HOTAIR in SBC-3 cells led to decreased proliferation activity and decreased invasiveness in vitro. Gene expression analysis indicated that depletion of HOTAIR resulted in upregulation of cell adhesion-related genes such as ASTN1, PCDHA1, and mucin production-related genes such as MUC5AC, and downregulation of genes involved in neuronal growth and signal transduction including NTM and PTK2B.	24591352	RID02214	expression association
Prostate cancer	AR	PCAT18	positively-E	RNAi	upregulation	qPCR;sequencing	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000265369	GRCh38_18:26687621-26703638	367	728606	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LINC01092	Identification of a long non-coding RNA as a novel biomarker and potential therapeutic target for metastatic prostate cancer. AR activation dramatically up-regulated PCAT18 expression in vitro and in vivo. PCAT18 silencing significantly (p<0.001) inhibited PCa cell proliferation and triggered caspase 3/7 activation, with no effect on non-neoplastic cells. PCAT18 silencing also inhibited PCa cell migration (p<0.01) and invasion (p<0.01).	24519926	RID02215	expression association
Ischemic stroke	CDKN2B-AS1	CARD8	positively-E	RNAi	NA	NA	NA	NA	predisposition(+)	NA	association	NA	NA	NA	NA	Cardiovascular system disease	Cerebrovascular disease	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105483	NA	100048912	22900	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CARDINAL|DACAR|DAKAR|NDPP|NDPP1|TUCAN	Regulation of CARD8 expression by ANRIL and association of CARD8 single nucleotide polymorphism rs2043211 (p.C10X) with ischemic stroke. Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.	24385277	RID02216	expression association
Urinary bladder cancer	H19	EZH2	interact	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression. Here we found that H19 levels are remarkably increased in bladder cancer tissues, and upregulated H19 promotes bladder cancer cell migration in vitro and in vivo. H19 is associated with enhancer of zeste homolog 2 (EZH2), and that this association results in Wnt/beta-catenin activation and subsequent downregulation of E-cadherin. A significant negative correlation is also observed between H19 levels and E-cad levels in vivo. These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression. Inhibition of E-cadherin expression by lnc-RNA H19 to facilitate bladder cancer metastasis;RNA interference is applied to knockdown H19 expression in bladder cancer cell, and found potentiated E-cadherin expression (p< 0.05), accompanied with weakened metastatic potency (p< 0.05)	23354591;29614625	RID02217	interact with protein
Breast cancer	HGF	H19	positively-E	northern blot;ISH	upregulation	qRT-PCR	NA	NA	cell migration(+);morphogenesis(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000019991	NA	ENSG00000130600	GRCh38_11:1995176-2001470	3082	283120	DFNB39|F-TCF|HGFB|HPTA|SF	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Cross-talk between mesenchyme and epithelium increases H19 gene expression during scattering and morphogenesis of epithelial cells. Using a blocking antibody, HGF/SF was identified as the fibroblast-derived growth factor capable of inducing H19 expression and cell morphogenesis. We further demonstrated that H19 promoter activity was stimulated by various growth factors using transient transfection in MDCK epithelial cells. HGF/SF was more efficient than EGF or FGF-2 in transactivating the H19 promoter, whereas IGF-2, TGFbeta-1, and TNF-alpha were ineffective. This activation by HGF/SF was prevented by pharmacological inhibition of MAP kinase or of phospholipase C. We conclude that H19 is a target gene for HGF/SF, a known regulator of epithelial/mesenchymal interactions, and suggest that the up-regulation of H19 may be implicated in morphogenesis and/or migration of epithelial cells.	11969291	RID02218	transcriptional regulation
Mantle cell lymphoma	MALAT1	EZH2	positively-F	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02219	interact with protein
Mantle cell lymphoma	MALAT1	CDKN1A	negatively-E	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000124762	NA	378938	1026	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02220	epigenetic regulation
Mantle cell lymphoma	MALAT1	CDKN1B	negatively-E	RNAi;RIP;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111276	NA	378938	1027	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.	27998273	RID02221	epigenetic regulation
Pancreatic cancer	NEAT1	miR-506-3p	negatively-F	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	miRNA	ENSG00000245532	GRCh38_11:65422774-65445540	NA	NA	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	NA	Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p. Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers. Additionally, our results confirmed that the tumor-promoting effects of NEAT1 in PC cells is at least partly through negative modulation of miR-506-3p.	27888106	RID02222	ceRNA or sponge
Endometrial adenocarcinoma	MALAT1	miR-200c	negatively-F	luciferase reporter assay;IHC	downregulation	qRT-PCR	NA	NA	cell invasion(-);cell migration(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma. In the present study, we first showed that miR-200c levels were higher in most EEC specimens than in non-tumor tissues, while MALAT1 levels were lower. Moreover, we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-beta increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro. In summary, miR-200c/MALAT1 axis is a target with therapeutic potential in EEC.	27693631	RID02223	ceRNA or sponge
Prostate cancer	PCA3	PRKD3	positively-E	IHC;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	ceRNA(miR-1261)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000225937	GRCh38_9:76691980-76863307	ENSG00000115825	NA	50652	23683	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	EPK2|PKC-NU|PKD3|PRKCN|nPKC-NU	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells. Prostate cancer antigen 3 (PCA3), also known as differential display code 3 (DD3), is one such lncRNA that maps to chromosome 9q21-22. PCA3 expression is highly specific to PCa. Here, we demonstrated that binding of Snail to the promoter region of PCA3 could activate the expression of PCA3. Down-regulation of PCA3 by silencing could increase the expression of the miRNA-1261, which then targeted at the PRKD3 gene (protein kinase D3) through competitive sponging. In summary, these results suggest that the transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	27743381	RID02224	ceRNA or sponge
Prostate cancer	SNAI1	PCA3	positively-E	IHC;luciferase reporter assay;ChIP	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000124216	NA	ENSG00000225937	GRCh38_9:76691980-76863307	6615	50652	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	DD3|NCRNA00019|PCAT3|PRUNE2-AS1	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells. Prostate cancer antigen 3 (PCA3), also known as differential display code 3 (DD3), is one such lncRNA that maps to chromosome 9q21-22. PCA3 expression is highly specific to PCa. Here, we demonstrated that binding of Snail to the promoter region of PCA3 could activate the expression of PCA3. Down-regulation of PCA3 by silencing could increase the expression of the miRNA-1261, which then targeted at the PRKD3 gene (protein kinase D3) through competitive sponging. In summary, these results suggest that the transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	27743381	RID02225	transcriptional regulation
Hepatocellular carcinoma	PCBP2-OT1	BMI1	interact	ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000168283	NA	102157401	648	NA	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long noncoding RNA uc.338 promotes cell proliferation through association with BMI1 in hepatocellular carcinoma. lncRNA ultraconserved element 338 (uc.338) was first found to be upregulated in HCC and promote cell growth. RNA-immunoprecipitation and RNA pull-down assays showed that uc.338 associated with BMI1. We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1.We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1. uc.338 also modulated the transcription of CDKN1A. The oncogenic activity of uc.338 is partially due to its repression of p21. uc.338 may be a potential target for HCC therapy.	27154519	RID02226	interact with protein
Hepatocellular carcinoma	PCBP2-OT1	CDKN1A	negatively-E	ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000282977	GRCh38_12:53464468-53465057	ENSG00000124762	NA	102157401	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA uc.338 promotes cell proliferation through association with BMI1 in hepatocellular carcinoma. lncRNA ultraconserved element 338 (uc.338) was first found to be upregulated in HCC and promote cell growth. RNA-immunoprecipitation and RNA pull-down assays showed that uc.338 associated with BMI1. We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1.We found that uc.338 promotes HCC cell proliferation and induces cell cycle progression through association with BMI1. uc.338 also modulated the transcription of CDKN1A. The oncogenic activity of uc.338 is partially due to its repression of p21. uc.338 may be a potential target for HCC therapy.	27154519	RID02227	transcriptional regulation
Atherosclerosis	SMILR	HAS2	positively-E	RNAi	upregulation	qRT-PCR;sequencing	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cardiovascular system disease	Atherosclerosis	lncRNA	PCG	ENSG00000255364	GRCh38_8:122414332-122428551	ENSG00000170961	NA	105375734	3037	NA	NA	Smooth Muscle Enriched Long Noncoding RNA (SMILR) Regulates Cell Proliferation.knockdown of SMILR markedly reduced cell proliferation. We focused on a novel lncRNA (Ensembl: RP11-94A24.1), which we termed smooth muscle-induced lncRNA enhances replication (SMILR). Following stimulation, SMILR expression was increased in both the nucleus and cytoplasm, and was detected in conditioned media. Furthermore, knockdown of SMILR markedly reduced cell proliferation. Mechanistically, we noted that expression of genes proximal to SMILR was also altered by interleukin-1alpha/platelet-derived growth factor treatment, and HAS2 expression was reduced by SMILR knockdown.	27052414	RID02228	expression association
Renal cell carcinoma	TGFB1	LNCRNA-ATB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+);cell proliferation(+);cell apoptosis(-);EMT(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Kidney cancer	PCG	lncRNA	ENSG00000105329	NA	NA	GRCh38_14:19126530-19128974	7040	114004396	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	NA	High expression of long non-coding RNA lncRNA-ATB is correlated with metastases and promotes cell migration and invasion in renal cell carcinoma. we found that long non-coding ribonucleic acid activated by transforming growth factor beta knockdown could (i) inhibit cell proliferation; (ii) trigger apoptosis; (iii) reduce epithelial-to-mesenchymal transition program; (iv) suppress cell migration and invasion.Our data have shown that long non-coding ribonucleic acid activated by transforming growth factor beta actively functions as a regulator of epithelial-to-mesenchymal transition during renal cell carcinoma metastasis, which suggests that long non-coding ribonucleic acid activated by transforming growth factor beta may be a potential prognostic biomarker and therapeutic target for renal cell carcinoma.	26848077	RID02229	expression association
Hepatocellular carcinoma	PRAL	TP53	positively-F	Immunocoprecipitation	downregulation	qPCR;microarray	NA	NA	cell growth(-);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000279296	GRCh38_17:6772831-6776116	ENSG00000141510	NA	109245082	7157	lncRNA-PRAL	BCC7|BMFS5|LFS1|P53|TRP53	Systemic genome screening identifies the outcome associated focal loss of long noncoding RNA PRAL in hepatocellular carcinoma. The integrative analysis of long noncoding RNA (lncRNA) expression profiles with SCNVs in hepatocellular carcinoma (HCC) led us to identify the recurrent deletion of lncRNA-PRAL (p53 regulation-associated lncRNA) on chromosome 17p13.1, whose genomic alterations were significantly associated with reduced survival of HCC patients. We found that lncRNA-PRAL could inhibit HCC growth and induce apoptosis in vivo and in vitro through p53. Subsequent investigations indicated that the three stem-loop motifs at the 5' end of lncRNA-PRAL facilitated the combination of HSP90 and p53 and thus competitively inhibited MDM2-dependent p53 ubiquitination, resulting in enhanced p53 stability.	26663434	RID02230	interact with protein
Gastric cancer	SNHG15	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000087245	NA	285958	4313	C7orf40|Linc-Myo1g|MYO1GUT	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Upregulated expression of long noncoding RNA SNHG15 promotes cell proliferation and invasion through regulates MMP2/MMP9 in patients with GC. In this study, we identified a novel lncRNA SNHG15, whose expression was upregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. knockdown of SNHG15 expression by siRNA could inhibit cell proliferation and invasion and induce apoptosis, while ectopic expression of SNHG15 promoted cell proliferation and invasion in GC cells partly via regulating MMP2 and MMP9 protein expression.	26662309	RID02231	expression association
Gastric cancer	SNHG15	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000232956	GRCh38_7:44983023-44986961	ENSG00000100985	NA	285958	4318	C7orf40|Linc-Myo1g|MYO1GUT	CLG4B|GELB|MANDP2|MMP-9	Upregulated expression of long noncoding RNA SNHG15 promotes cell proliferation and invasion through regulates MMP2/MMP9 in patients with GC. In this study, we identified a novel lncRNA SNHG15, whose expression was upregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. knockdown of SNHG15 expression by siRNA could inhibit cell proliferation and invasion and induce apoptosis, while ectopic expression of SNHG15 promoted cell proliferation and invasion in GC cells partly via regulating MMP2 and MMP9 protein expression.	26662309	RID02232	expression association
Liver cancer	HULC	SPHK1	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	angiogenesis(+)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000176170	NA	728655	8877	HCCAT1|LINC00078|NCRNA00078	SPHK	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).	26540633	RID02233	expression association
Urinary bladder cancer	UCA1	GLS2	positively-E	luciferase reporter assay	upregulation	qRT-PCR	NA	NA	glutamine metabolic process(+)	ceRNA(miR-16)	association	NA	NA	NA	NA	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000135423	NA	652995	27165	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	GA|GLS|LGA|hLGA	Long non-coding RNA UCA1 promotes glutamine metabolism by targeting miR-16 in human bladder cancer.Real-time reverse transcriptase-polymerase chain reaction demonstrated that the RNA level of urothelial carcinoma-associated 1 and GLS2 was positively correlated in bladder cancer tissues and cell lines.Furthermore, luciferase reporter assays indicated that there was a miR-16 binding site in urothelial carcinoma-associated 1, and it showed appreciable levels of sponge effects on miR-16 as readouts in a dose-dependent manner. Moreover, the seed region of miR-16 directly bound to the 3'UTR of GLS2 mRNA and regulated GLS2 expression level.Together, our results revealed that urothelial carcinoma-associated 1 regulated the expression of GLS2 through interfering with miR-16, and repressed ROS formation in bladder cancer cells.	26373319	RID02234	ceRNA or sponge
Papillary thyroid carcinoma	PTCSC3	S100A4	negatively-E	RNAi	downregulation	qRT-PCR;microarray	NA	NA	cell motility(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000259104	GRCh38_14:36136108-36176468	ENSG00000196154	NA	100886964	6275	NA	18A2|42A|CAPL|FSP1|MTS1|P9KA|PEL98	PTCSC3 Is Involved in Papillary Thyroid Carcinoma Development by Modulating S100A4 Gene Expression.Expression data from PTC cell lines pinpointed S100A4 as the most significantly downregulated gene in the presence of PTCSC3. S100A4 was upregulated in tumor tissue while PTCSC3 was strongly downregulated. PTCSC3 downregulates S100A4, leading to a reduction in cell motility and invasiveness. We propose that PTCSC3 impacts PTC predisposition and carcinogenesis through the S100A4 pathway.	26274343	RID02235	expression association
Urinary bladder cancer	miR-1-3p	UCA1	negatively-F	luciferase reporter assay	downregulation	qPCR	NA	NA	cell growth(-);apoptosis process(+);cell motility(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Urinary bladder cancer	miRNA	lncRNA	NA	NA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	Hsa-miR-1 downregulates long non-coding RNA urothelial cancer associated 1 in bladder cancer. Here, we report that downregulated hsa-miR-1 and upregulated lncRNA urothelial cancer associated 1 (UCA1) were inversely expressed in bladder cancer. The binding site between UCA1 and hsa-miR-1 was confirmed. Overexpression of hsa-miR-1 inhibited bladder cancer cell growth, induced apoptosis, and decreased cell motility. Knockdown of UCA1 expression phenocopied the effects of upregulation of hsa-miR-1. This study provides evidence for hsa-miR-1 to play tumor suppressive roles via downregulating lncRNA UCA1 in bladder cancer, which may have potential therapeutic significance.	25015192	RID02236	ceRNA or sponge
Cancer	ABALON	BCL2L1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	ENSG00000281376	GRCh38_20:31721507-31723409	ENSG00000171552	NA	103021294	598	INXS	BCL-XL/S|BCL2L|BCLX|Bcl-X|PPP1R52	Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis. We identified and characterized a long non-coding RNA (lncRNA) named INXS, transcribed from the opposite genomic strand of BCL-X, that was 5- to 9-fold less abundant in tumor cell lines from kidney, liver, breast and prostate and in kidney tumor tissues compared with non-tumors. Three apoptosis-inducing agents increased INXS lncRNA endogenous expression in the 786-O kidney tumor cell line, increased BCL-XS/BCL-XL mRNA ratio and activated caspases 3, 7 and 9. These effects were abrogated in the presence of INXS knockdown. Similarly, ectopic INXS overexpression caused a shift in splicing toward BCL-XS and activation of caspases, thus leading to apoptosis. BCL-XS protein accumulation was detected upon INXS overexpression.	24992962	RID02237	expression association
Liver cancer	YAP1	MALAT1	positively-E	luciferase reporter assay;IHC;RIP;ChIP	upregulation	qPCR	NA	NA	cell motility(-);cell growth(-)	transcriptional regulation;post-transcriptional level	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000251562	GRCh38_11:65497688-65506516	10413	378938	COB1|YAP|YAP2|YAP65|YKI	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. Here, we characterised the oncoprotein Yes-associated protein (YAP), which up-regulated metastasis-associated lung adenocarcinoma transcript 1 (Malat1) expression at both transcriptional and post-transcriptional levels, whereas serine/arginine-rich splicing factor 1 (SRSF1) played an opposing role. SRSF1 inhibited YAP activity by preventing its co-occupation with TCF/beta-catenin on the Malat1 promoter. We also revealed that overexpression of YAP combined with a knockdown of SRSF1 resulted in conspicuously enhanced transwell cell mobility, accelerated tumour growth rate, and loss of body weight in a tail vein-injected mouse models. Thus, disrupting the interaction between YAP and SRSF1 may serve as a crucial therapeutic method in liver cancer.	24468535	RID02238	transcriptional regulation
Liver cancer	SRSF1	MALAT1	negatively-E	luciferase reporter assay;IHC;RIP;ChIP	upregulation	qPCR	NA	NA	cell motility(-);cell growth(-)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Tissue Invasion and Metastasis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000136450	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6426	378938	ASF|SF2|SF2p33|SFRS1|SRp30a	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. Here, we characterised the oncoprotein Yes-associated protein (YAP), which up-regulated metastasis-associated lung adenocarcinoma transcript 1 (Malat1) expression at both transcriptional and post-transcriptional levels, whereas serine/arginine-rich splicing factor 1 (SRSF1) played an opposing role. SRSF1 inhibited YAP activity by preventing its co-occupation with TCF/beta-catenin on the Malat1 promoter. We also revealed that overexpression of YAP combined with a knockdown of SRSF1 resulted in conspicuously enhanced transwell cell mobility, accelerated tumour growth rate, and loss of body weight in a tail vein-injected mouse models. Thus, disrupting the interaction between YAP and SRSF1 may serve as a crucial therapeutic method in liver cancer.	24468535	RID02239	transcriptional regulation
Kawasaki disease	THRIL	TNF	interact	RNA pull-down assay	upregulation	NA	NA	NA	immune response(+)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Evading Immune Detection	Immune system disease	Lymph node disease	lncRNA	PCG	ENSG00000280634	GRCh38_12:125025434-125027410	ENSG00000232810	NA	102659353	7124	BRI3BP-AS1|BRI3BPAS1|Linc1992|TCONS_00020260	DIF|TNF-alpha|TNFA|TNFSF2|TNLG1F	The long noncoding RNA THRIL regulates TNFalpha expression through its interaction with hnRNPL.Finally, THRIL expression was correlated with the severity of symptoms in patients with Kawasaki disease, an acute inflammatory disease of childhood. Collectively, our data provide evidence that lincRNAs and their binding proteins can regulate TNFalpha expression and may play important roles in the innate immune response and inflammatory diseases in humans.	24371310	RID02240	transcriptional regulation
Colorectal cancer	IGF1	CRNDE	negatively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+)	NA	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	PCG	lncRNA	ENSG00000017427	NA	ENSG00000245694	GRCh38_16:54845189-54929189	3479	NA	IGF|IGF-I|IGFI|MGF	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	CRNDE, a long non-coding RNA responsive to insulin/IGF signaling, regulates genes involved in central metabolism.In colorectal cancer cells, we demonstrate that treatment with insulin and insulin-like growth factors (IGF) repressed CRNDE nuclear transcripts, including those encompassing gVC-In4. The results suggest that CRNDE expression promotes the metabolic changes by which cancer cells switch to aerobic glycolysis (Warburg effect). This is the first report of a lncRNA regulated by insulin/IGFs, and our findings indicate a role for CRNDE nuclear transcripts in regulating cellular metabolism which may correlate with their upregulation in colorectal cancer.	24184209	RID02241	expression association
B-cell acute lymphocytic leukemia	BALR-6	SP1	positively-E	luciferase reporter assay;northern blot	upregulation	qRT-PCR;microarray	NA	NA	cell proliferation(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Leukemia	lncRNA	TF	NA	GRCh38_3:17962572-18268922	ENSG00000185591	NA	NA	6667	NA	NA	BALR-6 regulates cell growth and cell survival in B-lymphoblastic leukemia.overexpression of BALR-6 isoforms in both human and mouse cell lines caused increased proliferation and decreased apoptosis. Luciferase reporter assays demonstrated an enhancement of SP1-mediated transcription in the presence of BALR-6. Specifically, our findings suggest that BALR-6 expression regulates the transcriptome downstream of SP1, and that this may underlie the function of BALR-6 in B-ALL.	26694754	RID02242	expression association
Prostate cancer	NDC80	BX647187	positively-E	RNAi;northern blot	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-);cell cycle(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Prostate cancer	PCG	lncRNA	ENSG00000080986	NA	NA	GRCh38_3:111096428-111098928	10403	NA	HEC|HEC1|HsHec1|KNTC2|TID3|hsNDC80	NA	The mitotic regulator Hec1 is a critical modulator of prostate cancer through the long non-coding RNA BX647187 in vitro. Our results showed that Hec1 mRNA and protein were significantly overexpressed in Human PCa tissues and several PCa cell lines.Through bioinformatics analysis and knockdown Hec1 in PCa cells, we found LncRNA BX647187 was positively regulated by Hec1. We further demonstrated that suppression of BX647187 in PCa cells significantly reduced cell proliferation and promoted apoptosis. Thus, we conclude that Hec1 is consistently overexpressed in human PCa and Hec1 is closely linked with human PCa progression through the meditator LncRNA BX647187.	26612002	RID02243	expression association
Gastric cancer	BC032469	TERT	positively-E	IHC;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-1207-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000249201	GRCh38_5:1173141-1178605	ENSG00000164362	NA	NA	7015	NA	CMM9|DKCA2|DKCB4|EST2|PFBMFT1|TCS1|TP2|TRT|hEST2|hTRT	Long noncoding RNA BC032469, a novel competing endogenous RNA, upregulates hTERT expression by sponging miR-1207-5p and promotes proliferation in gastric cancer. Here, we report that BC032469, a novel lncRNA, expressed highly in gastric cancer tissues. Mechanistically, BC032469 could directly bind to miR-1207-5p and effectively functioned as a sponge for miR-1207-5p to modulate the derepression of hTERT. Thus, BC032469 may function as a ceRNA to impair miR-1207-5p-dependent hTERT downregulation, suggesting that it may be clinically valuable as a poor prognostic biomarker of gastric cancer.	26549025	RID02244	ceRNA or sponge
Urinary bladder cancer	CDKN2B-AS1	BCL2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000171791	NA	100048912	596	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Bcl-2|PPP1R50	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02245	expression association
Urinary bladder cancer	CDKN2B-AS1	BAX	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000087088	NA	100048912	581	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	BCL2L4	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02246	expression association
Urinary bladder cancer	CDKN2B-AS1	CYCS	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000172115	NA	100048912	54205	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CYC|HCS|THC4	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02247	expression association
Urinary bladder cancer	CDKN2B-AS1	DIABLO	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000284934	NA	100048912	56616	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	DFNA64|SMAC	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02248	expression association
Urinary bladder cancer	CDKN2B-AS1	CASP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000132906	NA	100048912	842	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02249	expression association
Urinary bladder cancer	CDKN2B-AS1	CASP3	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000164305	NA	100048912	836	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CPP32|CPP32B|SCA-1	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02250	expression association
Urinary bladder cancer	CDKN2B-AS1	PARP1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000143799	NA	100048912	142	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ADPRT|ADPRT 1|ADPRT1|ARTD1|PARP|PARP-1|PPOL|pADPRT-1	Long non-coding RNA ANRIL is up-regulated in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic pathway. Knockdown of ANRIL repressed cell proliferation and increased cell apoptosis, along with decreased expression of Bcl-2 and increased expressions of Bax, cytoplasmic cytochrome c and Smac and cleaved caspase-9, caspase-3 and PARP. However, no change of cleaved caspase-8 level was observed. In conclusion, we first report that ANRIL possibly serves as an oncogene in bladder cancer and regulates bladder cancer cell proliferation and apoptosis through the intrinsic apoptosis pathway.	26449463	RID02251	expression association
Non-small cell lung cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR;RT-PCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long Noncoding RNA ANRIL Regulates Proliferation of Non-small Cell Lung Cancer and Cervical Cancer Cells.qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.	26408699	RID02252	expression association
Cervical cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR;RT-PCR	NA	NA	cell cycle(-);cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Long Noncoding RNA ANRIL Regulates Proliferation of Non-small Cell Lung Cancer and Cervical Cancer Cells.qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.	26408699	RID02253	expression association
Papillary thyroid carcinoma	BANCR	CCND1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000110092	NA	100885775	595	LINC00586	BCL1|D11S287E|PRAD1|U21B31	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02254	expression association
Papillary thyroid carcinoma	BANCR	TSHR	negatively-E	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000165409	NA	100885775	7253	LINC00586	CHNG1|LGR3|hTSHR-I	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02255	epigenetic regulation
Ovarian cancer	AB073614	MAPK3	positively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	GSE18521;GSE38666	GSE18521.zip;GSE38666.zip	cell proliferation(+);cell invasion(+);cell cycle(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000102882	NA	NA	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02256	expression association
Ovarian cancer	AB073614	MAPK1	positively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	GSE18521;GSE38667	GSE18521.zip;GSE38667.zip	cell proliferation(+);cell invasion(+);cell cycle(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000100030	NA	NA	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02257	expression association
Gastric cancer	FOXM1	FRGCA	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000111206	NA	ENSG00000236663	GRCh38_21:43140523-43141092	2305	NA	FKHL16|FOXM1A|FOXM1B|FOXM1C|HFH-11|HFH11|HNF-3|INS-1|MPHOSPH2|MPP-2|MPP2|PIG29|TRIDENT	NA	LncRNA-AP001631.9 promotes cell migration in gastric cancer. In the present study, through microarray analysis, we screened out a new LncRNA (LncRNA-AP001631.9), which was regulated by FOXM1, a well-known carcinogenetic factor and aimed to reveal the functional roles of this novel LncRNA in gastric cancer development. The data from qRT-PCR confirmed that the expression level of LncRNA-AP001631.9 was positively correlated with that of FOXM1.	26261500	RID02258	expression association
Gastric cancer	BANCR	NFKB1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000109320	NA	100885775	4790	LINC00586	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-kB1.BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-kB1 (P50/105) expression and 3'UTR of NF-kB1 activity. Overexpression of NF-kB1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-kB1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis.BANCR was highly expressed both in gastric tumor tissues and in cancer cells. NF-kB1 and miR-9 were involved in the role of BANCR in gastric cancer cell growth and apoptosis.	26248136	RID02259	expression association
Nasopharynx carcinoma	AFAP1-AS1	AFAP1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	Upregulated long non-coding RNA AFAP1-AS1 expression is associated with progression and poor prognosis of nasopharyngeal carcinoma. AFAP1-AS1 expression was upregulated in NPC and associated with NPC metastasis and poor prognosis. In vitro experiments demonstrated that AFAP1-AS1 knockdown significantly inhibited the NPC cell migration and invasive capability. AFAP1-AS1 knockdown also increased AFAP1 protein expression. AFAP1-AS1 promoted cancer cell metastasis via regulation of actin filament integrity.	26246469	RID02260	expression association
Lung cancer	AFAP1-AS1	AFAP1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000272620	GRCh38_4:7754090-7778928	ENSG00000196526	NA	84740	60312	AFAP1-AS|AFAP1AS	AFAP|AFAP-110|AFAP110	AFAP1-AS1, a long noncoding RNA upregulated in lung cancer and promotes invasion and metastasis. One lncRNA, actin filament associated protein 1 antisense RNA1 (AFAP1-AS1), was the most significantly upregulated in lung cancer and associated with poor prognosis. AFAP1-AS1 knockdown also increased the expression of its antisense protein coding gene, actin filament associated protein 1 (AFAP1), and affected the expression levels of several small GTPase family members and molecules in the actin cytokeratin signaling pathway, which suggested that AFAP1-AS1 promoted cancer cell metastasis via regulation of actin filament integrity.	26245991	RID02261	expression association
Pancreatic cancer	NUF2	AF339813	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell growth(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Pancreatic cancer	PCG	lncRNA	ENSG00000143228	NA	NA	GRCh38_13:93293507-93295109	83540	NA	CDCA1|CT106|NUF2R	NA	Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. Our results showed that NUF2 mRNA and protein were significantly overexpressed in Human PC tissues and several PC cell lines. Through bioinformatics analysis and knockdown NUF2 in PC cells, we found LncRNA AF339813 was positively regulated by NUF2.	26045769	RID02262	expression association
Hepatocellular carcinoma	SP1	CDKN2B-AS1	negatively-E	IHC;western blot;ChIP;RIP	upregulation	qRT-PCR	NA	NA	apoptosis process(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis	Cancer	Liver cancer	TF	lncRNA	ENSG00000185591	NA	ENSG00000240498	GRCh38_9:21994139-22128103	6667	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	25966845	RID02263	transcriptional regulation
Colorectal cancer	BANCR	CDKN1A	positively-E	RNAi;western blot	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	post-transcriptional level	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000124762	NA	100885775	1026	LINC00586	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Downregulated Long Noncoding RNA BANCR Promotes the Proliferation of Colorectal Cancer Cells via Downregualtion of p21 Expression. we show that BANCR expression was significantly down-regulated in colorectal cancer tissues compared with normal tissues. We also determined that pCDNA-BANCR-mediated colorectal cancer cell proliferation was associated with induction of G0/G1 cell-cycle arrest and apoptosis enhancement through regulation of p21, and its effects were most likely posttranscriptional.	25928067	RID02264	expression association
Gastric cancer	TUSC7	miR-23b-3p	negatively-F	luciferase reporter assay;ChIP;RIP	downregulation	microarray	NA	NA	cell growth(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000243197	GRCh38_3:116709235-116723581	NA	NA	285194	NA	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	NA	Reciprocal repression between TUSC7 and miR-23b in gastric cancer. The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients. Furthermore, we showed that TUSC7 was a direct transcriptional target of p53 via interaction of p53 with the putative p53-response element in the upstream region of TUSC7. Finally, we demonstrated reciprocal repression between TUSC7 and miR-23b; in contrast to TUSC7, miR-23b promoted cell growth. The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. Because there was one miR-23b binding site and two miR-320d binding sites (Fig. 5a) in TUSC7, we deleted these site (TUSC7-del) and determined that the corresponding construct no longer suppressed miR-23b or miR-320d	25765901	RID02265	ceRNA or sponge
Gastric cancer	TP53	TUSC7	positively-E	luciferase reporter assay;ChIP;RIP	upregulation	microarray	NA	NA	cell growth(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000243197	GRCh38_3:116709235-116723581	7157	285194	BCC7|BMFS5|LFS1|P53|TRP53	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	Reciprocal repression between TUSC7 and miR-23b in gastric cancer. The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients. Furthermore, we showed that TUSC7 was a direct transcriptional target of p53 via interaction of p53 with the putative p53-response element in the upstream region of TUSC7. Finally, we demonstrated reciprocal repression between TUSC7 and miR-23b; in contrast to TUSC7, miR-23b promoted cell growth. The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	25765901	RID02266	transcriptional regulation
Gastric cancer	NOTCH1	AK022798	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Gastric cancer	PCG	lncRNA	ENSG00000148400	NA	ENSG00000162757	GRCh38_1:209779208-209784559	4851	NA	AOS5|AOVD1|TAN1|hN1	NA	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02267	expression association
Gastric cancer	AK022798	ABCC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(-)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000103222	NA	NA	4363	NA	ABC29|ABCC|GS-X|MRP|MRP1	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02268	expression association
Gastric cancer	AK022798	CASP3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000164305	NA	NA	836	NA	CPP32|CPP32B|SCA-1	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02269	expression association
Gastric cancer	AK022798	CASP8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000162757	GRCh38_1:209779208-209784559	ENSG00000064012	NA	NA	841	NA	ALPS2B|CAP4|Casp-8|FLICE|MACH|MCH5	Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. First, we found that Notch 1 was highly expressed in the cisplatin-resistant gastric cancer cell lines SGC7901/DDP and BGC823/DDP cells. Furthermore, we used siRNA to interfere with lncRNA AK022798 expression, and found that the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8 obviously increased.	25763542	RID02270	expression association
Esophagus squamous cell carcinoma	BOK-AS1	CCN4	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	radioresistance(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000234235	GRCh38_2:241544403-241558977	ENSG00000104415	NA	100379249	8840	BOK-AS|BOKAS|NAToB|NCRNA00151	NA	Targeting WISP1 to sensitize esophageal squamous cell carcinoma to irradiation. We found that WISP1, a downstream target gene of Wnt/beta-catenin pathway, was re-expressed in 67.3% of ESCC patients as an oncofetal gene. Further studies revealed that WISP1 contributed to radioresistance primarily by repressing irradiation-induced DNA damage and activating PI3K kinase. LncRNA BOKAS was up-regulated following radiation and promoted WISP1 expression and resultant radioresistance.	25749038	RID02271	expression association
Lung cancer	BANCR	MAPK14	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000112062	NA	100885775	1432	LINC00586	CSBP|CSBP1|CSBP2|CSPB1|EXIP|Mxi2|PRKM14|PRKM15|RK|SAPK2A|p38|p38ALPHA	Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways. The results showed that BANCR levels were downregulated in LC cells. We further found that MAPK pathways were involved in the BANCR-mediated cell proliferation and migration of LC. Moreover, BANCR was found to regulate LC proliferation and migration via not ERK MAPK, but p38 MAPK and JNK inactivations.	25661343	RID02272	expression association
Lung cancer	BANCR	MAPK8	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000107643	NA	100885775	5599	LINC00586	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways. The results showed that BANCR levels were downregulated in LC cells. We further found that MAPK pathways were involved in the BANCR-mediated cell proliferation and migration of LC. Moreover, BANCR was found to regulate LC proliferation and migration via not ERK MAPK, but p38 MAPK and JNK inactivations.	25661343	RID02273	expression association
Non-small cell lung cancer	CDKN2B-AS1	KLF2	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000127528	NA	100048912	10365	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	LKLF	Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. In this study, we reported that ANRIL expression was increased in NSCLC tissues, and its expression level was significantly correlated with tumor-node-metastasis stages and tumor size. Furthermore, we uncover that ANRIL could not repress p15 expression in PC9 cells, but through silencing of KLF2 and P21 transcription.	25504755	RID02274	interact with protein
Non-small cell lung cancer	CDKN2B-AS1	CDKN1A	negatively-E	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000124762	NA	100048912	1026	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. In this study, we reported that ANRIL expression was increased in NSCLC tissues, and its expression level was significantly correlated with tumor-node-metastasis stages and tumor size. Furthermore, we uncover that ANRIL could not repress p15 expression in PC9 cells, but through silencing of KLF2 and P21 transcription.	25504755	RID02275	interact with protein
Gastric cancer	CDKN2B-AS1	miR-99a-5p	negatively-E	RIP;ChIP;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.	24810364;25504755	RID02276	epigenetic regulation
Gastric cancer	CDKN2B-AS1	miR-449a	negatively-E	RIP;ChIP;IHC	upregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.	24810364;25504755	RID02277	epigenetic regulation
Urinary bladder cancer	AATBC	CCND1	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000110092	NA	284837	595	NA	BCL1|D11S287E|PRAD1|U21B31	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02278	expression association
Urinary bladder cancer	AATBC	CDK4	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000135446	NA	284837	1019	NA	CMM3|PSK-J3	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02279	expression association
Urinary bladder cancer	AATBC	RB1	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000139687	NA	284837	5925	NA	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02280	expression association
Urinary bladder cancer	AATBC	CDKN2C	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000123080	NA	284837	1031	NA	INK4C|p18|p18-INK4C	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer.We found that AATBC was overexpressed in bladder cancer patient tissues and positively correlated with tumor grade and pT stage. We also found that inhibition of AATBC resulted in cell proliferation arrest through G1 cell cycle mediated by cyclin D1, CDK4, p18 and phosphorylated Rb.	25473900	RID02281	expression association
Urinary bladder cancer	AATBC	CASP9	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000132906	NA	284837	842	NA	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. inhibition of AATBC induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3.	25473900	RID02282	expression association
Urinary bladder cancer	AATBC	CASP3	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000164305	NA	284837	836	NA	CPP32|CPP32B|SCA-1	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. inhibition of AATBC induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3.	25473900	RID02283	expression association
Urinary bladder cancer	AATBC	MAPK8	negatively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000107643	NA	284837	5599	NA	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. The investigation for the signaling pathway revealed that the apoptosis following AATBC knockdown was mediated by activation of phosphorylated JNK and suppression of NRF2. Furthermore, JNK inhibitor SP600125 could attenuate the apoptotic effect achieved by AATBC knockdown, confirming the involvement of JNK signaling in the induced apoptosis.	25473900	RID02284	expression association
Urinary bladder cancer	AATBC	NFE2L2	positively-E	RNAi	upregulation	microarray;qRT-PCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000215458	GRCh38_21:43805758-43812567	ENSG00000116044	NA	284837	4780	NA	HEBP1|IMDDHH|NRF2	Knockdown of a novel lincRNA AATBC suppresses proliferation and induces apoptosis in bladder cancer. The investigation for the signaling pathway revealed that the apoptosis following AATBC knockdown was mediated by activation of phosphorylated JNK and suppression of NRF2. Furthermore, JNK inhibitor SP600125 could attenuate the apoptotic effect achieved by AATBC knockdown, confirming the involvement of JNK signaling in the induced apoptosis.	25473900	RID02285	expression association
Urinary bladder cancer	AB074278	EMP1	interact	RNAi	upregulation	qRT-PCR;microarray	GSE55433	GSE55433.zip	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	NA	GRCh38_17:63039470-63041178	ENSG00000134531	NA	NA	2012	NA	CL-20|EMP-1|TMP	Identification of differentially expressed long noncoding RNAs in bladder cancer. Focusing upon a promising candidate, we implicate upregulation of AB074278 in apoptosis avoidance and the maintenance of a proproliferative state in cancer through a potential interaction with EMP1, a tumor suppressor and a negative regulator of cell proliferation.	25165097	RID02286	interact with protein
Cervical cancer	TMPOP2	CDH1	negatively-E	RNAi;RIP	upregulation	microarray;qRT-PCR	GSE55940	GSE55940.zip	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	ENSG00000039068	NA	100533619	999	lncRNA-EBIC	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long noncoding RNA-EBIC promotes tumor cell invasion by binding to EZH2 and repressing E-cadherin in cervical cancer.Then, we found a specific differentially expressed lncRNA can physically bind to enhancer of zeste homolog2 (EZH2) by using RNA immunoprecipitation. We termed it as EZH2-binding lncRNA in cervical cancer [lncRNA-EBIC]. We also found that the association between lncRNA-EBIC and EZH2 was required for the repression of E-cadherin, which was a key molecular in the metastasis of cervical cancer. Conclusion: These results demonstrated that lncRNA-EBIC was an oncogenic lncRNA, which could promote tumor cell invasion in CC by binding to EZH2 and inhibiting E-cadherin expression.	25007342	RID02288	epigenetic regulation
Gastric cancer	miR-129-5p	GACAT3	negatively-F	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	prognosis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gastric cancer	miRNA	lncRNA	NA	NA	ENSG00000236289	GRCh38_2:16013928-16087201	NA	104797537	NA	LINC01458|lncRNA-AC130710	lncRNA-AC130710 targeting by miR-129-5p is upregulated in gastric cancer and associates with poor prognosis. Moreover, miR-129-5p may play an important role in the downregulation of AC130710 in gastric cancer cells.	24969565	RID02289	ceRNA or sponge
Melanoma	BANCR	MAPK3	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000102882	NA	100885775	5595	LINC00586	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02290	expression association
Melanoma	BANCR	MAPK1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000100030	NA	100885775	5594	LINC00586	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02291	expression association
Melanoma	BANCR	MAPK8	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);MAPK signaling pathway(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000107643	NA	100885775	5599	LINC00586	JNK|JNK-46|JNK1|JNK1A2|JNK21B1/2|PRKM8|SAPK1|SAPK1c	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component.	24967732	RID02292	expression association
Malignant glioma	DNMT1	ADAMTS9-AS2	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell migration(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	PCG	lncRNA	ENSG00000130816	NA	ENSG00000241684	GRCh38_3:64684909-65053439	1786	100507098	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	NA	A new tumor suppressor LncRNA ADAMTS9-AS2 is regulated by DNMT1 and inhibits migration of glioma cells. The results showed that the ADAMTS9-AS2 expression was significantly downregulated in tumor tissues compared with normal tissues and reversely associated with tumor grade and prognosis. We also found that ADAMTS9-AS2 expression was negatively correlated with DNA methyltransferase-1 (DNMT1). In addition, DNMT1 knockdown led to remarkable enhancement of ADAMTS9-AS2 expression. By 5-aza-dC treatment, the ADAMTS9-AS2 expression was also reactivated. The results suggested that ADAMTS9-AS2 is a novel tumor suppressor modulated by DNMT1 in glioma. LncRNA ADAMTS9-AS2 may serve as a potential biomarker and therapeutic target for glioma.	24833086	RID02293	expression association
Glioblastoma	APTR	CDKN1A	negatively-E	RIP;northern blot;ChIP;RNA pull-down assay;Immunoprecipitation;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000124762	NA	100505854	1026	RSBN1L-AS1	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. we performed an siRNA screen of human lncRNAs required for cell proliferation, and identified a novel lncRNA, APTR, that acts in trans to repress the CDKN1A/p21 promoter independent of p53 to promote cell proliferation. A different module of APTR associates with and recruits the Polycomb repressive complex 2 (PRC2) to epigenetically repress the p21 promoter. A decrease in APTR is necessary for the induction of p21 after heat stress and DNA damage by doxorubicin, and the levels of APTR and p21 are anti-correlated in human glioblastomas. Our data identify a new regulator of the cell-cycle inhibitor CDKN1A/p21 that acts as a proliferative factor in cancer cell lines and in glioblastomas and demonstrate that Alu elements present in lncRNAs can contribute to targeting regulatory lncRNAs to promoters.	24748121	RID02294	epigenetic regulation
Esophagus squamous cell carcinoma	CDKN2B-AS1	CDKN2B	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	ANRIL inhibits p15(INK4b) through the TGFbeta1 signaling pathway in human esophageal squamous cell carcinoma. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor beta1 (TGFbeta1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFbeta1 signaling pathways.	24747824	RID02295	expression association
Esophagus squamous cell carcinoma	CDKN2B-AS1	TGFB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105329	NA	100048912	7040	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	ANRIL inhibits p15(INK4b) through the TGFbeta1 signaling pathway in human esophageal squamous cell carcinoma. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor beta1 (TGFbeta1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFbeta1 signaling pathways.	24747824	RID02296	expression association
Non-small cell lung cancer	AK126698	CTNNB1	negatively-E	RNAi	upregulation	microarray;qRT-PCR	GSE43494	GSE43494.zip	chemoresistance(-);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_3:195715440-195719235	ENSG00000168036	NA	NA	1499	NA	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.Knockdown lncRNA AK126698 not only greatly decreased NKD2 which can negatively regulate Wnt/beta-catenin signaling but also increased the accumulation and nuclear translocation of beta-catenin, and significantly depressed apoptosis rate induced by cisplatin in A549 cells.Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	RID02297	expression association
Non-small cell lung cancer	AK126698	NKD2	positively-E	RNAi	upregulation	microarray;qRT-PCR	GSE43494	GSE43494.zip	chemoresistance(-);apoptosis process(+)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_3:195715440-195719235	ENSG00000145506	NA	NA	85409	NA	Naked2	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.Knockdown lncRNA AK126698 not only greatly decreased NKD2 which can negatively regulate Wnt/beta-catenin signaling but also increased the accumulation and nuclear translocation of beta-catenin, and significantly depressed apoptosis rate induced by cisplatin in A549 cells.Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	RID02298	expression association
Hepatocellular carcinoma	HEIH	EZH2	positively-E	RIP;ChIP;RNA pull-down assay	upregulation	microarray	GSE27462	GSE27462.zip	cell growth(+)	histone modification	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000106462	NA	100859930	2146	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans.We also found that lncRNA-HEIH plays a key role in G(0) /G(1) arrest, and further demonstrated that lncRNA-HEIH was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes.	21769904	RID02299	interact with protein
Acute lymphocytic leukemia	CDKN2B-AS1	CDKN2A	positively-E	RNAi	NA	NA	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147889	NA	100048912	1029	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	A polymorphism in the chromosome 9p21 ANRIL locus is associated to Philadelphia positive acute lymphoblastic leukemia.rs564398, mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype. We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.	21414664	RID02300	expression association
Acute lymphocytic leukemia	CDKN2B-AS1	CDKN2B	positively-E	RNAi	NA	NA	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	A polymorphism in the chromosome 9p21 ANRIL locus is associated to Philadelphia positive acute lymphoblastic leukemia.rs564398, mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype. We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.	21414664	RID02301	expression association
Osteosarcoma	LOC285194	FLT1	negatively-E	RNAi	downregulation	microarray;qRT-PCR;RT-qPCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709788-116717040	ENSG00000102755	NA	NA	2321	NA	FLT|FLT-1|VEGFR-1|VEGFR1	Recurrent focal copy-number changes and loss of heterozygosity implicate two noncoding RNAs and one tumor suppressor gene at chromosome 3q13.31 in osteosarcoma. Notably, these CNAs often involve the noncoding RNAs LOC285194 and BC040587 and, in some cases, a tumor suppressor gene that encodes the limbic system-associated membrane protein (LSAMP). depleting either LSAMP or LOC285194 promoted proliferation of normal osteoblasts by regulation of apoptotic and cell-cycle transcripts and also VEGF receptor 1.	20048075	RID02302	expression association
Cervical cancer	BOK-AS1	BOK	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000234235	GRCh38_2:241544403-241558977	ENSG00000176720	NA	100379249	666	BOK-AS|BOKAS|NAToB|NCRNA00151	BCL2L9|BOKL	A natural antisense transcript, BOKAS, regulates the pro-apoptotic activity of human Bok. Overexpression of BOKAS alone exhibited no significant anti- or pro-apoptotic activity but it was able to inhibit Bok-induced apoptosis in HeLa cells. Our results suggest that BOKAS may function specifically in the human testis, where it serves as an antisense molecule to regulate Bok-induced apoptosis.	19287972	RID02303	expression association
Cancer	CDKN2B-AS1	CDKN2B	negatively-E	ChIP	upregulation	qRT-PCR	NA	NA	cell growth(-);tumorigenesis(-)	epigenetic regulation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA. Here we show that many TSGs have nearby antisense RNAs, and we focus on the role of one RNA in silencing p15, a cyclin-dependent kinase inhibitor implicated in leukaemia. We found an inverse relation between p15 antisense (p15AS) and p15 sense expression in leukaemia. A p15AS expression construct induced p15 silencing in cis and in trans through heterochromatin formation but not DNA methylation; the silencing persisted after p15AS was turned off, although methylation and heterochromatin inhibitors reversed this process. The p15AS-induced silencing was Dicer-independent. Expression of exogenous p15AS in mouse embryonic stem cells caused p15 silencing and increased growth, through heterochromatin formation, as well as DNA methylation after differentiation of the embryonic stem cells.	18185590	RID02304	epigenetic regulation
Gastric cancer	lncRNA-LOWEG	LIFR	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENST00000508986	GRCh38_5:38425036-38427376	ENSG00000113594	NA	NA	3977	NA	CD118|LIF-R|SJS2|STWS|SWS	A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion.western blot and real-time PCR analysis suggested that lncRNA-LOWEG is positively correlated with the expression of leukemia inhibitory factor receptor (LIFR) gene at the translational level. LncRNA-LOWEG is a tumor suppressor that inhibits GC cell invasion. And LIFR gene is up-regulated by lncRNA-LOWEG.	26537802	RID02305	expression association
Endometrial cancer	GAS5	PTEN	positively-E	luciferase reporter assay;RNAi;western blot	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	ceRNA(miR-103a-3p)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells. The prediction of bioinformatics online revealed that GAS5 could bind to miR-103, which was further found to be regulated by GAS5. To further investigate the mechanism of the regulation of PTEN and miR-103 by GAS5, HHUA and JEC cells were transfected with luciferase reporter vector containing PTEN 3‘UTR and miR-103 mimic, or miR-103 mimic + GAS5 plasmid. Through measuring the luciferase activity and the mRNA level of PTEN, we found that they were both reduced in cells transfected with miR-103 mimic (Fig. 4a). we identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells.	26511107	RID02306	ceRNA or sponge
Epithelial ovarian cancer	GAS5	BAX	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000087088	NA	60674	581	NCRNA00030|SNHG2	BCL2L4	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02307	expression association
Epithelial ovarian cancer	GAS5	BAK1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000030110	NA	60674	578	NCRNA00030|SNHG2	BAK|BAK-LIKE|BCL2L7|CDN1	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02308	expression association
Epithelial ovarian cancer	GAS5	CASP3	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000164305	NA	60674	836	NCRNA00030|SNHG2	CPP32|CPP32B|SCA-1	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02309	expression association
Epithelial ovarian cancer	GAS5	CASP9	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000132906	NA	60674	842	NCRNA00030|SNHG2	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	Long non-coding RNA growth arrest-specific transcript 5 is involved in ovarian cancer cell apoptosis through the mitochondria-mediated apoptosis pathway. Finally, through mitochondrial potential and western blot analyses, GAS5 could disrupt mitochondrial membrane potential and promote BAX, BAK, cleaved-caspase 3 and cleaved-caspase 9 expression. Taken together, the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis. GAS5 can serve as a novel therapeutic target in patients with EOC.	26503132	RID02310	expression association
Intrahepatic cholangiocarcinoma	CPS1-IT1	CPS1	positively-E	IHC;RNAi;western blot	upregulation	qPCR;RT-PCR	NA	NA	cell proliferation(+);prognosis(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000280837	GRCh38_2:210617571-210619876	ENSG00000021826	NA	29034	1373	CPS1-IT|CPS1IT|CPS1IT1|PRO0132	CPSASE1|PHN	Co-expression of the carbamoyl-phosphate synthase 1 gene and its long non-coding RNA correlates with poor prognosis of patients with intrahepatic cholangiocarcinoma. Knockdown of CPS1 andor CPS1-IT1 reduced the proliferation and increased the apoptosis of ICC-9810 cells.Carbamoyl-phosphate synthase 1 (CPS1) and its lncRNA CPS1 intronic transcript 1 (CPS1-IT1) were observed to be upregulated in ICC.In conclusion, CPS1 and CPS1-IT1 may serve an important role in ICC development by promoting the proliferation of ICC cells. Furthermore, CPS1 and CPS1-IT1 were associated with poor liver function and reduced survival rates.	26499888	RID02311	expression association
Hepatocellular carcinoma	GAS5	PDCD4	positively-E	western blot;RNAi;luciferase reporter assay	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000150593	NA	60674	27250	NCRNA00030|SNHG2	H731	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21.The present report demonstrates that there are lower levels of GAS5, PDCD4, and PTEN and higher levels of microRNA-21 (miR-21) in HCC tissues than in adjacent normal tissues.Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive); in contrast, there are opposite changes in HCCLM3 cells (highly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Thus, GAS5 acts as a tumor suppressor in HCCs through negative regulation of miR-21 and its targets and proteins about migration and invasion in cancer cells, which may be a target for treating HCC.	26404135	RID02312	ceRNA or sponge
Hepatocellular carcinoma	GAS5	PTEN	positively-E	western blot;RNAi;luciferase reporter assay	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000171862	NA	60674	5728	NCRNA00030|SNHG2	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21.The present report demonstrates that there are lower levels of GAS5, PDCD4, and PTEN and higher levels of microRNA-21 (miR-21) in HCC tissues than in adjacent normal tissues.Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive); in contrast, there are opposite changes in HCCLM3 cells (highly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Thus, GAS5 acts as a tumor suppressor in HCCs through negative regulation of miR-21 and its targets and proteins about migration and invasion in cancer cells, which may be a target for treating HCC.	26404135	RID02313	ceRNA or sponge
Hepatocellular carcinoma	DBH-AS1	CDK6	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000105810	NA	138948	1021	NCRNA00118	MCPH12|PLSTIRE	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02314	expression association
Hepatocellular carcinoma	DBH-AS1	CCND1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000110092	NA	138948	595	NCRNA00118	BCL1|D11S287E|PRAD1|U21B31	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02315	expression association
Hepatocellular carcinoma	DBH-AS1	CCNE1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000105173	NA	138948	898	NCRNA00118	CCNE|pCCNE1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02316	expression association
Hepatocellular carcinoma	DBH-AS1	CDKN2A	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000147889	NA	138948	1029	NCRNA00118	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02317	expression association
Hepatocellular carcinoma	DBH-AS1	CDKN1A	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000124762	NA	138948	1026	NCRNA00118	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02318	expression association
Hepatocellular carcinoma	DBH-AS1	CDKN1B	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000225756	GRCh38_9:133654586-133657313	ENSG00000111276	NA	138948	1027	NCRNA00118	CDKN4|KIP1|MEN1B|MEN4|P27KIP1	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27.	26393879	RID02319	expression association
Hepatocellular carcinoma	HBX	DBH-AS1	positively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell survival(+);MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	PCG	lncRNA	NA	NA	ENSG00000225756	GRCh38_9:133654586-133657313	NA	138948	NA	NCRNA00118	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC.	26393879	RID02320	expression association
Hepatocellular carcinoma	TP53	DBH-AS1	negatively-E	western blot;IHC;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell survival(+);MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals;Evading Apoptosis;Reprogramming Energy Metabolism;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000225756	GRCh38_9:133654586-133657313	7157	138948	BCC7|BMFS5|LFS1|P53|TRP53	NCRNA00118	HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC.	26393879	RID02321	expression association
Colon cancer	DACOR1	CBS	negatively-E	RIP;western blot	downregulation	qRT-PCR;sequencing	TCGA	COAD.zip	cell growth(-)	DNA methylation	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	PCG	NA	GRCh38_15:67000001-67200000	ENSG00000160200	NA	100131796	875	LP2570|TCONS_00023265	CBSL|HIP4	DNMT1-associated long non-coding RNAs regulate global gene expression and DNA methylation in colon cancer. One lncRNA, TCONS_00023265, which we named DACOR1 (DNMT1-associated Colon Cancer Repressed lncRNA 1), shows high, tissue-specific expression in the normal colon (including colon crypts) but was repressed in a panel of colon tumors and patient-derived colon cancer cell lines. DACOR1 induction resulted in down-regulation of Cystathionine beta-synthase, which is known to lead to increased levels of S-adenosyl methionine-the key methyl donor for DNA methylation. Induction of DACOR1 in colon cancer cell lines significantly reduced their ability to form colonies in vitro, suggesting a growth suppressor function.	26307088	RID02322	epigenetic regulation
Gastric cancer	FER1L4	PTEN	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	ceRNA(miR-106a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000088340	GRCh38_20:35558737-35607562	ENSG00000171862	NA	80307	5728	C20orf124	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition.	26306906	RID02323	ceRNA or sponge
Hepatocellular carcinoma	EGFR-AS1	EGFR	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000224057	GRCh38_7:55179750-55188934	ENSG00000146648	NA	100507500	1956	NA	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long noncoding RNA, EGFR-AS1, a target of GHR, increases the expression of EGFR in hepatocellular carcinoma. EGFR-AS1 has been found to inhibit the expression of EGFR. We found that impeded expression of GHR decreased the expression of EGFR and EGFR-AS1 in vivo and in vitro. Then, it was verified that EGFR and EGFR-AS1 were relatively upregulated in HCC tissue, and they were significantly related to some clinical characteristics and patient prognosis. Furthermore, EGFR-AS1 was determined to promote HCC development by improving the ability of invasion and proliferation of HCC cells in vitro, and it was also found to affect the cell cycle. Our study identified that EGFR-AS1 may promote HCC genesis and development. EGFR-AS1 may act as a prognostic factor in HCC.	26271667	RID02324	expression association
Hepatocellular carcinoma	GHR	EGFR-AS1	positively-E	RNAi	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(+);cell proliferation(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	PCG	lncRNA	ENSG00000112964	NA	ENSG00000224057	GRCh38_7:55179750-55188934	2690	100507500	GHBP|GHIP	NA	The long noncoding RNA, EGFR-AS1, a target of GHR, increases the expression of EGFR in hepatocellular carcinoma. EGFR-AS1 has been found to inhibit the expression of EGFR. We found that impeded expression of GHR decreased the expression of EGFR and EGFR-AS1 in vivo and in vitro. Then, it was verified that EGFR and EGFR-AS1 were relatively upregulated in HCC tissue, and they were significantly related to some clinical characteristics and patient prognosis. Furthermore, EGFR-AS1 was determined to promote HCC development by improving the ability of invasion and proliferation of HCC cells in vitro, and it was also found to affect the cell cycle. Our study identified that EGFR-AS1 may promote HCC genesis and development. EGFR-AS1 may act as a prognostic factor in HCC.	26271667	RID02325	expression association
Lung adenocarcinoma	DLX6-AS1	DLX6	negatively-E	RNAi;western blot	upregulation	qRT-PCR;microarray	NA	NA	cell differentiation(+);TNM stage(+)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000231764	GRCh38_7:96955141-97014088	ENSG00000006377	NA	285987	1750	DLX6-AS|DLX6AS|Evf-2|NCRNA00212	NA	Expression of long non-coding RNA DLX6-AS1 in lung adenocarcinoma. The expression level of lncRNA DLX6-AS1 in LAC tissues was significantly higher compared to paired adjacent normal lung tissues (P<0.05). High DLX6-AS1 expression levels were significantly associated with both histological differentiation and TNM stage. Down-regulation of lncRNA DLX6-AS1 expression decreased the DLX6 mRNA and protein levels.	26052251	RID02326	expression association
Hepatocellular carcinoma	DANCR	CTNNB1	negatively-E	RNAi;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell stemness(+)	RNA stability	binding/interaction	RNA-RNA	NA	CSC	Limitless Replicative Potential	Cancer	Liver cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000168036	NA	57291	1499	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1. We found that lncRNA-DANCR is overexpressed in stem-like HCC cells, and this can serve as a prognostic biomarker for HCC patients. Experiments showed that DANCR markedly increased stemness features of HCC cells to promote tumorigenesis and intra-/extrahepatic tumor colonization. Experiments showed that DANCR markedly increased stemness features of HCC cells to promote tumorigenesis and intra-/extrahepatic tumor colonization. Additionally, we found that the role of DANCR relied largely on an association with, and regulation of, CTNNB1. Association of DANCR with CTNNB1 blocked the repressing effect of microRNA (miR)-214, miR-320a, and miR-199a on CTNNB1.	25964079	RID02329	interact with mRNA
Myeloid leukemia	CCDC26	KIT	positively-E	IHC;western blot	downregulation	qPCR;microarray	NA	NA	cell growth(-)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000229140	GRCh38_8:128634199-129683770	ENSG00000157404	NA	137196	3815	RAM	C-Kit|CD117|MASTC|PBT|SCFR	Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression. We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. DNA microarray and quantitative polymerase chain reaction screening for differentially expressed genes between KD clones and non-KD control cells revealed significant up-regulation of the tyrosine kinase receptor, KIT, hyperactive mutations of which are often found in AML. We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression. A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered.	25928165	RID02330	expression association
Lung adenocarcinoma	GAS5	EGFR	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000146648	NA	60674	1956	NCRNA00030|SNHG2	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib, which could be reversed by overexpressing GAS5.	25925741	RID02331	expression association
Lung adenocarcinoma	GAS5	IGF1R	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(+)	NA	association	NA	gefitinib	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000140443	NA	60674	3480	NCRNA00030|SNHG2	CD221|IGFIR|IGFR|JTK13	The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib, which could be reversed by overexpressing GAS5.	25925741	RID02332	expression association
Cervical cancer	CCEPR	PCNA	positively-F	western blot;RNA pull-down assay;RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	NA	GRCh38_10:59173963-59176464	ENSG00000132646	NA	105682749	5111	CCHE1|lncRNA-CCHE1	ATLD2	Long noncoding RNA CCHE1 promotes cervical cancer cell proliferation via upregulating PCNA. In this study, we found that cervical carcinoma high-expressed lncRNA 1 (lncRNA-CCHE1) was significantly upregulated in cervical cancer tissues.By contrast, the depletion of CCHE1 inhibits the proliferation of cervical cancer cells. RNA pull-down assays confirmed that CCHE1 physically associates with proliferating cell nuclear antigen (PCNA) messenger RNA, consequently enhances the expression of PCNA.The expression of CCHE1 and PCNA is significantly correlated in cervical cancer tissues. The depletion of PCNA abolishes the effects of CCHE1 on the proliferation of cervical cancer cells. Taken together, these findings indicate that CCHE1 plays a pivotal role in cervical cancer cell proliferation via increasing PCNA expression and serves as a potential prognostic biomarker and therapeutic target in human cervical cancer.	25921283	RID02333	interact with mRNA
Prostate cancer	AR	DRAIC	negatively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENSG00000245750	GRCh38_15:69462921-69843120	367	145837	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02337	transcriptional regulation
Prostate cancer	AR	PCAT29	negatively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000169083	NA	ENST00000560655	GRCh38_15:69592200-69695750	367	104472713	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02338	transcriptional regulation
Prostate cancer	FOXA1	DRAIC	positively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000129514	NA	ENSG00000245750	GRCh38_15:69462921-69843120	3169	145837	HNF3A|TCF3A	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02339	transcriptional regulation
Prostate cancer	FOXA1	PCAT29	positively-E	ChIP	downregulation	qPCR;RT-PCR	NA	NA	cell migration(-);cell invasion(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	TF	lncRNA	ENSG00000129514	NA	ENST00000560655	GRCh38_15:69592200-69695750	3169	104472713	HNF3A|TCF3A	NA	The lncRNA DRAIC/PCAT29 Locus Constitutes a Tumor-Suppressive Nexus. Here, we report a novel tumor-suppressive locus on human chromosome 15q23 that contains two multiexonic lncRNA genes of 100 kb each: DRAIC (LOC145837) and the recently reported PCAT29. Androgen induced androgen receptor (AR) binding to the DRAIC locus and repressed DRAIC expression. In contrast, FOXA1 and NKX3-1 are recruited to the DRAIC locus to induce DRAIC, and FOXA1 specifically counters the repression of DRAIC by AR. The decrease of FOXA1 and NKX3-1, and aberrant activation of AR, thus accounts for the decrease of DRAIC during prostate cancer progression to the CR state. Consistent with DRAIC being a good prognostic marker, DRAIC prevents the transformation of cuboidal epithelial cells to fibroblast-like morphology and prevents cellular migration and invasion. A second tumor-suppressive lncRNA PCAT29, located 20 kb downstream of DRAIC, is regulated identically by AR and FOXA1 and also suppresses cellular migration and metastasis.ChIP-seq dataset for AR, FOXA1 and NKX3-1 and identified that these transcriptional factors are also recruited to PCAT29 locus.	25700553	RID02340	transcriptional regulation
Gallbladder cancer	CCAT1	BMI1	positively-E	luciferase reporter assay;RNA pull-down assay;western blot	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	ceRNA(miR-218-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gallbladder cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000168283	NA	100507056	648	CARLO5|CARLo-5|onco-lncRNA-40	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Long non-coding RNA CCAT1 promotes gallbladder cancer development via negative modulation of miRNA-218-5p. In this study, we demonstrated that CCAT1 was upregulated in gallbladder cancer (GBC) tissues. CCAT1 silencing downregulated, whereas CCAT1 overexpression enhanced the expression of miRNA-218-5p target gene Bmi1 through competitively 'spongeing' miRNA-218-5p. Our data revealed that CCAT1 knockdown impaired the proliferation and invasiveness of GBC cells, at least in part through affecting miRNA-218-5p-mediated regulation of Bmi1. Moreover, CCAT1 transcript level was correlated with Bmi1 mRNA level in GBC tissues. Together, these results suggest that CCAT1 is a driver of malignancy, which acts in part through 'spongeing' miRNA-218-5p.	25569100	RID02341	ceRNA or sponge
Malignant glioma	CASC2	miR-21-5p	negatively-F	luciferase reporter assay;RNA pull-down assay;RIP	downregulation	qRT-PCR	NA	NA	tumor-suppressive function(-)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Brain glioma	lncRNA	miRNA	ENSG00000177640	GRCh38_10:118046279-118210158	NA	NA	255082	NA	C10orf5	NA	Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21.In this study, we confirmed that CASC2 was lowly expressed in glioma tissues as well as in U251 and U87 glioma cell lines. We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner. Furthermore, bioinformatics, luciferase reporter assays and pull-down assay confirmed that miR-21 binds to CASC2 in a sequence-specific manner. Introduction of miR-21 largely abrogated CASC2-mediated inhibition of glioma cell proliferation, migration, and invasion, and promotion of cell apoptosis. This study demonstrated that CASC2 plays a tumor suppressive role in glioma via negative regulation of miR-21, which may be a novel therapeutic target for treating gliomas.	25446261	RID02342	ceRNA or sponge
Peripheral primitive neuroectodermal tumor	EWSR1	EWSAT1	positively-E	RNAi;western blot	upregulation	microarray;sequencing	GSE60949	GSE60949.zip	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Sarcoma	PCG	lncRNA	ENSG00000182944	NA	ENSG00000212766	GRCh38_15:69072926-69095820	2130	283673	EWS|EWS-FLI1|bK984G1.4	LINC00277|NCRNA00277|TMEM84	Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis. We determined that long noncoding RNA-277 (Ewing sarcoma-associated transcript 1 [EWSAT1]) is upregulated by EWS-FLI1 in pMPCs. Inhibition of EWSAT1 expression diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in soft agar, whereas EWSAT1 inhibition had no effect on other cell types tested. Together, our data reveal that EWSAT1 is a downstream target of EWS-FLI1 that facilitates the development of Ewing sarcoma via the repression of target genes.	25401475	RID02343	expression association
Pancreatic ductal adenocarcinoma	RPL13AP23	OS9	positively-E	RNAi;IHC;luciferase reporter assay;ChIP	downregulation	qRT-PCR	NA	NA	cell invasion(-)	transcriptional regulation	binding/interaction	RNA-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000242990	GRCh38_12:57674665-57675250	ENSG00000135506	NA	441641	10956	RPL13A_10_1240	ERLEC2|OS-9	A novel long non-coding RNA ENST00000480739 suppresses tumour cell invasion by regulating OS-9 and HIF-1alpha in pancreatic ductal adenocarcinoma. We determined that the ENST00000480739 expression level was remarkably decreased in tumorous tissues compared with their corresponding non-tumorous tissues. Besides, enforced expression of ENST00000480739 suppressed PDAC cells' invasion in vitro. Overexpression of ENST00000480739 significantly increased both mRNA and protein levels of OS-9, and the luciferase assays confirmed that ENST00000480739 positively regulates OS-9 by activating the transcription level of the OS-9 promoter. We further found that ENST00000480739 may target hypoxia-inducible factor-1alpha (HIF-1alpha) expression by upregulating OS-9.	25314054	RID02344	transcriptional regulation
Pancreatic ductal adenocarcinoma	RPL13AP23	HIF1A	positively-E	RNAi;luciferase reporter assay	downregulation	qRT-PCR	NA	NA	cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	TF	ENSG00000242990	GRCh38_12:57674665-57675250	ENSG00000100644	NA	441641	3091	RPL13A_10_1240	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	A novel long non-coding RNA ENST00000480739 suppresses tumour cell invasion by regulating OS-9 and HIF-1alpha in pancreatic ductal adenocarcinoma.	25314054	RID02345	expression association
Gastric cancer	GAPLINC	CD44	positively-E	RNAi;luciferase reporter assay	upregulation	microarray	GSE50710	GSE50710.zip	cell invasion(-);cell proliferation(-);prognosis	ceRNA(miR-211-3p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000266835	GRCh38_18:3466250-3478978	ENSG00000026508	NA	100505592	960	LINC01540	CDW44|CSPG8|ECMR-III|HCELL|HUTCH-I|IN|LHR|MC56|MDU2|MDU3|MIC4|Pgp1	Long noncoding RNA GAPLINC regulates CD44-dependent cell invasiveness and associates with poor prognosis of gastric cancer.GAPLINC is a 924-bp-long lncRNA that is highly expressed in gastric cancer tissues. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effects of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression. Mechanistic investigations revealed that GAPLINC regulates CD44 as a molecular decoy for miR211-3p, a microRNA that targets both CD44 and GAPLINC.	25277524	RID02346	ceRNA or sponge
Colon cancer	MYC	CCAT1	positively-E	RNAi;IHC;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Colon cancer	TF	lncRNA	ENSG00000136997	NA	NA	GRCh38_8:127207382-127219268	4609	100507056	MRTL|MYCC|bHLHe39|c-Myc	CARLO5|CARLo-5|onco-lncRNA-40	C-Myc-activated long noncoding RNA CCAT1 promotes colon cancer cell proliferation and invasion. Our results revealed that CCAT1 was significantly overexpressed in colon cancer tissues when compared with normal tissues, and its increased expression was correlated with patients' clinical stage, lymph nodes metastasis, and survival time after surgery. Moreover, c-Myc could promote CCAT1 transcription by directly binding to its promoter region, and upregulation of CCAT1 expression in colon cancer cells promoted cell proliferation and invasion.	25185650	RID02347	transcriptional regulation
Gastric cancer	FENDRR	FN1	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000115414	NA	400550	2335	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CIG|ED-B|FINC|FN|FNZ|GFND|GFND2|LETS|MSF|SMDCF	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02348	expression association
Gastric cancer	FENDRR	MMP2	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000087245	NA	400550	4313	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02349	expression association
Gastric cancer	FENDRR	MMP9	negatively-E	RNAi;IHC;western blot	downregulation	qRT-PCR	NA	NA	cell metastasis(-);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000268388	GRCh38_16:86474529-86509099	ENSG00000100985	NA	400550	4318	FOXF1-AS1|FOXF1AS1|TCONS_00024240|lincFOXF1|onco-lncRNA-21	CLG4B|GELB|MANDP2|MMP-9	Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression.	25167886	RID02350	expression association
Esophagus squamous cell carcinoma	FOXCUT	FOXC1	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cancer progression(+);prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000280916	GRCh38_6:1601654-1607354	ENSG00000054598	NA	101927703	2296	LINC01379|TCONS_00011636	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	A novel long non-coding RNA FOXCUT and mRNA FOXC1 pair promote progression and predict poor prognosis in esophageal squamous cell carcinoma. Here, we showed that a novel long non-coding RNA FOXCUT (FOXC1 promoter upstream transcript) and its neighboring gene FOXC1 played a similar important role in the oncogenesis and progression of esophageal squamous cell carcinoma (ESCC). Notably elevated FOXCUT and FOXC1 expression levels were observed in cancerous tissues compared to adjacent noncancerous tissues the expression of FOXCUT was positively correlated with expression of FOXC1 in ESCC specimens.Assays in vitro demonstrated that knockdown of either FOXCUT or FOXC1 remarkably inhibited cell proliferation, colony formation, migration, invasion in ESCC cells. In conclusion, FOXCUT may be functionally involved in the tumor progression and survival of ESCC patients, at least in part, by modulating FOXC1. FOXCUT and FOXC1 may function as a lncRNA-mRNA gene pair, which may represent a potential prognostic biomarker and therapeutic target for ESCC patients.	25031703	RID02351	expression association
Gastric cancer	GAS5	E2F1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000101412	NA	60674	1869	NCRNA00030|SNHG2	E2F-1|RBAP1|RBBP3|RBP3	Decreased expression of long noncoding RNA GAS5 indicates a poor prognosis and promotes cell proliferation in gastric cancer. We found that GAS5 expression was markedly downregulated in gastric cancer tissues, and associated with larger tumor size and advanced pathologic stage. Finally, we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression.The results showed that the expression of E2F1 was significantly decreased and the expression of cyclin D1 was also downregulated in gastric cancer cells transfected with pCDNA3.1-GAS5.	24884417	RID02352	expression association
Breast cancer	MTOR	GAS5	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(-);apoptosis process(+)	NA	regulation	NA	docetaxel;5-fluorouracil	NA	Evading Apoptosis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000198793	NA	ENSG00000234741	GRCh38_1:173858559-173868882	2475	60674	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	NCRNA00030|SNHG2	Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy. GAS5 silencing attenuated cell responses to apoptotic stimuli, including classical chemotherapeutic agents; the extent of cell death was directly proportional to cellular GAS5 levels. Imatinib action in contrast, was independent of GAS5. GAS5 lncRNA promoted the apoptosis of triple-negative and oestrogen receptor-positive cells but only dual PI3K/mTOR inhibition was able to enhance GAS5 levels in all cell types. Reduced GAS5 expression attenuates apoptosis induction by classical chemotherapeutic agents in breast cancer cells, providing an explanation for the relationship between GAS5 expression and breast cancer patient prognosis. Clinically, this relationship may be circumvented by the use of GAS5-independent drugs such as imatinib, or by restoration of GAS5 expression. The latter may be achieved by the use of a dual PI3K/mTOR inhibitor, to improve apoptotic responses to conventional chemotherapies.GAS5 silencing diminished docetaxel-induced apoptosis and the associated loss of culture viability in both MCF7 (Fig. 3c) and T-47D cells (Fig. 3d). Similar effects were observed regarding 5-FU action in MCF7 (Fig. 3e) and T-47D (Fig. 3f) cells, whereas, imatinib action was unaffected by GAS5 silencing.	24789445	RID02353	expression association
Breast cancer	PI3K	GAS5	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	chemoresistance(-);apoptosis process(+)	NA	regulation	NA	docetaxel;5-fluorouracil	NA	Evading Apoptosis	Cancer	Breast cancer	PCG	lncRNA	NA	NA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	60674	NA	NCRNA00030|SNHG2	Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy. GAS5 silencing attenuated cell responses to apoptotic stimuli, including classical chemotherapeutic agents; the extent of cell death was directly proportional to cellular GAS5 levels. Imatinib action in contrast, was independent of GAS5. GAS5 lncRNA promoted the apoptosis of triple-negative and oestrogen receptor-positive cells but only dual PI3K/mTOR inhibition was able to enhance GAS5 levels in all cell types. Reduced GAS5 expression attenuates apoptosis induction by classical chemotherapeutic agents in breast cancer cells, providing an explanation for the relationship between GAS5 expression and breast cancer patient prognosis. Clinically, this relationship may be circumvented by the use of GAS5-independent drugs such as imatinib, or by restoration of GAS5 expression. The latter may be achieved by the use of a dual PI3K/mTOR inhibitor, to improve apoptotic responses to conventional chemotherapies.GAS5 silencing diminished docetaxel-induced apoptosis and the associated loss of culture viability in both MCF7 (Fig. 3c) and T-47D cells (Fig. 3d). Similar effects were observed regarding 5-FU action in MCF7 (Fig. 3e) and T-47D (Fig. 3f) cells, whereas, imatinib action was unaffected by GAS5 silencing.	24789445	RID02354	expression association
Colorectal cancer	CCAT1	MYC	positively-E	northern blot;ISH;ChIP;RNA pull-down assay	upregulation	qPCR;RT-PCR	NA	NA	tumorigenesis(+)	chromatin looping;super-enhancer	regulation	NA	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	TF	NA	GRCh38_8:127207382-127219268	ENSG00000136997	NA	100507056	4609	CARLO5|CARLo-5|onco-lncRNA-40	MRTL|MYCC|bHLHe39|c-Myc	Human colorectal cancer-specific CCAT1-L lncRNA regulates long-range chromatin interactions at the MYC locus. Here we demonstrate that a long noncoding RNA (lncRNA), CCAT1-L, is transcribed specifically in human colorectal cancers from a locus 515 kb upstream of MYC. This lncRNA plays a role in MYC transcriptional regulation and promotes long-range chromatin looping. Importantly, the CCAT1-L locus is located within a strong super-enhancer and is spatially close to MYC. Knockdown of CCAT1-L reduced long-range interactions between the MYC promoter and its enhancers. In cis overexpression of CCAT1-L enhances MYC expression and promotes tumorigenesis.	24662484	RID02355	chromatin looping
Gastric cancer	GHET1	MYC	positively-E	RIP;RNAi;RNA pull-down assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	RNA stability	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	TF	ENSG00000281189	GRCh38_7:148987527-148989432	ENSG00000136997	NA	102723099	4609	lncRNA-GHET1	MRTL|MYCC|bHLHe39|c-Myc	Long non-coding RNA GHET1 promotes gastric carcinoma cell proliferation by increasing c-Myc mRNA stability. In this study, we found that lncRNA gastric carcinoma high expressed transcript 1 (lncRNA-GHET1) was up-regulated in gastric carcinoma. RNA pull-down and immunoprecipitation assays confirmed that GHET1 physically associates with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) and enhances the physical interaction between c-Myc mRNA and IGF2BP1, consequently increasing the stability of c-Myc mRNA and expression. The expression of GHET1 and c-Myc is strongly correlated in gastric carcinoma tissues. these findings indicate that GHET1 plays a pivotal role in gastric carcinoma cell proliferation via increasing c-Myc mRNA stability and expression, which suggests potential use of GHET1 for the prognosis and treatment of gastric carcinoma.	24397586	RID02356	interact with mRNA
Non-small cell lung cancer	GAS5	TP53	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000141510	NA	60674	7157	NCRNA00030|SNHG2	BCC7|BMFS5|LFS1|P53|TRP53	A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer.The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues (P<0.05) and was highly related to tumor size and TNM stage (P<0.05). Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up-regulated p53 expression and down-regulated transcription factor E2F1 expression.	24357161	RID02357	expression association
Non-small cell lung cancer	GAS5	E2F1	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Lung cancer	lncRNA	TF	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000101412	NA	60674	1869	NCRNA00030|SNHG2	E2F-1|RBAP1|RBBP3|RBP3	A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer.The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues (P<0.05) and was highly related to tumor size and TNM stage (P<0.05). Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up-regulated p53 expression and down-regulated transcription factor E2F1 expression.	24357161	RID02358	expression association
Urinary bladder cancer	GAS5	CDK6	negatively-E	RIP;RNA pull-down assay	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	RNA stability	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	Downregulation of GAS5 promotes bladder cancer cell proliferation, partly by regulating CDK6. In the present study, we found that the GAS5 expression is commonly downregulated in bladder cancer cell lines and human specimens. Knockdown of GAS5 promotes bladder cancer cell proliferation, whereas forced expression of GAS5 suppresses cell proliferation. We further demonstrated that knockdown of GAS5 increases CDK6 mRNA and protein levels in bladder cancer cells.	24069260	RID02359	interact with mRNA
Pancreatic cancer	GAS5	CDK6	negatively-E	RNAi	downregulation	qRT-PCR	NA	NA	cell proliferation(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000234741	GRCh38_1:173858559-173868882	ENSG00000105810	NA	60674	1021	NCRNA00030|SNHG2	MCPH12|PLSTIRE	Downregulation of gas5 increases pancreatic cancer cell proliferation by regulating CDK6. We verify that the expression level of gas5 is significantly decreased in pancreatic cancer tissues compared with normal control. We further demonstrate that gas5 negatively regulates CDK6 (cyclin-dependent kinase 6) expression in vitro and in vivo. knockdown of CDK6 partially abrogates gas5-siRNA-induced cell proliferation. More importantly, knockdown of CDK6 partially abrogates gas5-siRNA-induced cell proliferation.	24026436	RID02360	expression association
Colon cancer	CCAT2	MYC	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colon cancer	lncRNA	TF	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000136997	NA	101805488	4609	LINC00873|NCCP1	MRTL|MYCC|bHLHe39|c-Myc	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02361	expression association
Colon cancer	CCAT2	miR-17-5p	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02362	expression association
Colon cancer	CCAT2	miR-20a-5p	positively-E	RNAi	upregulation	sequencing	NA	NA	cell growth(+);cell metastasis(+);chromosomal instability(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Genome Instability and Mutation	Cancer	Colon cancer	lncRNA	miRNA	ENSG00000280997	GRCh38_8:127400399-127402150	NA	NA	101805488	NA	LINC00873|NCCP1	NA	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.We demonstrate that MYC, miR-17-5p, and miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability.	23796952	RID02363	expression association
Prostate cancer	CTBP1-AS	CTBP1	negatively-E	immunoprecipitation;northern blot;RNAi;IHC	upregulation	sequencing	NA	NA	cell cycle(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000280927	GRCh38_4:1210120-1218591	ENSG00000159692	NA	285463	1487	PCAT10	BARS|HADDTS	Androgen-responsive long noncoding RNA CTBP1-AS promotes prostate cancer. CTBP1-AS directly represses CTBP1 expression by recruiting the RNA-binding transcriptional repressor PSF together with histone deacetylases. CTBP1-AS also exhibits global androgen-dependent functions by inhibiting tumour-suppressor genes via the PSF-dependent mechanism thus promoting cell cycle progression.	23644382	RID02364	epigenetic regulation
Gastric cancer	MYC	CCAT1	positively-E	ChIP;RNAi;ChIP;luciferase reporter assay	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	TF	lncRNA	ENSG00000136997	NA	NA	GRCh38_8:127207382-127219268	4609	100507056	MRTL|MYCC|bHLHe39|c-Myc	CARLO5|CARLo-5|onco-lncRNA-40	Long noncoding RNA CCAT1, which could be activated by c-Myc, promotes the progression of gastric carcinoma.c-Myc directly binds to the E-box element in the promoter region of CCAT1, and when ectopically expressed increased promoter activity and expression of CCAT1. abnormally expressed CCAT1 promotes cell proliferation and migration.	23143645	RID02365	transcriptional regulation
Chronic lymphocytic leukemia	DLEU2	miR-15a-5p	positively-E	ChIP;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-)	host	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000231607	GRCh38_13:49956670-50125720	NA	NA	8847	NA	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	NA	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1. Here we demonstrate that the putative tumor suppressor DLEU2 acts as a host gene of these microRNAs. Mature miR-15a/miR-16-1 are produced in a Drosha-dependent process from DLEU2 and binding of the Myc oncoprotein to two alterative DLEU2 promoters represses both the host gene transcript and levels of mature miR-15a/miR-16-1. We additionally show that DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	19591824	RID02366	expression association
Chronic lymphocytic leukemia	DLEU2	miR-16-1-3p	positively-E	ChIP;luciferase reporter assay	downregulation	RT-PCR	NA	NA	cell proliferation(-)	host	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	miRNA	ENSG00000231607	GRCh38_13:49956670-50125720	NA	NA	8847	NA	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	NA	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1. Here we demonstrate that the putative tumor suppressor DLEU2 acts as a host gene of these microRNAs. Mature miR-15a/miR-16-1 are produced in a Drosha-dependent process from DLEU2 and binding of the Myc oncoprotein to two alterative DLEU2 promoters represses both the host gene transcript and levels of mature miR-15a/miR-16-1. We additionally show that DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	19591824	RID02367	expression association
Breast cancer	GAS5	SNORD50A	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	apoptosis process(+)	host(snoRNA)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Breast cancer	lncRNA	snoRNA	ENSG00000234741	GRCh38_1:173858559-173868882	NA	NA	60674	26799	NCRNA00030|SNHG2	RNU50|U50	GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer.GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. The GAS5 gene has no significant protein-coding potential but expression encodes small nucleolar RNAs (snoRNAs) in its introns. Taken together with the recent demonstration of tumor suppressor characteristics in the related snoRNA U50, our observations suggest that such snoRNAs form a novel family of genes controlling oncogenesis and sensitivity to therapy in cancer.	18836484	RID02368	expression association
Hepatocellular carcinoma	HULC	SNAI1	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000124216	NA	728655	6615	HCCAT1|LINC00078|NCRNA00078	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Molecular mechanism of HEIH and HULC in the proliferation and invasion of hepatoma cells. The expression of HEIH and HULC in hepatocellular carcinoma cell line was significantly increased compared with human normal hepatocyte line (P<0.05). Over-expression of HULC up-regulated the expression of Snail in HepG2.	26550214	RID02369	expression association
Gastric cancer	HNF1A-AS1	RRM1	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000167325	NA	283460	6240	C12orf27|HAS1|NCRNA00262	R1|RIR1|RR1	Expression and clinical significance of long non-coding RNA HNF1A-AS1 in human gastric cancer. LncRNAs microarray analysis results exhibited that HNF1A-AS1 was downregulated in GCs tissues (mean fold change 2.06, p<0.05), which was further confirmed by qRT-PCR.Furthermore, low HNF1A-AS1 expression was associated with tumor size/diameter (p=0.005, multivariate analysis), levels of serum carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9), and RRM1 expression in tissue samples (p=0.028, p=0.009, and p=0.006, respectively).Taken together, our data indicate that lncRNA HNF1A-AS1 may be a regulator of GC, and thus, it may have potential as a novel biomarker and treatment target for this type of cancer.	26472090	RID02370	expression association
Gastric cancer	HNF1A-AS1	CEACAM5	positively-E	RNAi	downregulation	qRT-PCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000105388	NA	283460	1048	C12orf27|HAS1|NCRNA00262	CD66e|CEA	Expression and clinical significance of long non-coding RNA HNF1A-AS1 in human gastric cancer. LncRNAs microarray analysis results exhibited that HNF1A-AS1 was downregulated in GCs tissues (mean fold change 2.06, p<0.05), which was further confirmed by qRT-PCR.Furthermore, low HNF1A-AS1 expression was associated with tumor size/diameter (p=0.005, multivariate analysis), levels of serum carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9), and RRM1 expression in tissue samples (p=0.028, p=0.009, and p=0.006, respectively).Taken together, our data indicate that lncRNA HNF1A-AS1 may be a regulator of GC, and thus, it may have potential as a novel biomarker and treatment target for this type of cancer.	26472090	RID02371	expression association
Prostate cancer	HOTAIR	AR	interact	ISH;ChIP;RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell growth(-);cell invasion(-)	protein stability	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000169083	NA	100124700	367	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	LncRNA HOTAIR Enhances the Androgen-Receptor-Mediated Transcriptional Program and Drives Castration-Resistant Prostate Cancer. Here, we report HOTAIR as an androgen-repressed lncRNA, and, as such, it is markedly upregulated following androgen deprivation therapies and in CRPC. We further demonstrate a distinct mode of lncRNA-mediated gene regulation, wherein HOTAIR binds to the AR protein to block its interaction with the E3 ubiquitin ligase MDM2, thereby preventing AR ubiquitination and protein degradation. Consequently, HOTAIR expression is sufficient to induce androgen-independent AR activation and drive the AR-mediated transcriptional program in the absence of androgen. Functionally, HOTAIR overexpression increases, whereas HOTAIR knockdown decreases, prostate cancer cell growth and invasion.	26411689;25895025;28082728	RID02372	interact with protein
Breast cancer	ESR1	HOTAIR	negatively-E	Chromosome conformation capture (3C) assay;RIP;RNA pull-down assay;ChIP	upregulation	microarray;sequencing	GSE61270	GSE61270.zip	chemoresistance(+);cancer progression(+)	chromatin looping;enhancer;interact with protein	regulation	NA	tamoxifen	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000091831	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2099	100124700	ER|ESR|ESRA|ESTRR|Era|NR3A1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer. In this study, we report that HOTAIR (HOX antisense intergenic RNA) is upregulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or by tamoxifen treatment. In conclusion, the long non-coding RNA HOTAIR is directly repressed by ER and its upregulation promotes ligand-independent ER activities and contributes to tamoxifen resistance. Further, chromosome conformation capture (3C) experiment demonstrated estrogen-induced DNA looping between the transcription start site (TSS) of the HOTAIR gene (anchor primer- AP) and the ER-bound enhancer (P4). HOTAIR directly interacts with ER and enhances ER transcriptional activities.	26364613;23375982	RID02373	chromatin looping;interact with protein
Urinary bladder cancer	H19	TP53	negatively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+)	host(miR-675)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000141510	NA	283120	7157	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BCC7|BMFS5|LFS1|P53|TRP53	H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation. Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro.Western blotting analysis further identified that miR-675 inhibited p53 activation, decreased the ratio of Bax/Bcl-2 and cyclin D1 expression in bladder cancer cells;	26198047	RID02374	expression association
Gastric cancer	HOTAIR	HLA-G	positively-E	luciferase reporter assay;RNAi	upregulation	qRT-PCR	NA	NA	immune evasion(+)	ceRNA(miR-152)	regulation	NA	NA	NA	Evading Immune Detection	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000204632	NA	100124700	3135	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	MHC-G	Long non-coding RNA HOTAIR promotes HLA-G expression via inhibiting miR-152 in gastric cancer cells. Significant HOTAIR overexpression was observed in GC tissues, as well as strong positive correlations with HLA-G levels in both tissue and peripheral blood samples, detected by real-time PCR and ELISA assays respectively.bioinformatics analysis indicated the interaction between HOTAIR and miR-152, which shows potential regulation on HLA-G.Moreover, the negative regulation of miR-152 on HLA-G was verified in GC cells, while miR-152 induced decrease of HLA-G 3'UTR activity could be attenuated by HOTAIR co-overexpression with the assistant of mutation studies. Therefore, it was concluded that HOTAIR overexpression might also get involved in tumor escape mechanisms, involving HLA-G upregulation via inhibiting miR-152. Furthermore, this study recommended the potential application of HOTAIR in GC immunotherapy for better prognosis and improved survival.	26187665	RID02375	ceRNA or sponge
Urinary bladder cancer	YAP1	H19	positively-E	RNAi	upregulation	qRT-PCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	PCG	lncRNA	ENSG00000137693	NA	ENSG00000130600	GRCh38_11:1995176-2001470	10413	283120	COB1|YAP|YAP2|YAP65|YKI	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	The YAP1 oncogene contributes to bladder cancer cell proliferation and migration by regulating the H19 long noncoding RNA. YAP1 and H19 expression levels were markedly elevated in bladder cancer tissues and cells, and H19 expression was found to be significantly associated with YAP1 expression. YAP1 was found to enhance H19 expression, whereas H19 had no significant effect on YAP1 expression in bladder cancer cells. Our results emphasize the importance of YAP1 and H19 in bladder cancer progression and indicate that H19, at least in part, is induced by YAP1 overexpression.	26163939	RID02376	expression association
Gastric cancer	H19	ZEB1	positively-E	luciferase reporter assay;western blot	upregulation	RT-PCR	NA	NA	cell proliferation(-);cell migration(-)	ceRNA(miR-141)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer. H19 expression was found to be inversely correlated to miR-141 expression in gastric cancer cells and tissues. MiR-141 binds to H19 in a sequence specific manner, and suppresses H19 expression and functions including proliferation and invasion. MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1. These results were the first to demonstrate that H19 and miR-141 could compete with each other and affect their target genes in gastric cancer, which provide important clues for understanding the key roles of lncRNA-miRNA functional network in cancer.	26160158	RID02377	ceRNA or sponge
Colorectal cancer	H19	VIM	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000026025	NA	283120	7431	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02378	ceRNA or sponge
Colorectal cancer	H19	ZEB1	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000148516	NA	283120	6935	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02379	ceRNA or sponge
Colorectal cancer	H19	ZEB2	positively-E	luciferase reporter assay;western blot;RIP	upregulation	qRT-PCR	NA	NA	epithelial to mesenchymal transition(+)	ceRNA(miR-138;miR-200a)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000169554	NA	283120	9839	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.	26068968	RID02380	ceRNA or sponge
Papillary thyroid carcinoma	MEG3	RAC1	negatively-F	luciferase reporter assay;western blot	downregulation	qRT-PCR	NA	NA	cell migration(-);cell invasion(-)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000136238	NA	55384	5879	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	MIG5|MRD48|Rac-1|TC-25|p21-Rac1	Long non-coding RNA MEG3 suppresses migration and invasion of thyroid carcinoma by targeting of Rac1. the present study demonstrates that MEG3 was significantly down-regulated in papillary thyroid carcinoma (PTC) tissues with lymph-node metastasis than in primary thyroid cancer. In addition, we also showed that Rac1 was negatively regulated by lncRNA-MEG3 at the posttranscriptional level, via a specific target site within the 3'UTR by dual luciferase reporter assay. The expression of Rac1 was inversely correlated with lncRNA-MEG3 expression in PTC tissues.	25997963	RID02381	interact with mRNA
Breast cancer	BCAR4	SNIP1	interact	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000163877	NA	400500	79753	NA	PML1|PMRED	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02382	interact with protein
Breast cancer	BCAR4	PPP1R10	interact	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000204569	NA	400500	5514	NA	CAT53|FB19|PNUTS|PP1R10|R111|p99	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02383	interact with protein
Breast cancer	BCAR4	GLI2	positively-E	pull-down assay;mass spectrometry	upregulation	qRT-PCR	NA	NA	cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000262117	GRCh38_16:11819829-11828845	ENSG00000074047	NA	400500	2736	NA	CJS|HPE9|PHS2|THP1|THP2	lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The lncRNA BCAR4 is required for phospho-GLI2 dependent gene activation via its direct interaction with Smad nuclear-interacting protein 1 (SNIP1) and Serine/threonine-protein phosphatase 1 regulatory subunit 10 (PPP1R10, also known as PNUTS). Mechanistically, the BCAR4-SNIP1 binding releases the inhibitory role of SNIP1 on p300 histone acetyltransferase (HAT) activity, leading to the acetylation of histones including a novel mark, H3K18ac, on the promoters of GLI2 target transcription units. The acetylated H3K18 can be further recognized by PNUTS, which is recruited to the promoters of GLI2 target genes by BCAR4, to attenuate the protein's inhibitory effect on the enzymatic activity of PP1, leading to hypophosphorylation of RNA polymerase II at Ser5.	25416949	RID02384	epigenetic regulation
B-cell lymphoma	DLEU2	MYB	negatively-E	western blot;northern blot;luciferase reporter assay	downregulation	RT-PCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lymphoma	lncRNA	TF	ENSG00000231607	GRCh38_13:49956670-50125720	ENSG00000118513	NA	8847	4602	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	Cmyb|c-myb|c-myb_CDS|efg	c-Myb oncoprotein is an essential target of the dleu2 tumor suppressor microRNA cluster. Here we demonstrate that the Pax5 oncoprotein downregulates the dleu2 gene and at the same time boosts expression of its own heterodimeric partner c-Myb.Moreover, forced overexpression of miR-15a/16 reduces endogenous c-Myb levels and compromises Pax5 function. Conversely, restoration of c-Myb levels partly alleviates tumors suppressive effects of miR-15a/16, suggesting that c-Myb is a key downstream target of this microRNA cluster.	18708755	RID02385	expression association
B-cell lymphoma	PAX5	DLEU2	negatively-E	western blot;northern blot;luciferase reporter assay	downregulation	RT-PCR	NA	NA	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lymphoma	TF	lncRNA	ENSG00000196092	NA	ENSG00000231607	GRCh38_13:49956670-50125720	5079	8847	ALL3|BSAP	ALT1|BCMSUN|DLB2|LEU2|LINC00022|MIR15AHG|NCRNA00022|RFP2|RFP2OS|TRIM13OS	c-Myb oncoprotein is an essential target of the dleu2 tumor suppressor microRNA cluster. Here we demonstrate that the Pax5 oncoprotein downregulates the dleu2 gene and at the same time boosts expression of its own heterodimeric partner c-Myb.Moreover, forced overexpression of miR-15a/16 reduces endogenous c-Myb levels and compromises Pax5 function. Conversely, restoration of c-Myb levels partly alleviates tumors suppressive effects of miR-15a/16, suggesting that c-Myb is a key downstream target of this microRNA cluster.	18708755	RID02386	expression association
Breast cancer	HOTAIR	EZH2	interact	ISH;RNAi;ChIP	upregulation	qRT-PCR	NA	NA	cell proliferation(-);cell invasion(-);cell metastasis(-);chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	platinum	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	20393566;28420874;30048163	RID02387	interact with protein
Breast cancer	HOTAIR	SUZ12	interact	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.	20393566	RID02388	interact with protein
Breast cancer	HOTAIR	EED	interact	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000074266	NA	100124700	8726	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	COGIS|HEED|WAIT1	The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. We transduced vector- or HOTAIR-expressing MDA-MB-231 cells with short hairpin RNAs (shRNAs) targeting PRC2 subunits EZH2 or SUZ12. Immunoblot analyses confirmed efficient depletion of the targeted proteins (Fig. 4a). Depletion of either SUZ12 or EZH2 had little impact on the invasiveness of control cells, but completely reversed the ability of HOTAIR to promote matrix invasion (Fig. 4b). These results suggest that PRC2 is specifically required for HOTAIR to promote cellular invasiveness.	20393566	RID02389	interact with protein
Breast cancer	HOTAIR	JAM2	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154721	NA	100124700	58494	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	C21orf43|CD322|JAM-B|JAMB|PRO245|VE-JAM|VEJAM	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02390	epigenetic regulation
Breast cancer	HOTAIR	ABL2	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000143322	NA	100124700	27	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABLL|ARG	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02391	epigenetic regulation
Breast cancer	HOTAIR	SNAI1	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02392	epigenetic regulation
Breast cancer	HOTAIR	LAMB3	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196878	NA	100124700	3914	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AI1A|BM600-125KDA|LAM5|LAMNB1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02393	epigenetic regulation
Breast cancer	HOTAIR	LAMC2	positively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cell invasion(-);cell metastasis(-)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000058085	NA	100124700	3918	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	B2T|BM600|CSF|EBR2|EBR2A|LAMB2T|LAMNB2	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion (Fig. 4d). HOTAIR-induced genes were also reversed upon PRC2 depletion (Fig. 4d). Of note, many of the genes induced by HOTAIR are known positive regulators of cancer metastasis, including ABL2, SNAIL, and laminins.	20393566	RID02394	epigenetic regulation
Breast cancer	HOTAIR	HOXD10	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000128710	NA	100124700	3236	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOX4|HOX4D|HOX4E|Hox-4.4	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02395	epigenetic regulation
Breast cancer	HOTAIR	PRG1	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	23574	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02396	epigenetic regulation
Breast cancer	HOTAIR	PCDH10	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000138650	NA	100124700	57575	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	OL-PCDH|PCDH19	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion.	20393566	RID02397	epigenetic regulation
Breast cancer	HOTAIR	PCDHB5	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000113209	NA	100124700	26167	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PCDH-BETA5	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis. Quantitative RT-PCR confirmed that HOTAIR-induced PRC2 target genes, such as JAM2, PCDH10, PCDHB5, were transcriptionally repressed upon HOTAIR expression and de-repressed upon concomitant PRC2 depletion.	20393566	RID02398	epigenetic regulation
Breast cancer	HOTAIR	PGR	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	cancer progression(+)	histone modification	regulation	NA	NA	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000082175	NA	100124700	5241	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NR3C3|PR	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02399	epigenetic regulation
Breast cancer	HOTAIR	EPHA1	negatively-E	RNAi;ChIP	upregulation	qRT-PCR;microarray	NA	NA	angiogenesis(+)	histone modification	regulation	NA	NA	NA	Sustained Angiogenesis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000146904	NA	100124700	2041	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	EPH|EPHT|EPHT1	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.A number of the genes with HOTAIR-induced PRC2 occupancy are implicated in inhibiting breast cancer progression, including transcription factors HOXD10 and PRG1, encoding progesterone receptor (a classic favorable prognostic factor); cell adhesion molecules of the protocadherin (PCDH) gene family and JAM2; and EPHA1, encoding an ephrin receptor involved in tumor angiogenesis.	20393566	RID02400	epigenetic regulation
Prostate cancer	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);PI3K/AKT signaling pathway(-);cell growth(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	ectopic expression of PTENP1 resulted in the upregulation of PTEN, accompanied by the blockage of PI3K/AKT pathway and growth inhibition in prostate (DU145) and renal (ACHN and SN12PM6) cancer cells [3, 6]. Specifically, PTENP1 can modulate PTEN levels by sponging miR21 in ACHN and SN12PM6 renal cancer cells, while exerting its decoy effect by trapping miR17, miR19b and miR20a, which would otherwise target PTEN and several autophagy gene transcripts in Mahlavu HCC cells.	20577206;24172333	RID02401	ceRNA or sponge
Clear cell renal cell carcinoma	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+);PI3K/AKT signaling pathway(-);cell growth(-)	ceRNA(miR-21)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	ectopic expression of PTENP1 resulted in the upregulation of PTEN, accompanied by the blockage of PI3K/AKT pathway and growth inhibition in prostate (DU145) and renal (ACHN and SN12PM6) cancer cells [3, 6]. Specifically, PTENP1 can modulate PTEN levels by sponging miR21 in ACHN and SN12PM6 renal cancer cells, while exerting its decoy effect by trapping miR17, miR19b and miR20a, which would otherwise target PTEN and several autophagy gene transcripts in Mahlavu HCC cells.We found that PTENP1 is downregulated in ccRCC tissues and cells due to methylation.	25249556;24172333	RID02402	ceRNA or sponge
Hepatocellular carcinoma	PTENP1	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(-);cell proliferation(-);cell migration(-);cell invasion(-);cell autophagy(+);apoptosis process(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000171862	NA	11191	5728	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02403	ceRNA or sponge
Hepatocellular carcinoma	PTENP1	ULK1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000177169	NA	11191	8408	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	ATG1|ATG1A|UNC51|Unc51.1|hATG1	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02404	ceRNA or sponge
Hepatocellular carcinoma	PTENP1	ATG7	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000197548	NA	11191	10533	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	APG7-LIKE|APG7L|GSA7	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02405	ceRNA or sponge
Hepatocellular carcinoma	PTENP1	SQSTM1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	cell autophagy(+)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000161011	NA	11191	8878	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	A170|DMRV|FTDALS3|NADGP|OSIL|PDB3|ZIP3|p60|p62|p62B	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02406	ceRNA or sponge
Hepatocellular carcinoma	PTENP1	PHLPP1	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(-)	ceRNA(miR-17;miR-19b;miR-20a)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000237984	GRCh38_9:33673504-33677499	ENSG00000081913	NA	11191	23239	PTEN-rs|PTEN2|PTENpg1|PTH2|psiPTEN	PHLPP|PLEKHE1|PPM3A|SCOP	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. Co-transduction of HCC cells with the SB-BV vector expressing PTENP1 elevated the levels of PTENP1 and PTEN, which suppressed the oncogenic PI3K/AKT pathway, inhibited cell proliferation, migration/invasion as well as induced autophagy and apoptosis. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	25617127;24172333	RID02407	ceRNA or sponge
Breast cancer	HOTAIR	LAMTOR5	interact	RIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000134248	NA	100124700	10542	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HBXIP|XIP	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02408	interact with protein
Breast cancer	HOTAIR	KDM1A	interact	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02409	interact with protein
Breast cancer	HOTAIR	CCNA2	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000145386	NA	100124700	890	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCN1|CCNA	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02410	epigenetic regulation
Breast cancer	HOTAIR	EIF4E	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000151247	NA	100124700	1977	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AUTS19|CBP|EIF4E1|EIF4EL1|EIF4F|eIF-4E	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02411	epigenetic regulation
Breast cancer	HOTAIR	LDHA	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000134333	NA	100124700	3939	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	GSD11|HEL-S-133P|LDHM|PIG19	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02412	epigenetic regulation
Breast cancer	HOTAIR	CCNA1	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell growth(+)	histone modification	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000133101	NA	100124700	8900	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CT146	HBXIP and LSD1 Scaffolded by lncRNA Hotair Mediate Transcriptional Activation by c-Myc. We confirmed that the HBXIP expression correlated with expression of the c-Myc target genes cyclin A, eIF4E, and LDHA. RNAi-mediated silencing of HBXIP abolished c-Myc-mediated upregulation of these target genes. Mechanistically, HBXIP interacted directly with c-Myc through the leucine zippers and recruited the lncRNA Hotair along with the histone demethylase LSD1, for which Hotair serves as a scaffold. Silencing of HBXIP, Hotair, or LSD1 was sufficient to block c-Myc-enhanced cancer cell growth in vitro and in vivo. Taken together, our results support a model in which the HBXIP/Hotair/LSD1 complex serves as a critical effector of c-Myc in activating transcription of its target genes, illuminating long-standing questions on how c-Myc drives carcinogenesis.	26719542	RID02413	epigenetic regulation
Lung cancer	HOTAIR	MMP9	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Role of HOTAIR long noncoding RNA in metastatic progression of lung cancer. Among the tested lncRNAs, HOTAIR and NEAT1 were most highly expressed in lymph node metastasis. However, only HOTAIR was subsequently found to be involved in lung cancer cell motility and invasion, as assessed by in vitro migration and invasion assay. Finally, our experiments suggest that HOTAIR promoted gelatinase activity in these cells.Our data indicates that HOTAIR is overexpressed in metastatic lung cancer tissue, which is prospectively associated with the ability of HOTAIR to promote lung cancer cell motility and invasion.	25010625	RID02414	expression association
Lung adenocarcinoma	MALAT1	MIA2	negatively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150527	NA	378938	4253	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTAGE5|MEA6|MGEA|MGEA11|MGEA6|TALI	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02415	expression association
Lung adenocarcinoma	MALAT1	ROBO1	negatively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169855	NA	378938	6091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DUTT1|SAX3	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02416	expression association
Lung adenocarcinoma	MALAT1	GPC6	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000183098	NA	378938	10082	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OMIMD1	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02417	expression association
Lung adenocarcinoma	MALAT1	ADGRL2	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000117114	NA	378938	23266	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CIRL2|CL2|LEC1|LPHH1|LPHN2	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02418	expression association
Lung adenocarcinoma	MALAT1	CDCP1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163814	NA	378938	64866	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD318|SIMA135|TRASK	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02419	expression association
Lung adenocarcinoma	MALAT1	ABCA1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000165029	NA	378938	19	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ABC-1|ABC1|CERP|HDLDT1|TGD	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02420	expression association
Lung adenocarcinoma	MALAT1	DRD1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000184845	NA	378938	1812	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DADR|DRD1A	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02421	expression association
Lung adenocarcinoma	MALAT1	COL6A1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142156	NA	378938	1291	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BTHLM1|OPLL|UCHMD1	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02422	expression association
Lung adenocarcinoma	MALAT1	STC1	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000159167	NA	378938	6781	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	STC	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02423	expression association
Lung adenocarcinoma	MALAT1	MCAM	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Sustained Angiogenesis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000076706	NA	378938	4162	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD146|HEMCAM|METCAM|MUC18|MelCAM	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02424	expression association
Lung adenocarcinoma	MALAT1	PRKCE	positively-E	RNAi	NA	NA	NA	NA	cell metastasis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000171132	NA	378938	5581	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	PKCE|nPKC-epsilon	The non-coding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. MALAT1 regulates gene expression including metastasis-associated transcripts.MIA2 (Melanoma inhibitory activity 2), a negative regulator of tumor growth and invasion (31), or ROBO1 (Roundabout 1), an inhibitor of glioma migration and invasion (32-33), were increased in all KO cells compared to all WT cells. In turn, GPC6 (Glypican 6), a promoter of breast cancer metastasis (34), LPHN2 (Latrophilin 2), an important factor for the Epithelial-to-Mesenchmyal-Transition (EMT) of endothelial cells in the atrioventricular canal of the heart and involved in cancer cell invasion (35-36), CDCP1 (Cub domain containing protein 1), a promoter of lung adenocarcinoma metastasis in a mouse model (37), and ABCA1 (ATP-binding cassette, sub-family A, member 1), an important factor for prostate cancer cell migration and EMT (38-39), were strongly reduced by loss of MALAT1.The expression of several other MALAT1 target genes was associated with metastasis (e.g. DRD1, COL6A1, STC1) or they represented critical regulators of metastasis formation (e.g. GPC6, MCAM, PRKCE).	23243023	RID02425	expression association
Non-small cell lung cancer	MVIH	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:78038556-78040701	ENSG00000087245	NA	NA	4313	NA	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Long non-coding RNA MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion.  In this study, we found that lncRNA MVIH levels were increased in NSCLC tissues compared with adjacent normal tissues. Furthermore, knockdown of MVIH expression by siRNA could inhibit cell proliferation and invasion, while ectopic expression of MVIH promoted cell proliferation and invasion in NSCLC cells partly via regulating MMP2 and MMP9 protein expression. Our findings present that increased lncRNA MVIH could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and invasion.	24793017;25491133	RID02426	expression association
Non-small cell lung cancer	MVIH	MMP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	NA	GRCh38_10:78038556-78040701	ENSG00000100985	NA	NA	4318	NA	CLG4B|GELB|MANDP2|MMP-9	Long non-coding RNA MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion.  In this study, we found that lncRNA MVIH levels were increased in NSCLC tissues compared with adjacent normal tissues. Furthermore, knockdown of MVIH expression by siRNA could inhibit cell proliferation and invasion, while ectopic expression of MVIH promoted cell proliferation and invasion in NSCLC cells partly via regulating MMP2 and MMP9 protein expression. Our findings present that increased lncRNA MVIH could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and invasion.	24793017;25491133	RID02427	expression association
Non-small cell lung cancer	NFE2L2	LUCAT1	interact	ChIP;western blot;RNAi	upregulation	qPCR;microarray	GSE29006	GSE29006.zip	cytotoxicity(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tumor Promoting Inflammation	Cancer	Lung cancer	TF	lncRNA	ENSG00000116044	NA	ENSG00000248323	GRCh38_5:91054834-91314547	4780	100505994	HEBP1|IMDDHH|NRF2	SCAL1|SCAT5	The expression of SCAL1 is regulated transcriptionally by nuclear factor erythroid 2-related factor (NRF2), as determined by the small, interfering RNA (siRNA) knockdown of NRF2 and kelch-like ECH-associated protein 1 (KEAP1). A nuclear factor erythroid-derived 2 (NF-E2) motif was identified in the promoter region that shows binding to NRF2 after its activation. Functionally, the siRNA knockdown of SCAL1 in human bronchial epithelial cells shows a significant potentiation of cytotoxicity induced by CSE in vitro.	23672216;25491133	RID02428	transcriptional regulation
Non-small cell lung cancer	GAS6-AS1	GAS6	negatively-E	RNAi	downregulation	qPCR	NA	NA	prognosis(+);cancer progression(-)	NA	association	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000233695	GRCh38_13:113815630-113845744	ENSG00000183087	NA	650669	2621	NA	AXLLG|AXSF	Low expression of long noncoding RNA GAS6-AS1 predicts a poor prognosis in patients with NSCLC.In this study, we reported a new lncRNA GAS6-AS1 (GAS6 antisense RNA 1), whose expression was downregulated in tumor tissues in 50 patients with non-small cell lung cancer (NSCLC) compared with those in the adjacent normal tissues (P<0.001).GAS6-AS1 level was inversely correlated with GAS6 (growth-arrest-specific gene6) mRNA level (Pearson's correlation -0.620). In conclusion, our study demonstrated that altered lncRNA GAS6-AS1 expression might be involved in the development and progression of NSCLC by influencing its host gene and promised to be a potential diagnostic target in patients with NSCLC.	23979857;25491133	RID02429	expression association
Lung cancer	TARID	TCF21	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;25491133	RID02430	epigenetic regulation
Lung cancer	TARID	GADD45A	interact	ChIP;RIP	downregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;25491133	RID02431	interact with protein
Gallbladder cancer	HOTAIR	miR-130a	negatively-F	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	oncogenic role(+)	sponge	binding/interaction	RNA-RNA	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer.We demonstrate that HOTAIR is a direct target of c-Myc through interaction with putative c-Myc target response element (RE) in the upstream region of HOTAIR in gallbladder cancer cells. A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. We predicted that HOTAIR harbors a miRNA-130a binding site. Our data showed that this binding site is vital for the regulation of miRNA-130a by HOTAIR. Moreover, a negative correlation between HOTAIR and miRNA-130a was observed in gallbladder cancer tissues. Finally, we demonstrate that the oncogenic activity of HOTAIR is in part through its negative regulation of miRNA-130a.	24953832;25491133	RID02432	ceRNA or sponge
Gallbladder cancer	MYC	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Gallbladder cancer	TF	lncRNA	ENSG00000136997	NA	ENSG00000228630	GRCh38_12:53962308-53974956	4609	100124700	MRTL|MYCC|bHLHe39|c-Myc	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer.We demonstrate that HOTAIR is a direct target of c-Myc through interaction with putative c-Myc target response element (RE) in the upstream region of HOTAIR in gallbladder cancer cells. A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. We predicted that HOTAIR harbors a miRNA-130a binding site. Our data showed that this binding site is vital for the regulation of miRNA-130a by HOTAIR. Moreover, a negative correlation between HOTAIR and miRNA-130a was observed in gallbladder cancer tissues. Finally, we demonstrate that the oncogenic activity of HOTAIR is in part through its negative regulation of miRNA-130a.	24953832;25491133	RID02433	transcriptional regulation
Laryngeal squamous cell carcinoma	HOTAIR	PTEN	negatively-E	RNAi;Methylation-Specific and Bisulfite Sequencing PCR	upregulation	qPCR	NA	NA	oncogenic role(+)	DNA methylation	regulation	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171862	NA	100124700	5728	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	Long intergenic noncoding RNA HOTAIR is overexpressed and regulates PTEN methylation in laryngeal squamous cell carcinoma. HOTAIR levels were significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues. Moreover, PTEN methylation was significantly reduced in Hep-2 cells depleted of HOTAIR. Taken together, these results suggest that the oncogenic role of HOTAIR in LSCC is related to promotion of PTEN methylation. HOTAIR could serve as a marker for LSCC prognosis and a potential target for therapeutic intervention.	23141928;25491133	RID02434	epigenetic regulation
Colorectal cancer	HOTAIR	SUZ12	positively-E	RNAi	upregulation	qPCR;microarray	GSE21815	GSE21815.zip	cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	Long noncoding RNA HOTAIR regulates polycomb-dependent chromatin modification and is associated with poor prognosis in colorectal cancers.In this study, we examined the status and function of HOTAIR in patients with stage IV colorectal cancer (CRC) who have liver metastases and a poor prognosis. HOTAIR expression levels were higher in cancerous tissues than in corresponding noncancerous tissues and high HOTAIR expression correlated tightly with the presence of liver metastasis.gene set enrichment analysis using cDNA array data revealed a close correlation between expression of HOTAIR and members of the PRC2 complex (SUZ12, EZH2, and H3K27me3). Our findings suggest that HOTAIR expression is associated with a genome-wide reprogramming of PRC2 function not only in breast cancer but also in CRC, where upregulation of this long ncRNA may be a critical element in metastatic progression.	21862635	RID02435	expression association
Colorectal cancer	HOTAIR	EZH2	interact	RIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	5-fluorouracil	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer. To investigate whether HOTAIR is associated with EZH2 in CRC, an RNA immunoprecipitation (RIP) assay was performed, and the results showed a significant enrichment of HOTAIR with EZH2 antibody compared with the non-specific IgG (immunoglobulin G) antibody in both HT29 and SW480 cells	28918035;21862635	RID02436	interact with protein
Renal cell carcinoma	miR-141	HOTAIR	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Kidney cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Long non-coding RNA HOTAIR is targeted and regulated by miR-141 in human cancer cells. We found that HOTAIR expression is inversely correlated to miR-141 expression in renal carcinoma cells. HOTAIR promotes malignancy, including proliferation and invasion, whereas miR-141 suppresses malignancy in human cancer cells. miR-141 binds to HOTAIR in a sequence-specific manner and suppresses HOTAIR expression and functions, including proliferation and invasion.	20333681	RID02437	ceRNA or sponge
Gastric cancer	HOTAIR	MMP1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000196611	NA	100124700	4312	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG|CLGN	Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer.The expression level of HOTAIR in cancer tissues was higher than that in adjacent noncancerous tissues. In vitro, inhibition of HOTAIR in GC cells could reduce invasiveness, as well as the expression of MMP1 and MMP3. In addition, suppression of HOTAIR could reverse EMT process.	23847441	RID02438	expression association
Gastric cancer	HOTAIR	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell invasion(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000149968	NA	100124700	4314	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer.The expression level of HOTAIR in cancer tissues was higher than that in adjacent noncancerous tissues. In vitro, inhibition of HOTAIR in GC cells could reduce invasiveness, as well as the expression of MMP1 and MMP3. In addition, suppression of HOTAIR could reverse EMT process.	23847441	RID02439	expression association
Non-small cell lung cancer	COL1A1	HOTAIR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	tumorigenesis(+)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	PCG	lncRNA	ENSG00000108821	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1277	100124700	EDSARTH1|EDSC|OI1|OI2|OI3|OI4	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Induction of long intergenic non-coding RNA HOTAIR in lung cancer cells by type I collagen. Our findings indicate that tumor-promoting Col-1 up-regulates the expression of HOTAIR in NSCLC cells. These initial results warrant further investigation of HOTAIR and other lincRNA genes in lung tumorigenesis. Moreover the expression of HOTAIR and Col-1 was concurrently up-regulated in human non-small cell lung cancer.	23668363	RID02440	expression association
Breast cancer	KMT2A	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000118058	NA	ENSG00000228630	GRCh38_12:53962308-53974956	4297	100124700	ALL-1|CXXC7|HRX|HTRX1|MLL|MLL1|MLL1A|TRX1|WDSTS	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02441	transcriptional regulation
Breast cancer	KMT2C	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000055609	NA	ENSG00000228630	GRCh38_12:53962308-53974956	58508	100124700	HALR|KLEFS2|MLL3	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02442	transcriptional regulation
Breast cancer	CREBBP	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000005339	NA	ENSG00000228630	GRCh38_12:53962308-53974956	1387	100124700	CBP|KAT3A|MKHK1|RSTS|RSTS1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02443	transcriptional regulation
Breast cancer	EP300	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000100393	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2033	100124700	KAT3B|MKHK2|RSTS2|p300	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. Estrogen receptors (ERs) along with various ER coregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding protein/p300 bind to the promoter of HOTAIR in an E2-dependent manner. Level of histone H3 lysine-4 trimethylation, histone acetylation, and RNA polymerase II recruitment is enriched at the HOTAIR promoter in the presence of E2. Knockdown of ERs and MLLs downregulated the E2-induced HOTAIR expression. Thus, similar to protein-coding gene transcription, E2-induced transcription of antisense transcript HOTAIR is coordinated via ERs and ER coregulators, and this mechanism of HOTAIR overexpression potentially contributes towards breast cancer progression.	23375982	RID02444	transcriptional regulation
Cancer	NBR2	PRKAG1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000181929	NA	10230	5571	NCRNA00192	AMPKG	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02445	interact with protein
Cancer	NBR2	PRKAA1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000132356	NA	10230	5562	NCRNA00192	AMPK|AMPKa1	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02446	interact with protein
Cancer	NBR2	PRKAA2	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000162409	NA	10230	5563	NCRNA00192	AMPK|AMPK2|AMPKa2|PRKAA	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02447	interact with protein
Cancer	NBR2	PRKAB1	interact	RNA pull-down assay	downregulation	sequencing	TCGA	NA	energy metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Reprogramming Energy Metabolism	Cancer	Cancer	lncRNA	PCG	ENSG00000198496	GRCh38_17:43125551-43153671	ENSG00000111725	NA	10230	5564	NCRNA00192	AMPK|HAMPKb	LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress.Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1-AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress.NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo.Since AMPK alpha, beta and gamma subunits form a very stable complex at the endogenous level, we also observed a glucose starvation-induced binding between NBR2 and endogenous AMPK beta and gamma subunits (Fig. 5d), likely mediated by NBR2 interaction with endogenous AMPK alpha subunit. In vitro binding assay using purified AMPK alpha and in vitro-synthesized biotinylated NBR2 confirmed the direct binding between NBR2 and AMPK alpha	26999735;30134946	RID02448	interact with protein
Urinary bladder cancer	UCA1	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000198793	NA	652995	2475	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02449	expression association
Urinary bladder cancer	UCA1	STAT3	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000168610	NA	652995	6774	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ADMIO|ADMIO1|APRF|HIES	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02450	expression association
Urinary bladder cancer	UCA1	miR-143	negatively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	miRNA	ENSG00000214049	GRCh38_19:15828206-15836328	NA	NA	652995	NA	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	NA	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02451	expression association
Urinary bladder cancer	UCA1	HK2	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000159399	NA	652995	3099	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	HKII|HXK2	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR-STAT3/microRNA143-HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells.	24890811;30134946	RID02452	expression association
Hepatocellular carcinoma	LINC00462	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+);PI3K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233610	GRCh38_13:48576974-48578088	NA	NA	100129597	NA	NA	NA	Long noncoding RNA linc00462 promotes hepatocellular carcinoma progression. Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway.	28622593;30134946	RID02453	expression association
Hepatocellular carcinoma	LINC00462	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	metabolic process(+);PI4K/AKT signaling pathway(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000233610	GRCh38_13:48576974-48578088	ENSG00000142208	NA	100129597	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA linc00462 promotes hepatocellular carcinoma progression. Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway.	28622593;30134946	RID02454	expression association
Cholangiocarcinoma	MALAT1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);PI3K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells.The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway.	28592124;30134946	RID02455	expression association
Cholangiocarcinoma	MALAT1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);PI4K/AKT signaling pathway(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000142208	NA	378938	207	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells.The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway.	28592124;30134946	RID02456	expression association
Chronic myeloid leukemia	HULC	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	NA	NA	728655	NA	HCCAT1|LINC00078|NCRNA00078	NA	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548;30134946	RID02457	expression association
Chronic myeloid leukemia	HULC	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	PI4K/AKT signaling pathway(+);cell proliferation(-);apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Leukemia	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000142208	NA	728655	207	HCCAT1|LINC00078|NCRNA00078	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2.Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	28069548;30134946	RID02458	expression association
Cervical cancer	CDKN2B-AS1	PI3K	positively-E	RNAi	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	NA	NA	100048912	NA	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Long non-coding RNA ANRIL indicates a poor prognosis of cervical cancer and promotes carcinogenesis via PI3K/Akt pathways.Our results showed that the expression of lncRNA ANRIL was significantly increased both in cervical cancer tissues and cell lines.Finally, western blot indicated that the PI3K/Akt pathway was found to be inactivated in cervical cancer cells after ANRIL inhibition.	27899255;30134946	RID02459	expression association
Cervical cancer	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	PI4K/AKT signaling pathway(+);tumorigenesis(+)	NA	association	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	Long non-coding RNA ANRIL indicates a poor prognosis of cervical cancer and promotes carcinogenesis via PI3K/Akt pathways.Our results showed that the expression of lncRNA ANRIL was significantly increased both in cervical cancer tissues and cell lines.Finally, western blot indicated that the PI3K/Akt pathway was found to be inactivated in cervical cancer cells after ANRIL inhibition.	27899255;30134946	RID02460	expression association
Non-small cell lung cancer	LINC00473	STK11	negatively-E	luciferase reporter assay	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cell growth(+);metabolic process(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000118046	NA	90632	6794	C6orf176|LNC473|bA142J11.1	LKB1|PJS|hLKB1	cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth.Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription.	27140397;30134946	RID02461	expression association
Non-small cell lung cancer	LINC00473	NONO	interact	RIP;western blot	upregulation	qPCR;microarray	TCGA	LUSC_LUAD.zip	cAMP signaling pathway(+);metabolic process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000112541	GRCh38_6:165924048-165988039	ENSG00000147140	NA	90632	4841	C6orf176|LNC473|bA142J11.1	MRXS34|NMT55|NRB54|P54|P54NRB|PPP1R114	cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth.Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription.	27140397;30134946	RID02462	interact with protein
Nasopharynx carcinoma	CDKN2B-AS1	SLC2A1	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000117394	NA	100048912	6513	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CSE|DYT17|DYT18|DYT9|EIG12|GLUT|GLUT-1|GLUT1|GLUT1DS|HTLVR|PED|SDCHCN	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02463	expression association
Nasopharynx carcinoma	CDKN2B-AS1	LDHA	positively-E	RNAi	upregulation	qPCR	NA	NA	glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000134333	NA	100048912	3939	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	GSD11|HEL-S-133P|LDHM|PIG19	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02464	expression association
Nasopharynx carcinoma	CDKN2B-AS1	AKT1	positively-E	RNAi	upregulation	qPCR	NA	NA	mTOR signaling pathway(+);glucose metabolic process(+)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Nasopharynx carcinoma	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000142208	NA	100048912	207	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells.Taken together, these data demonstrated that ANRIL could increase the expression of Glut1 and LDHA in NPC cells. Both ANRIL and Glut1 or LDHA can contribute to NPC progression. The possible mechanism of how ANRIL regulating the expression of Glut1 and LDHA may be that ANRIL promotes the phosphorylation of Akt to activate the mTOR signal pathway, which can up-regulate the expression of Glut1 and LDHA. Subsequently, the glucose uptake would be enhanced, and the increased glucose could be reprogrammed to aerobic glycolysis for rapid ATP production for proliferation.	27557514;30134946	RID02465	expression association
Malignant glioma	CRNDE	MTOR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell invasion(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000198793	NA	NA	2475	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	CRNDE, a long-noncoding RNA, promotes glioma cell growth and invasion through mTOR signaling. In this study, the upregulation of CRNDE was confirmed in both primary specimens from glioma patients and in vitro with cell lines. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma.	25813405;30134946	RID02466	expression association
Cervical cancer	LNMICC	NPM1	interact	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	lipid metabolic process(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENST00000518880	GRCh38_8:81279871-81281446	ENSG00000181163	NA	NA	4869	NA	B23|NPM	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02467	interact with protein
Cervical cancer	LNMICC	FABP5	interact	RNAi	upregulation	qPCR	NA	NA	lipid metabolic process(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENST00000518880	GRCh38_8:81279871-81281446	ENSG00000164687	NA	NA	2171	NA	E-FABP|EFABP|KFABP|PA-FABP|PAFABP	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02468	expression association
Cervical cancer	miR-190	LNMICC	negatively-F	RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	lipid metabolic process(-);cell metastasis(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	miRNA	lncRNA	NA	NA	ENST00000518880	GRCh38_8:81279871-81281446	NA	NA	NA	NA	LNMICC Promotes Nodal Metastasis of Cervical Cancer by Reprogramming Fatty Acid Metabolism. Functional investigations demonstrated that LNMICC promoted lymph node metastasis by reprogramming fatty acid metabolism, by recruiting the nuclear factor NPM1 to the promoter of the fatty acid binding protein FABP5. We also found that the prometastatic effects of LNMICC were directly targeted and suppressed by miR-190.More importantly, we found that LNMICC targeted the FABP5 promoter region through directly interaction with NPM1, thus mediating fatty acid metabolism reprogramming and finally promoting the process of lymphangiogenesis and EMT in cervical cancer. Meanwhile, our data also indicated that the function of LNMICC could be suppressed by miR-190 via directly targeting the miRNA-binding site in cervical cancer cells.	29229603;30134946	RID02469	ceRNA or sponge
Cholangiocarcinoma	TUG1	SIRT3	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	glutamine metabolic process(+);prognosis(-)	ceRNA(miR-145)	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000142082	NA	55000	23410	LINC00080|NCRNA00080|TI-227H	SIR2L3	LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis. We found that TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that sponges miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. In view of the above results, we used the TargetScan algorithm to find out whether glutaminase (GLS), glutamate dehydrogenase (GDH), and/or their regulators are targets of miR-145. Results revealed Sirt3, a positive regulator of GDH [21], and glutaminase 1 (GLS1) as potential targets of miR-145 (Figure 7A). Transfection experiments showed that ectopic expression of miR-145 significantly reduced Sirt3 and GDH, but not GLS1 protein levels (Figure 7B). To confirm that Sirt3 is a direct target of miR-145, the full length 3-UTR fragments of Sirt3 and corresponding mutant counterparts were cloned directly downstream of the firefly luciferase gene.	29371936	RID02470	ceRNA or sponge
Cholangiocarcinoma	TUG1	GLUD1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	glutamine metabolic process(+);prognosis(-)	NA	regulation	NA	NA	NA	NA	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000148672	NA	55000	2746	LINC00080|NCRNA00080|TI-227H	GDH|GDH1|GLUD	LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis. We found that TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that sponges miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. In view of the above results, we used the TargetScan algorithm to find out whether glutaminase (GLS), glutamate dehydrogenase (GDH), and/or their regulators are targets of miR-145. Results revealed Sirt3, a positive regulator of GDH [21], and glutaminase 1 (GLS1) as potential targets of miR-145 (Figure 7A). Transfection experiments showed that ectopic expression of miR-145 significantly reduced Sirt3 and GDH, but not GLS1 protein levels (Figure 7B). To confirm that Sirt3 is a direct target of miR-145, the full length 3-UTR fragments of Sirt3 and corresponding mutant counterparts were cloned directly downstream of the firefly luciferase gene.	29371936	RID02471	expression association
Esophagus squamous cell carcinoma	SBF2-AS1	CDKN1A	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000124762	NA	283104	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	Upregulated long non-coding RNA SBF2-AS1 promotes proliferation in esophageal squamous cell carcinoma. Patients with advanced ESCC exhibited increased upregulation of SBF2-AS1.Gene Set Enrichment Analysis revealed that genes associated with cell cycle biological processes, including the cancer suppressor gene cyclin-dependent kinase 1A (CDKN1A), were significantly associated with SBF2-AS1 in ESCC tissues. Further validation confirmed that CDKN1A expression levels were increased in ECA-109 cells following SBF2-AS1 silencing. The results of the present study demonstrate that SBF2-AS1 is significantly upregulated in ESCC, and that silencing of SBF2-AS1 inhibits the proliferative and invasive ability of ESCC cells. SBF2-AS1 may be a novel biomarker and therefore a potential therapeutic target for ESCC.	29552140	RID02472	expression association
Non-small cell lung cancer	SBF2-AS1	CDKN1A	negatively-E	RNAi;RIP;ChIP	upregulation	microarray	GSE19804	GSE19804.zip	cell proliferation(+)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000124762	NA	283104	1026	NA	CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1	High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer. High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer.We speculated that SBF2-AS1 might negatively regulate P21. RNA immunoprecipitation discovered that SBF2-AS2 could bind with a core component of polycomb repressive complex2, SUZ12. Additionally chromatin immunoprecipitation assay demonstrated that, after silencing SBF2-AS1, the enrichment of SUZ12 and trimethylation of histone 3 lysine 27 decreased at the promoter region of P21.We demonstrated that SBF2-AS1 is upregulated in NSCLC and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients.	27154193	RID02473	epigenetic regulation
Non-small cell lung cancer	SBF2-AS1	SUZ12	interact	RIP	upregulation	microarray	GSE19804	GSE19804.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000246273	GRCh38_11:9758268-9811335	ENSG00000178691	NA	283104	23512	NA	CHET9|JJAZ1	High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer. High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer.We speculated that SBF2-AS1 might negatively regulate P21. RNA immunoprecipitation discovered that SBF2-AS2 could bind with a core component of polycomb repressive complex2, SUZ12. Additionally chromatin immunoprecipitation assay demonstrated that, after silencing SBF2-AS1, the enrichment of SUZ12 and trimethylation of histone 3 lysine 27 decreased at the promoter region of P21.We demonstrated that SBF2-AS1 is upregulated in NSCLC and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients.	27154193	RID02474	interact with protein
Esophagus squamous cell carcinoma	CASC9	LAMC2	positively-E	ChIP	upregulation	qPCR	NA	NA	cell metastasis(+);PI3K/AKT signaling pathway(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000058085	NA	101805492	3918	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	B2T|BM600|CSF|EBR2|EBR2A|LAMB2T|LAMNB2	LncRNA CASC9 promotes esophageal squamous cell carcinoma metastasis through upregulating LAMC2 expression by interacting with the CREB-binding protein. In this study, we found that CASC9 was significantly upregulated in ESCC tissues, with further analysis revealing that elevated CASC9 expression was associated with ESCC prognosis and metastasis. Mechanistically, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assay indicated that CASC9 could bind with the transcriptional coactivator CREB-binding protein (CBP) in the nucleus. Chromatin immunoprecipitation (ChIP) assay additionally illustrated that CASC9 increased the enrichment of CBP and H3K27 acetylation in the LAMC2 promoter, thereby upregulating LAMC2 expression. In conclusion, we demonstrate that CASC9 upregulates LAMC2 expression by binding with CBP and modifying histone acetylation. Activates the FAK-PI3K/Akt signaling pathways through upregulating LAMC2 expression by interacting with the CREB-binding protein	29511340;30223861	RID02475	epigenetic regulation
Esophagus squamous cell carcinoma	CASC9	CREBBP	interact	RIP	upregulation	qPCR	NA	NA	cell metastasis(+);PI4K/AKT signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000249395	GRCh38_8:75223127-75324741	ENSG00000005339	NA	101805492	1387	ESCCAL-1|ESSCAL1|LINC00981|linc-JPH1	CBP|KAT3A|MKHK1|RSTS|RSTS1	LncRNA CASC9 promotes esophageal squamous cell carcinoma metastasis through upregulating LAMC2 expression by interacting with the CREB-binding protein. In this study, we found that CASC9 was significantly upregulated in ESCC tissues, with further analysis revealing that elevated CASC9 expression was associated with ESCC prognosis and metastasis. Mechanistically, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assay indicated that CASC9 could bind with the transcriptional coactivator CREB-binding protein (CBP) in the nucleus. Chromatin immunoprecipitation (ChIP) assay additionally illustrated that CASC9 increased the enrichment of CBP and H3K27 acetylation in the LAMC2 promoter, thereby upregulating LAMC2 expression. In conclusion, we demonstrate that CASC9 upregulates LAMC2 expression by binding with CBP and modifying histone acetylation. Activates the FAK-PI3K/Akt signaling pathways through upregulating LAMC2 expression by interacting with the CREB-binding protein	29511340;30223861	RID02476	interact with protein
Esophagus squamous cell carcinoma	LUCAT1	DNMT1	interact	RIP	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	tumorigenesis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000130816	NA	100505994	1786	SCAL1|SCAT5	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The long noncoding RNA LUCAT1 promotes tumorigenesis by controlling ubiquitination and stability of DNA methyltransferase 1 in esophageal squamous cell carcinoma. LUCAT1 was significantly upregulated in ESCC cell lines and cancer tissue compared with normal cells and adjacent normal tissues.Moreover, LUCAT1 siRNA reduced DNA methyltransferase 1 (DNMT1) protein levels without affecting transcription. Patients with high LUCAT1 expression had significantly lower survival rates than patients with low LUCAT1 expression. Our results thus suggest that LUCAT1 regulates the stability of DNMT1 and inhibits the expression of tumor suppressors through DNA methylation, leading to the formation and metastasis of ESCC. We identified LUCAT1 as a potential target for drug development and as a biomarker for ESCC. Binds to DNMT1 and regulates its stability, inhibits the expression of tumor suppressors through DNA methylation.	29247823;30223861	RID02477	interact with protein
Esophagus squamous cell carcinoma	LINC01672	BPTF	interact	RIP	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/2 signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000171634	NA	100505887	2186	NMR	FAC1|FALZ|NEDDFL|NURF301	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02478	interact with protein
Esophagus squamous cell carcinoma	LINC01672	MMP3	positively-E	RNAi	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/3 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000149968	NA	100505887	4314	NMR	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02479	expression association
Esophagus squamous cell carcinoma	LINC01672	MMP10	positively-E	RNAi	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(+);cell invasion(+);chemoresistance(+);ERK1/4 signaling pathway(+)	NA	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228750	GRCh38_1:6724637-6730012	ENSG00000166670	NA	100505887	4319	NMR	SL-2|STMY2	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02480	expression association
Esophagus squamous cell carcinoma	NSUN2	LINC01672	negatively-E	RIP;RNA pull-down assay;mass spectrometry;RNA methylation assay	upregulation	sequencing;microarray	TCGA;GSE53625	ESCA.zip;GSE53625.zip	cell migration(-);cell invasion(-);chemoresistance(-);ERK1/5 signaling pathway(-)	DNA methylation	regulation	NA	cisplatin	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	PCG	lncRNA	ENSG00000037474	NA	ENSG00000228750	GRCh38_1:6724637-6730012	54888	100505887	MISU|MRT5|SAKI|TRM4	NMR	Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1beta and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. NMR could directly bind to chromatin regulator BPTF, and potentially promote MMP3 and MMP10 expression by ERK1/2 pathway through recruiting BPTF to chromatin.	29763634	RID02481	epigenetic regulation
Esophagus squamous cell carcinoma	SNHG16	ZEB1	positively-E	RIP;RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);epithelial to mesenchymal transition(+)	ceRNA(miR-140-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000163597	GRCh38_17:76557764-76565348	ENSG00000148516	NA	100507246	6935	Nbla10727|Nbla12061|ncRAN	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	SNHG16/miR-140-5p axis promotes esophagus cancer cell proliferation, migration and EMT formation through regulating ZEB1. RIP, RNA pulldown system and dual luciferase reporter assay further provided evidence that SNHG16 directly targets miR-140-5p by binding with microRNA binding site harboring in the SNHG16 sequence. Furthermore, bioinformatics analysis revealed that ZEB1 is a target of miR-140-5p in ESCC. Collectively, our findings suggested that SNHG16 could act as an oncogenic lncRNA that promotes tumor progression through acting as an endogenous 'sponge' by competing with miR-140-5p, thereby regulating target ZEB1.	29416674;30223861	RID02482	ceRNA or sponge
Esophagus squamous cell carcinoma	HOTAIR	CCND1	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell cycle(-)	ceRNA(miR-1)	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma.The lncRNA HOX transcript antisense RNA (HOTAIR) was reported to be dysregulated and correlated with the progression of ESCC.Besides, we found that HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. Taken together, our study elucidated a novel HOTAIR /miR-1/CCND1 regulatory axis in which HOTAIR acted as a competing endogenous RNA by sponging miR-1 and upregulated CCND1 expression, thereby facilitating the tumorigenesis of ESCC.	27816685	RID02483	ceRNA or sponge
Esophagus squamous cell carcinoma	HOTAIR	HK2	positively-E	RNAi;RIP;luciferase reporter assay	upregulation	qPCR	NA	NA	glucose metabolic process(+)	ceRNA(miR-125;miR-143)	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000159399	NA	100124700	3099	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HKII|HXK2	HOTAIR regulates HK2 expression by binding endogenous miR-125 and miR-143 in oesophageal squamous cell carcinoma progression.We highlight the molecular mechanisms by which HOTAIR could influence the expression of Hexokinase 2 (HK2) in ESCC through binding miR-125 and miR-143 directly. Taken together, this study identified a functional lncRNA HOTAIR involved with regulation of glycolysis via miRNA-125/miRNA-143-HK2 in ESCC cells. The competitive endogenous RNA(ceRNA) model of HOTAIR/miR-125 and miR143/HK2 interaction might serve as important targets for ESCC diagnosis and therapy.	29156804	RID02484	ceRNA or sponge
Esophagus squamous cell carcinoma	XIST	EZH2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell growth(+)	ceRNA(miR-101)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2.Our data indicated that XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines.Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression. Moreover, enforced expression of EZH2 significantly attenuated the anti-proliferation activity upon XIST knockdown. Conclusively, XIST plays an important role in malignant progression of ESCC via modulation of miR-101/EZH2 axis.Luciferase assays further confirmed that miR-101 could bind to the 3-UTR of EZH2. Based on the online database (http://starbase.sysu.edu.cn/), we searched for miRNAs containing complementary bases with XIST and focused on miR-101.XIST promotes tumor growth of ESCC via regulation of miR-101/EZH2 axis in vivo	29100288	RID02485	ceRNA or sponge
Esophagus squamous cell carcinoma	TUSC7	TMPRSS11E	positively-E	RIP;luciferase reporter assay;western blot	downregulation	qPCR	NA	NA	chemoresistance(-);cell proliferation(-)	ceRNA(miR-224)	regulation	NA	cisplatin;5-fluorouracil	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000243197	GRCh38_3:116709235-116723581	ENSG00000087128	NA	285194	28983	LINC00902|LSAMP-AS1|LSAMP-AS3|LSAMPAS3|NCRNA00295	DESC1|TMPRSS11E2	LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1.TUSC7 was downregulated in ESCC tissues and cells, and low TUSC7 indicated worse overall survival. TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224. We also confirmed DESC1 inhibited chemotherapy resistance of ESCC cells via EGFR/AKT.miR-224 could bind to the two sites of TUSC7.DESC1 was a direct target of miR-224.TUSC7 inhibited cell proliferation and chemotherapy resistance via miR-224-regulated DESC1	29530057	RID02486	ceRNA or sponge
Esophagus squamous cell carcinoma	LINC01503	DUSP6	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000139318	NA	100506119	1848	NA	HH19|MKP3|PYST1	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02487	interact with protein
Esophagus squamous cell carcinoma	LINC01503	MAPK1	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000100030	NA	100506119	5594	NA	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02488	expression association
Esophagus squamous cell carcinoma	LINC01503	MAPK3	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000102882	NA	100506119	5595	NA	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation.phospho-p44/42 MAPK (Erk1/2)	29454790	RID02489	expression association
Esophagus squamous cell carcinoma	LINC01503	PI3K	interact	RNAi;RNA pull-down assay	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	NA	regulation	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	NA	NA	100506119	NA	NA	NA	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02490	expression association
Esophagus squamous cell carcinoma	LINC01503	PA2G4	interact	RNA pull-down assay;western blot	upregulation	qPCR;microarray	TCGA	ESCA.zip	cell migration(+);cell invasion(+);ERK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233901	GRCh38_9:129332300-129359541	ENSG00000170515	NA	100506119	5036	NA	EBP1|HG4-1|p38-2G4	Super-Enhancer-Driven Long Non-Coding RNA LINC01503, Regulated by TP63, Is Over-Expressed and Oncogenic in Squamous Cell Carcinoma. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients. LINC01503 Interacts With Both EBP-1 and ERK2.LINC01503 Activates Both PI3K/Akt and ERK/MAPK Signaling Pathways.we performed co-immunoprecipitation, which revealed that the interaction between DUSP-6 and ERK2 was increased in LINC01503 knockdown cells with or without EGF treatment, suggesting that binding of LINC01503 to ERK2 suppresses the interaction between DUSP-6 and ERK2 and thus inhibits ERK2 dephosphorylation	29454790	RID02491	interact with protein
Esophagus squamous cell carcinoma	EZR-AS1	SMYD3	interact	ChIP;RIP	upregulation	sequencing	SRP064894	SRP064894	cell motility(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000185420	NA	101409257	64754	NA	KMT3E|ZMYND1|ZNFN3A1|bA74P14.1	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.	29253179	RID02492	interact with protein
Esophagus squamous cell carcinoma	EZR-AS1	EZR	positively-E	RNAi;Immunofluorescence;RNA pull-down assay;luciferase reporter assay	upregulation	sequencing	SRP064895	SRP064895	cell motility(+);cell invasion(+)	transcriptional regulation;histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233893	GRCh38_6:158817979-158822252	ENSG00000092820	NA	101409257	7430	NA	CVIL|CVL|HEL-S-105|VIL2	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.	29253179	RID02493	transcriptional regulation;epigenetic regulation
Esophagus squamous cell carcinoma	AK001796	MDM2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111196350-111344098	ENSG00000135679	NA	NA	4193	NA	ACTFS|HDMX|hdm2	The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma. we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples.The results showed that MDM2 was downregulated and the expression of p53 and its target gene p21 were significantly upregulated in both Eca-109 and TE-1 cell lines after transfection with siRNA-AK001796 (Fig. 3a-c).	29568233;30223861	RID02494	expression association
Esophagus squamous cell carcinoma	AK001796	TP53	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000172965	GRCh38_2:111196350-111344098	ENSG00000141510	NA	NA	7157	NA	BCC7|BMFS5|LFS1|P53|TRP53	The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma. we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples.The results showed that MDM2 was downregulated and the expression of p53 and its target gene p21 were significantly upregulated in both Eca-109 and TE-1 cell lines after transfection with siRNA-AK001796 (Fig. 3a-c).	29568233;30223861	RID02495	expression association
Esophagus squamous cell carcinoma	CYTOR	EGFR	positively-E	starBase	upregulation	microarray	GSE53624	GSE53624.zip	cell growth(+)	ceRNA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000146648	NA	112597	1956	C2orf59|LINC00152|NCRNA00152	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	Construction of differential mRNA-lncRNA crosstalk networks based on ceRNA hypothesis uncover key roles of lncRNAs implicated in esophageal squamous cell carcinoma.crosstalks between LINC00152 and EGFR, LINC00240 and LOX gene family were identified, which were associated with the function of response to wounding and extracellular matrix-receptor interaction.	27966444;30223861	RID02496	ceRNA or sponge
Esophagus squamous cell carcinoma	CASC2	PTEN	positively-E	luciferase reporter assay	downregulation	qPCR	NA	NA	tumorigenesis(-);cell proliferation(-);cell invasion(-);apoptosis process(+)	ceRNA(miR-18a-5p)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000177640	GRCh38_10:118046279-118210158	ENSG00000171862	NA	255082	5728	C10orf5	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	The long noncoding RNA CASC2 inhibits tumorigenesis through modulating the expression of PTEN by targeting miR-18a-5p in esophageal carcinoma.We found the expression of CASC2 to be significantly downregulated in EC tissues and EC cell lines; moreover, low expression of CACS2 was associated with advanced TNM stage and lymph node metastases.Furthermore, upregulation of CASC2 significantly inhibited the proliferation of EC cells both in vitro and in vivo as well as their invasion in vitro; it also induced the apoptosis of EC9706 and EC1 cells. Our experiments suggest that CASC2, acting as a competing endogenous RNAs (ceRNAs) of miR-18a-5p, exerts its biological effects by modulating the expression of PTEN. These findings indicate that the CASC2-miR-18a-5p-PTEN axis may be a novel target for further studies aimed at the prevention and treatment of EC.	28964779;30223861	RID02497	ceRNA or sponge
Esophageal cancer	MALAT1	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway.Meanwhile, expression of Ezh2, Notch1, Hes1, MMP-9, and Vimentin was significantly decreased and expression of E-cadherin was significantly increased when cells were transfected with sh-MALAT1 compared with the nontransfected cells (P<0.05). However, when cells were cotransfected with both sh-MALAT1 and pcDNA3.1-Ezh2, the protein expression changes induced by sh-MALAT1 were recovered. MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	29916899;30223861	RID02498	expression association
Esophageal cancer	MALAT1	NOTCH1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148400	NA	378938	4851	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AOS5|AOVD1|TAN1|hN1	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway.Meanwhile, expression of Ezh2, Notch1, Hes1, MMP-9, and Vimentin was significantly decreased and expression of E-cadherin was significantly increased when cells were transfected with sh-MALAT1 compared with the nontransfected cells (P<0.05). However, when cells were cotransfected with both sh-MALAT1 and pcDNA3.1-Ezh2, the protein expression changes induced by sh-MALAT1 were recovered. MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	29916899;30223861	RID02499	expression association
Esophagus squamous cell carcinoma	TTN-AS1	SNAI1	positively-E	luciferase reporter assay	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000124216	NA	100506866	6615	NA	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02500	ceRNA or sponge
Esophagus squamous cell carcinoma	TTN-AS1	FSCN1	positively-E	luciferase reporter assay	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	ceRNA(miR-133b)	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000075618	NA	100506866	6624	NA	FAN1|HSN|SNL|p55	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02501	ceRNA or sponge
Esophagus squamous cell carcinoma	TTN-AS1	ELAVL1	positively-E	RIP	upregulation	microarray	GSE97051	GSE97051.zip	cell invasion(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000237298	GRCh38_2:178521183-178779963	ENSG00000066044	NA	100506866	1994	NA	ELAV1|HUR|Hua|MelG	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade. Moreover, lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR, which further promotes ESCC invasion cascades.	29101304;30223861	RID02502	expression association
Esophagus squamous cell carcinoma	HOTTIP	WDR5	positively-F	RIP;RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196363	NA	100316868	11091	HOXA-AS6|HOXA13-AS1|NCRNA00213	BIG-3|CFAP89|SWD3	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells;harboring a miR-30b-binding site, HOTTIP as a molecular sponge mainly regulated miR-30b level in the nucleus and modulated the repression of HOXA13 mediated by miR-30b in the cytoplasm, resulting in the positive HOTTIP/HOXA13 correlation;HOTTIP upregulation snail1 by competitively binding miR-30b, subsequently promoting epithelial-mesenchymal transition (EMT) and invasion. HOTTIP recruits WDR5 to the HOXA13 promoter and activates HOXA13 transcription. HOTTIP directly bound the adaptor protein WDR5 and drove histone H3 lysine 4 trimethylation and HOXA13 gene transcription in ESCC cells.	28534516	RID02503	interact with protein
Esophagus squamous cell carcinoma	HNF1A-AS1	VEGFA	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000112715	NA	283460	7422	C12orf27|HAS1|NCRNA00262	MVCD1|VEGF|VPF	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4; HAS1-siRNA also restrained the expression of migration marker proteins matrix metalloproteinase-9 (MMP-9) and vascular endothelial cell growth factor (VEGF).	28656277;30223861	RID02504	expression association
Esophagus squamous cell carcinoma	HNF1A-AS1	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000100985	NA	283460	4318	C12orf27|HAS1|NCRNA00262	CLG4B|GELB|MANDP2|MMP-9	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR-214 to upregulate the expression of SOX-4; HAS1-siRNA also restrained the expression of migration marker proteins matrix metalloproteinase-9 (MMP-9) and vascular endothelial cell growth factor (VEGF).	28656277;30223861	RID02505	expression association
Esophagus squamous cell carcinoma	POU6F2-AS2	YBX1	interact	RIP	upregulation	qPCR	NA	NA	DNA repair(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Genome Instability and Mutation	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000233854	GRCh38_7:38980370-39013551	ENSG00000065978	NA	100689074	4904	NA	BP-8|CBF-A|CSDA2|CSDB|DBPB|EFI-A|MDR-NF1|NSEP-1|NSEP1|YB-1|YB1	Long noncoding RNA POU6F2-AS2 is associated with oesophageal squamous cell carcinoma. Here, we describe a novel lncRNA POU6F2-AS2 specifically expressed in OSCC. POU6F2-AS2 is involved in the DNA damage response and regulates cells survival after ionizing radiation. POU6F2-AS2 interacts with Ybx1 protein and regulates its chromatin localization. Our current study represents the first description of an OSCC associated lncRNA that modulates DNA repair.	27033944;30223861	RID02506	interact with protein
Esophagus squamous cell carcinoma	MALAT1	POU5F1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204531	NA	378938	5460	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	In vitro studies revealed that knock-down of MALAT1 reduced cell proliferation, migration and number of tumor spheres representing putative stem cell-like cells, along with increasing cell apoptosis. Moreover, MALAT1 downregulation induced a decrease of Beta-catenin, Lin28, EZH2 and EMT stem genes as OCT4, while promoted E-cadherin expression. Of note, EZH2 overexpression completely reverted repression of Beta-catenin and Lin28 induced by MALAT1-targeting siRNAs, thus supporting EZH2-dependent activity of MALAT1 in ESCC.	29739426;27015363	RID02507	expression association
Esophagus squamous cell carcinoma	MALAT1	NANOG	positively-E	RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	NA	association	NA	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000111704	NA	378938	79923	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting beta-catenin via Ezh2.We found that the MALAT1 expression level was higher in human ESCC tissues.  In our report, we found that down-regulation of MALAT1 notably declined the expression of beta-catenin, Lin28, Ezh2 and EMT stem genes, such as OCT4 and Nanog, while increased the E-cadherin expression level	27015363	RID02508	expression association
Gastric cancer	HOTAIR	EZH2	interact	RIP	upregulation	qPCR	NA	NA	chemoresistance(+);PI3K/AKT signaling pathway(+);WNT/beta-catenin signaling pathway(+);epithelial to mesenchymal transition(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	cisplatin	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/beta-catenin signaling pathways by up-regulating miR-34a;HOTAIR directly bound to miR-34a. LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer.RIP experiments were performed using the EZH2 antibodies for immunoprecipitation. The results of chromatin immunoprecipitation (ChIP) assays showed that EZH2 could directly bind to the promoter region of miR34a and mediate H3K27me3 modification, while knockdown of HOTAIR and EZH2 led to reduced EZH2 and H3K27 binding ability.	29080815;26136075;28970725	RID02509	interact with protein
Gastric cancer	HOTAIR	CDH1	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	HOX transcript antisense intergenic RNA represses E-cadherin expression by binding to EZH2 in gastric cancer. The expression of HOTAIR was up-regulated in GC tumorous tissues compared with the para-tumorous tissues. Significantly negative correlation between HOTAIR and E-cadherin was found in GC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 with the E-cadherin promoter. Knockdown of HOTAIR by siRNA in GC cells suppressed the migration and invasion of GC cells.	28970725	RID02510	epigenetic regulation
Gastric cancer	MALAT1	EZH2	interact	RIP	upregulation	sequencing	TCGA	STAD.zip	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 long ncRNA promotes gastric cancer metastasis by suppressing PCDH10.In particular, we found that long noncoding RNA (lncRNA) MALAT1 binds EZH2, suppresses the tumor suppressor PCDH10, and promotes gastric cellular migration and invasion.	26871474	RID02511	interact with protein
Anaplastic large cell lymphoma	MALAT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02512	interact with protein
Anaplastic large cell lymphoma	MALAT1	SUZ12	interact	RIP	upregulation	qPCR	NA	NA	prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178691	NA	378938	23512	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CHET9|JJAZ1	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02513	interact with protein
Anaplastic large cell lymphoma	MALAT1	BMI1	positively-E	RIP	upregulation	qPCR	NA	NA	prognosis(-)	histone modification	association	NA	NA	NA	NA	Cancer	Lymphoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000168283	NA	378938	648	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FLVI2/BMI1|PCGF4|RNF51|flvi-2/bmi-1	Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma. MALAT1 was most highly expressed in clinical samples and cell lines. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.	28412742	RID02514	epigenetic regulation
Breast cancer	MALAT1	TEAD1	interact	ChIRP-MS	upregulation	qPCR	NA	NA	cell metastasis(+)	protein stability	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000187079	NA	378938	7003	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AA|NTEF-1|REF1|TCF-13|TCF13|TEAD-1|TEF-1	Long noncoding RNA MALAT1 suppresses breast cancer metastasis.Mechanistically, the MALAT1 lncRNA binds and inactivates the prometastatic transcription factor TEAD, preventing TEAD from associating with its co-activator YAP and target gene promoters.Malat1 interacts with TEAD1's transactivation domain, the same domain that mediates the YAP-TEAD1 interaction. MALAT1 inhibits the transcriptional activity of TEAD. ITGB4 and VEGFA are TEAD target genes regulated by MALAT1.  Taken together, these data demonstrate that ITGB4 and VEGFA are TEAD target genes and are negatively regulated by MALAT1.	30349115	RID02515	interact with protein
Breast cancer	MALAT1	VEGFA	interact	RIP;ChIP;ChIRP	upregulation	qPCR	NA	NA	angiogenesis(-);cell metastasis(+)	interact with mRNA	binding/interaction	RNA-RNA	NA	NA	Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000112715	NA	378938	7422	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MVCD1|VEGF|VPF	The mutant p53-ID4 complex controls VEGFA isoforms by recruiting lncRNA MALAT1.In this study, we demonstrate that oncogenic splicing factor SRSF1 bridges MALAT1 to mutant p53 and ID4 proteins in breast cancer cells. Mutant p53 and ID4 delocalize MALAT1 from nuclear speckles and favor its association with chromatin. This enables aberrant recruitment of MALAT1 on VEGFA pre-mRNA and modulation of VEGFA isoforms expression. Interestingly, VEGFA-dependent expression signatures associate with ID4 expression specifically in basal-like breast cancers carrying TP53 mutations. Our results highlight a key role for MALAT1 in control of VEGFA isoforms expression in breast cancer cells expressing gain-of-function mutant p53 and ID4 proteins.In BC cells, oncogenic splicing factor SRSF1 bridges MALAT1 to mutant p53 and ID4 proteins, favoring its chromatin association and thus inducing the expression of various VEGF-A isoforms, indicating a role of MALAT1 in the promotion of angiogenesis	28652379;30349115	RID02516	interact with mRNA
Urinary bladder cancer	MALAT1	ZEB1	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000148516	NA	378938	6935	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AREB6|BZP|DELTAEF1|FECD6|NIL2A|PPCD3|TCF8|ZFHEP|ZFHX1A	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02517	expression association
Urinary bladder cancer	MALAT1	ZEB2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169554	NA	378938	9839	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	HSPC082|SIP-1|SIP1|SMADIP1|ZFHX1B	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02518	expression association
Urinary bladder cancer	MALAT1	SNAI2	positively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000019549	NA	378938	6591	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02519	expression association
Urinary bladder cancer	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);WNT signaling pathway(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition. We verified that MALAT-1 levels were upregulated in bladder cancer tissues compared with adjacent normal tissues. Downregulation of MALAT-1 resulted in a decrease of the epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. We further demonstrated that MALAT-1 promoted EMT by activating Wnt signaling in vitro.	22722759	RID02520	expression association
Hepatocellular carcinoma	MALAT1	MTOR	positively-E	RNAi	upregulation	sequencing	NA	NA	cancer progression(+);mTOR signaling pathway(+)	NA	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000198793	NA	378938	2475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FRAP|FRAP1|FRAP2|RAFT1|RAPT1|SKS	Long Noncoding RNA MALAT1 Promotes Hepatocellular Carcinoma Development by SRSF1 Upregulation and mTOR Activation. Here we report that the lncRNA MALAT1 is upregulation in hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induction of the oncogenic splicing factor SRSF1. Our results reveal a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulation.	27993818	RID02521	expression association
Osteosarcoma	MALAT1	RET	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	PI3K/AKT signaling pathway(+);cell stemness(+)	ceRNA(miR-129-5p)	regulation	NA	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis;Tissue Invasion and Metastasis;Limitless Replicative Potential	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000165731	NA	378938	5979	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CDHF12|CDHR16|HSCR1|MEN2A|MEN2B|MTC1|PTC|RET-ELE1	MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. Moreover, rescue experiment and luciferase reporter assay results indicated that MALAT1 modulates RET expression by sponging miR-129-5p in osteosarcomas. Furthermore, MALAT1 augmented the expression of downstream proteins of the RET-Akt pathway. Our data revealed for the first time that MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway and provides potential therapeutic targets for osteosarcoma treatment.	30481748	RID02522	ceRNA or sponge
Malignant glioma	MALAT1	MMP9	positively-E	RNAi	downregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100985	NA	378938	4318	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CLG4B|GELB|MANDP2|MMP-9	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02523	expression association
Malignant glioma	MALAT1	MAPK3	negatively-E	RNAi	downregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000102882	NA	378938	5595	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK-1|ERK1|ERT2|HS44KDAP|HUMKER1A|P44ERK1|P44MAPK|PRKM3|p44-ERK1|p44-MAPK	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02524	expression association
Malignant glioma	MALAT1	MAPK1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);ERK/MAPK signaling pathway(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000100030	NA	378938	5594	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ERK|ERK-2|ERK2|ERT1|MAPK2|P42MAPK|PRKM1|PRKM2|p38|p40|p41|p41mapk|p42-MAPK	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by downregulation of MMP2 and inactivation of ERK/MAPK signaling.In this study, quantitative reverse transcription PCR (qRT-PCR) was used to demonstrate that the expression of MALAT1 was lower than that in normal brain tissues.Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2). In conclusion, overall data demonstrated the tumor-suppressive role of MALAT1 in glioma by attenuating ERK/MAPK-mediated growth and MMP2-mediated invasiveness.Western blot analysis showed that downregulation of MALAT1 significantly increased the levels of phosphorylated ERK1/2, and upregulation of MALAT1 reduced the levels of phosphorylated ERK1/2, while no detectable changes were observed in the total levels of ERK1/2. Moreover, MALAT1 was shown to promote the invasion of cancer cell by inducing the expression of MMP9, and the activation of the ERK/MAPK pathway participates in this process	26938295	RID02525	expression association
Epithelial ovarian cancer	LINC01118	miR-134	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	sponge	binding/interaction	RNA-RNA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000222005	GRCh38_2:46698940-46822804	NA	NA	388948	NA	NA	NA	LINC01118 Modulates Paclitaxel Resistance of Epithelial Ovarian Cancer by Regulating miR-134/ABCC1. LINC01118 was highly expressed in EOC tissues and chemoresistant cells. Biological function experiments showed LINC01118 could facilitate paclitaxel resistance and promote migration and invasion while inhibiting apoptosis of EOC cells. Moreover, LINC01118 targets miR-134 and then affects ABCC1 expression. CONCLUSIONS LINC01118 acted as an oncogene and modulated EOC paclitaxel sensitivity by regulating miR-134/ABCC1.	30521500	RID02526	ceRNA or sponge
Epithelial ovarian cancer	LINC01118	ABCC1	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	paclitaxel	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000222005	GRCh38_2:46698940-46822804	ENSG00000103222	NA	388948	4363	NA	ABC29|ABCC|GS-X|MRP|MRP1	LINC01118 Modulates Paclitaxel Resistance of Epithelial Ovarian Cancer by Regulating miR-134/ABCC1. LINC01118 was highly expressed in EOC tissues and chemoresistant cells. Biological function experiments showed LINC01118 could facilitate paclitaxel resistance and promote migration and invasion while inhibiting apoptosis of EOC cells. Moreover, LINC01118 targets miR-134 and then affects ABCC1 expression. CONCLUSIONS LINC01118 acted as an oncogene and modulated EOC paclitaxel sensitivity by regulating miR-134/ABCC1.	30521500	RID02527	expression association
Ovarian cancer	PVT1	SOX2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell proliferation(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000181449	NA	5820	6657	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ANOP3|MCOPS3	Long non-coding RNA PVT1 functions as an oncogene in ovarian cancer via upregulating SOX2.Compared with normal tissues, the expression of lnc-PVT1 T1 was remarkably upregulated in tumor tissues.Moreover, both the mRNA and protein levels of SOX2 were suppressed after knockdown of lnc-PVT1 in vitro. Besides, the expression of SOX2 in tumor tissues was positively correlated to lnc-PVT1. Lnc-PVT1 could enhance the invasion and proliferation of ovarian cancer cells through upregulating SOX2, which might serve as a new therapeutic target for the treatment of ovarian cancer.	30468460	RID02528	expression association
Colon cancer	PVT1	RUNX2	positively-E	luciferase reporter assay;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);cell proliferation(+)	ceRNA(miR-30d-5p)	regulation	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Colon cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000124813	NA	5820	860	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	AML3|CBF-alpha-1|CBFA1|CCD|CCD1|CLCD|OSF-2|OSF2|PEA2aA|PEBP2aA	Long non-coding RNA PVT1 functions as an oncogene in human colon cancer through miR-30d-5p/RUNX2 axis. PVT1 expression was significantly higher in tumor tissues than in peritumoral tissues, and was associated with lymph node metastasis, tumor stage and survival time of these patients.PVT1 expression was significantly higher in tumor tissues than in peritumoral tissues, and was associated with lymph node metastasis, tumor stage and survival time of these patients.These results indicate that PVT1 could promote metastasis and proliferation of colon cancer via suppressing miR-30d-5p/RUNX2 axis, which may offer a new way for interpreting the mechanism of colon cancer development.	29552759	RID02529	ceRNA or sponge
Ovarian cancer	PVT1	EZH2	interact	RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA PVT1 promotes ovarian cancer progression by silencing miR-214.The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines.The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.	30197791	RID02530	interact with protein
Ovarian cancer	PVT1	miR-214	negatively-E	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000249859	GRCh38_8:127794526-128187101	NA	NA	5820	NA	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	NA	LncRNA PVT1 promotes ovarian cancer progression by silencing miR-214.The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines.The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.	30197791	RID02531	epigenetic regulation
Ovarian cancer	DANCR	IGF2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000167244	NA	57291	3481	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	C11orf43|GRDF|IGF-II|PP9974	Long non-coding RNA DANCR upregulates IGF2 expression and promotes ovarian cancer progression.The expression of DANCR in ovarian cancer samples was significantly higher than that of the corresponding normal tissues.In addition, both the mRNA and protein expression levels of insulin-like growth factor 2 (IGF2) were remarkably upregulated after DANCR overexpression. Furthermore, the results found that the expression level of IGF2 was positively correlated with DANCR expression in ovarian cancer tissues. In this study, we revealed that DANCR could enhance the proliferation, migration and invasion capacities of ovarian cancer cells by upregulating IGF2. Our findings might offer a potential therapeutic choice for patients with ovarian cancer.	31114986	RID02532	expression association
Gastric cancer	HOXA11-AS	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell cycle(-);cell metastasis(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948;27651312	RID02533	interact with protein
Gastric cancer	HOXA11-AS	KDM1A	interact	RIP	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000004487	NA	221883	23028	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	AOF2|BHC110|CPRF|KDM1|LSD1	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02534	interact with protein
Gastric cancer	HOXA11-AS	DNMT1	interact	RIP	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000130816	NA	221883	1786	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02535	interact with protein
Gastric cancer	HOXA11-AS	miR-1297	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE58828;GSE50710;GSE51575;GSE65801;TCGA	GSE58828.zip;GSE50710.zip;GSE51575.zip;GSE65801.zip;STAD.zip	cell proliferation(+);cell invasion(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000240990	GRCh38_7:27184507-27189298	NA	NA	221883	NA	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer.	27651312	RID02536	ceRNA or sponge
Cancer	H19	miR-675	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02537	expression association
Cancer	H19	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000039068	NA	283120	999	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02538	expression association
Cancer	H19	SNAI2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000019549	NA	283120	6591	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	SLUG|SLUGH|SLUGH1|SNAIL2|WS2D	Oncofetal H19 RNA promotes tumor metastasis. Our results present novel mechanistic insights into a critical role for H19 RNA in tumor progression and indicate a previously unknown link between H19/miR-675, Slug and E-cadherin in the regulation of cancer cell EMT programs. In patients, we detected high H19 expression in all common metastatic sites tested, regardless of tumor primary origin. H19 RNA suppressed the expression of E-cadherin protein. H19 up-regulated Slug expression concomitant with the suppression of E-cadherin protein through a mechanism that involved miR-675. Slug also up-regulated H19 expression and activated its promoter. Altogether, these results may support the existence of a positive feedback loop between Slug and H19/miR-675, that regulates E-cadherin expression. H19 RNA enhanced the invasive potential of cancer cells in vitro and enhanced tumor metastasis in vivo.	24703882	RID02539	expression association
Endometrial cancer	H19	let-7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02540	expression association
Endometrial cancer	H19	HMGA2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02541	expression association
Endometrial cancer	H19	IGF2BP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136231	NA	283120	10643	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CT98|IMP-3|IMP3|KOC|KOC1|VICKZ3	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02542	expression association
Endometrial cancer	H19	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136997	NA	283120	4609	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MRTL|MYCC|bHLHe39|c-Myc	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02543	expression association
Ovarian cancer	H19	let-7	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000130600	GRCh38_11:1995176-2001470	NA	NA	283120	NA	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	NA	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02544	expression association
Ovarian cancer	H19	HMGA2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000149948	NA	283120	8091	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02545	expression association
Ovarian cancer	H19	IGF2BP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136231	NA	283120	10643	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	CT98|IMP-3|IMP3|KOC|KOC1|VICKZ3	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02546	expression association
Ovarian cancer	H19	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000136997	NA	283120	4609	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	MRTL|MYCC|bHLHe39|c-Myc	Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation.Here, we report that H19 promotes tumor cell migration and invasion by inhibiting let-7, a potent tumor suppressor microRNA that functions to posttranscriptionally suppress the expression of oncogenes that regulate cell growth and motility. We show that H19 depletion impairs, whereas its overexpression enhances the motility and invasiveness of tumor cells. These phenomena occur, at least in part through affecting let-7-mediated regulation of metastasis-promoting genes, including Hmga2, c-Myc and Igf2bp3. This H19/let-7-dependent regulation is recapitulated in vivo where co-expressions of oncogenes and H19 exist in both primary human ovarian and endometrial cancers.	25088204	RID02547	expression association
Ovarian cancer	CDKN2B-AS1	MET	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000105976	NA	100048912	4233	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	AUTS9|DFNB97|HGFR|RCCP2|c-Met	Long non-coding RNA ANRIL predicts poor prognosis and promotes invasion/metastasis in serous ovarian cancer. We found that ANRIL levels were elevated in SOC tissues compared with normal controls and were highly correlated with advanced FIGO stage, high histological grade, lymph node metastasis, and poor prognosis. SiRNA-mediated ANRIL silencing in these cells impaired cell migration and invasion. Based on the metastasis-related mRNA microarray analysis and subsequent western blotting confirmation, we found that MET and MMP3 are key downstream genes of ANRIL involved in SOC cell migration/invasion.	25845387	RID02548	expression association
Ovarian cancer	CDKN2B-AS1	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000149968	NA	100048912	4314	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Long non-coding RNA ANRIL predicts poor prognosis and promotes invasion/metastasis in serous ovarian cancer. We found that ANRIL levels were elevated in SOC tissues compared with normal controls and were highly correlated with advanced FIGO stage, high histological grade, lymph node metastasis, and poor prognosis. SiRNA-mediated ANRIL silencing in these cells impaired cell migration and invasion. Based on the metastasis-related mRNA microarray analysis and subsequent western blotting confirmation, we found that MET and MMP3 are key downstream genes of ANRIL involved in SOC cell migration/invasion.	25845387	RID02549	expression association
Prostate cancer	CDKN2B-AS1	CBX7	interact	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000100307	NA	100048912	23492	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	NA	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02550	interact with protein
Prostate cancer	CDKN2B-AS1	CDKN2B	negatively-E	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147883	NA	100048912	1030	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CDK4I|INK4B|MTS2|P15|TP15|p15INK4b	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02551	epigenetic regulation
Prostate cancer	CDKN2B-AS1	CDKN2A	negatively-E	RNAi;western blot;ChIP;RNAi	upregulation	qPCR	NA	NA	senescence(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000147889	NA	100048912	1029	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ARF|CDK4I|CDKN2|CMM2|INK4|INK4A|MLM|MTS-1|MTS1|P14|P14ARF|P16|P16-INK4A|P16INK4|P16INK4A|P19|P19ARF|TP16	Molecular Interplay of the Non-coding RNA ANRIL and Methylated Histone H3 Lysine 27 by Polycomb CBX7 in Transcriptional Silencing of INK4a. Here we report that chromobox 7 (CBX7) within the Polycomb Repressive Complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between non-coding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a new mechanism by which non-coding RNA participates directly in epigenetic transcriptional repression. Model of ncRNA-mediated gene repression of the INK4b/ARF/INK4a locus by the Polycomb group complexes. Schematic model illustrating molecular interplay between methylated H3K27 (by EZH2 of PRC2) and ncRNA transcripts ANRIL for silencing of the INK4b/ARF/INK4a locus by Polycomb CBX7. Both PRC1 and PRC2 complexes are retained at a repression site of a target gene through their association with the nascent ANRIL transcripts of Pol II. Note that the stem loop RNA structure is used for illustration only; RNA/CBX7 binding could result in dissociation of PRC1 from H3K27me, leading to a reversal of transcriptional repression of the target gene.	20541999;21828241	RID02552	epigenetic regulation
Ovarian cancer	HOXA11-AS	VEGFA	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000112715	NA	221883	7422	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	MVCD1|VEGF|VPF	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02553	expression association
Ovarian cancer	HOXA11-AS	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000100985	NA	221883	4318	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CLG4B|GELB|MANDP2|MMP-9	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02554	expression association
Ovarian cancer	HOXA11-AS	CTNNB1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000168036	NA	221883	1499	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02555	expression association
Ovarian cancer	HOXA11-AS	CDH1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000039068	NA	221883	999	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02556	expression association
Ovarian cancer	HOXA11-AS	SNAI1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124216	NA	221883	6615	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02557	expression association
Ovarian cancer	HOXA11-AS	TWIST1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000122691	NA	221883	7291	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ACS3|BPES2|BPES3|CRS|CRS1|CSO|SCS|SWCOS|TWIST|bHLHa38	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02558	expression association
Ovarian cancer	HOXA11-AS	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000026025	NA	221883	7431	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	NA	Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer.HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin.	27737536	RID02559	expression association
Epithelial ovarian cancer	HOTAIR	MMP9	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02560	expression association
Epithelial ovarian cancer	HOTAIR	MMP3	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000149968	NA	100124700	4314	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02561	expression association
Epithelial ovarian cancer	HOTAIR	VIM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell metastasis(+);prognosis(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000026025	NA	100124700	7431	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival (OS) and disease-free survival (DFS).Moreover, the pro-metastatic effects of HOTAIR were partially mediated by the regulation of certain matrix metalloproteinases (MMPs) and epithelial-to-mesenchymal transition (EMT)-related genes. MMP9 and MMP3 are the downstream mediators of HOTAIR activity affecting EOC cell migration and invasion. As anticipated, the siRNA-mediated silencing of HOTAIR resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin and snail, suggesting that HOTAIR influences the EMT in EOC cells.	24662839	RID02562	expression association
Lung cancer	MEG3	PHLPP1	positively-E	IHC;luciferase reporter assay	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000081913	NA	55384	23239	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	PHLPP|PLEKHE1|PPM3A|SCOP	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02563	expression association
Lung cancer	MEG3	JUN	interact	RIP;RNAi	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000177606	NA	55384	3725	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	AP-1|AP1|c-Jun|p39	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02564	interact with protein
Lung cancer	MEG3	HIF1A	positively-E	RNAi	downregulation	qPCR	NA	NA	tumor malignant transformation(-)	NA	regulation	NA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000100644	NA	55384	3091	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	HIF-1-alpha|HIF-1A|HIF-1alpha|HIF1|HIF1-ALPHA|MOP1|PASD8|bHLHe78	LncRNA MEG3 downregulation mediated by DNMT3b contributes to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1a translation. In the present study, we discovered that nickel exposure led to MEG3 downregulation through its promoter hypermethylation, and MEG3 downregulation resulted in PHLPP1 transcriptional inhibition, consequently leading to HIF-1a protein translation elevation, and in turn promoting malignant transformation of human bronchial epithelial cells. Mechanistically, MEG3 downregulation was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, whereas PHLPP1 transcriptional inhibition was due to the decreasing interaction of MEG3 with its inhibitory transcription factor c-Jun. Moreover, HIF-1a protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1a protein translation, as well as malignant transformation of human bronchial epithelial cells.	28263966	RID02565	expression association
Epithelial ovarian cancer	CERNA2	HMGA2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000149948	NA	642934	8091	HOST2|lncRNA-HOST2	BABL|HMGI-C|HMGIC|LIPO|STQTL9	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02566	expression association
Epithelial ovarian cancer	CERNA2	DICER1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000100697	NA	642934	23405	HOST2|lncRNA-HOST2	DCR1|Dicer|Dicer1e|GLOW|HERNA|K12H4.8-LIKE|MNG1|RMSE2	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02567	expression association
Epithelial ovarian cancer	CERNA2	MYC	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000136997	NA	642934	4609	HOST2|lncRNA-HOST2	MRTL|MYCC|bHLHe39|c-Myc	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02568	expression association
Epithelial ovarian cancer	CERNA2	IMP3	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000285972	GRCh38_10:84167228-84172093	ENSG00000177971	NA	642934	55272	HOST2|lncRNA-HOST2	BRMS2|C15orf12|MRPS4	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Obvious down-regulation of HMGA2, c-Myc, Dicer and Imp3 were shown after transfection with siHOST2 and iCon, while co-transfection with siHOST2 and ilet-7 apparently relieved this inhibition.	25292198	RID02569	expression association
Epithelial ovarian cancer	CERNA2	let-7b	negatively-F	RNAi;western blot	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-);cell proliferation(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000285972	GRCh38_10:84167228-84172093	NA	NA	642934	NA	HOST2|lncRNA-HOST2	NA	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. Here we report, for the first time, that HOST2 promotes tumor cell migration, invasion and proliferation in epithelial ovarian cancer by working in key aspects of biological behaviors. In the present study, bioinformatics analysis indicated that HOST2 binds with microRNA let-7b, a potent tumor suppressor, which was then verified to target HOST2. Our results showed that HOST2 harbors a let-7b binding site and modulates let-7b availability by acting as a molecular sponge. HOST2 inhibits let-7b functions, which post-transcriptionally suppress the expression of targets, including some oncogenes that regulate cell growth and motility. Additionally, understanding HOST2/let-7b-dependent regulation may lead to alternative approaches for the diagnosis and cure of this deadly disease.	25292198	RID02570	ceRNA or sponge
Ovarian cancer	LSINCT5	NEAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000245532	GRCh38_11:65422774-65445540	101234261	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02571	expression association
Ovarian cancer	LSINCT5	PSPC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000121390	NA	101234261	55269	NA	PSP1	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02572	expression association
Breast cancer	LSINCT5	NEAT1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	lncRNA	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000245532	GRCh38_11:65422774-65445540	101234261	283131	NA	LINC00084|NCRNA00084|TncRNA|VINC	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02573	expression association
Breast cancer	LSINCT5	PSPC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000281560	GRCh38_5:2712591-2715237	ENSG00000121390	NA	101234261	55269	NA	PSP1	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation. We chose a subset of these genes to validate using qPCR and found that ten of these genes were indeed significantly affected by the LSINCT5 knockdown. Interestingly, two genes that were significantly downregulated were the lncRNA NEAT-1 and a protein coding gene PSPC1. We have therefore characterized a novel lncRNA that is overexpressed in breast and ovarian cancers, enhances cellular proliferation and may play a significant role in multiple processes.	21532345	RID02574	expression association
Ovarian cancer	LNCOC1	miR-34a	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE36668;GSE18520;GSE9891;GSE26193;GSE63885	GSE36668.zip;GSE18520.zip;GSE9891.zip;GSE26193.zip;GSE63885.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000253741	GRCh38_8:142701857-142727016	NA	NA	100288181	NA	Lnc-OC1	NA	A novel lncRNA, Lnc-OC1, promotes ovarian cancer cell proliferation and migration by sponging miR-34a and miR-34c.In the present study, we identified a novel lncRNA, LOC100288181 (named as Lnc-OC1), which acted as a key regulator in the development and progression of OC.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34a and miR-34c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34a and miR-34c. In conclusion, our results suggest that the Lnc-OC1-miR-34a/34c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.	29576507	RID02575	ceRNA or sponge
Ovarian cancer	LNCOC1	miR-34c	negatively-F	western blot;luciferase reporter assay	upregulation	qPCR;microarray;sequencing	GSE36668;GSE18520;GSE9891;GSE26193;GSE63885	GSE36668.zip;GSE18520.zip;GSE9891.zip;GSE26193.zip;GSE63885.zip	cell proliferation(+);cell migration(+)	sponge	binding/interaction	RNA-RNA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	miRNA	ENSG00000253741	GRCh38_8:142701857-142727016	NA	NA	100288181	NA	Lnc-OC1	NA	A novel lncRNA, Lnc-OC1, promotes ovarian cancer cell proliferation and migration by sponging miR-34a and miR-34c.In the present study, we identified a novel lncRNA, LOC100288181 (named as Lnc-OC1), which acted as a key regulator in the development and progression of OC.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34a and miR-34c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34a and miR-34c. In conclusion, our results suggest that the Lnc-OC1-miR-34a/34c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.	29576507	RID02576	ceRNA or sponge
Ovarian cancer	H19	NFE2L2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	regulation	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000116044	NA	283120	4780	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	HEBP1|IMDDHH|NRF2	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02577	expression association
Ovarian cancer	H19	NQO1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000181019	NA	283120	1728	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DHQU|DIA4|DTD|NMOR1|NMORI|QR1	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02578	expression association
Ovarian cancer	H19	GSR	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	Reprogramming Energy Metabolism	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000104687	NA	283120	2936	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GR|HEL-75|HEL-S-122m	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02579	expression association
Ovarian cancer	H19	G6PD	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000160211	NA	283120	2539	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	G6PD1	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02580	expression association
Ovarian cancer	H19	GCLC	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000001084	NA	283120	2729	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GCL|GCS|GLCL|GLCLC	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02581	expression association
Ovarian cancer	H19	GCLM	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000023909	NA	283120	2730	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	GLCLR	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02582	expression association
Ovarian cancer	H19	GSTP1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	chemoresistance(+);glutathione metabolic process(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000084207	NA	283120	2950	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	DFN7|FAEES3|GST3|GSTP|HEL-S-22|PI	The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.Additionally, we verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance.	27193186	RID02583	expression association
Ovarian cancer	ERLNC1	MMP2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000087245	NA	101929441	4313	ElncRNA1|TC0101441	CLG4|CLG4A|MMP-2|MMP-II|MONA|TBE-1	Effects of oestrogen on long noncoding RNA expression in oestrogen receptor alpha-positive ovarian cancer cells. Particularly, elevated TC0101441 expression was correlated with lymph node metastasis, showing a metastatic potential. Results of in vitro assays further confirmed the pro-metastatic effect of TC0101441 and revealed that knockdown of TC0101441 also impaired E2-induced EOC cell migration/invasion by at least partly, regulating MMP2 and MMP3.	24380700	RID02584	expression association
Ovarian cancer	ERLNC1	MMP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000230550	GRCh38_1:204141404-204143327	ENSG00000149968	NA	101929441	4314	ElncRNA1|TC0101441	CHDS6|MMP-3|SL-1|STMY|STMY1|STR1	Effects of oestrogen on long noncoding RNA expression in oestrogen receptor alpha-positive ovarian cancer cells. Particularly, elevated TC0101441 expression was correlated with lymph node metastasis, showing a metastatic potential. Results of in vitro assays further confirmed the pro-metastatic effect of TC0101441 and revealed that knockdown of TC0101441 also impaired E2-induced EOC cell migration/invasion by at least partly, regulating MMP2 and MMP3.	24380700	RID02585	expression association
Ovarian cancer	HOTAIR	CCNE1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000105173	NA	100124700	898	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CCNE|pCCNE1	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02586	expression association
Ovarian cancer	HOTAIR	BRCA1	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000012048	NA	100124700	672	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BRCAI|BRCC1|BROVCA1|FANCS|IRIS|PNCA4|PPP1R53|PSCP|RNF53	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02587	expression association
Ovarian cancer	HOTAIR	BCL2	positively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02588	expression association
Ovarian cancer	HOTAIR	CASP3	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02589	expression association
Ovarian cancer	HOTAIR	CASP9	negatively-E	RNAi;western blot	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(-);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000132906	NA	100124700	842	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	APAF-3|APAF3|ICE-LAP6|MCH6|PPP1R56	The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis.Mechanistic research demonstrated that HOTAIR silencing retarded SOC cell cycle progression and promoted cell apoptosis by decreasing cyclin E, histone H1 (a histone mark associated with cyclin E), anti-apoptotic protein Bcl-2, tumour suppressor gene BRCA1 expression and increasing pro-apoptotic proteins caspase-9 and caspase-3 expression, which were related with cell cycle and apoptosis	25796453	RID02590	expression association
Ovarian cancer	HOTAIR	MMP9	positively-E	RNAi	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+)	NA	regulation	NA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28420874	RID02591	expression association
Ovarian cancer	PVT1	MYC	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 was suggested as a MYC activator. Investigation of the mechanism of silencing of PVT1 or MYC in ovarian and breast cancer cell lines demonstrated reduced levels of PVT1 or MYC inhibited cell proliferation, reduced levels of PVT1 but not MYC increased cell apoptosis, indicating that increased expression of both MYC and PVT1 contributed to the pathophysiology of ovarian cancer and breast cancer pathophysiology; however, PVT1 acted independently of MYC in generation of the apoptotic phenotype	17908964	RID02592	expression association
Breast cancer	PVT1	MYC	positively-E	RNAi;western blot	upregulation	qPCR;sequencing	TCGA	BRCA.zip	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	TF	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000136997	NA	5820	4609	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	MRTL|MYCC|bHLHe39|c-Myc	Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 was suggested as a MYC activator. Investigation of the mechanism of silencing of PVT1 or MYC in ovarian and breast cancer cell lines demonstrated reduced levels of PVT1 or MYC inhibited cell proliferation, reduced levels of PVT1 but not MYC increased cell apoptosis, indicating that increased expression of both MYC and PVT1 contributed to the pathophysiology of ovarian cancer and breast cancer pathophysiology; however, PVT1 acted independently of MYC in generation of the apoptotic phenotype	17908964;25043044	RID02593	expression association
Epithelial ovarian cancer	MEG3	TP53	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000141510	NA	55384	7157	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	BCC7|BMFS5|LFS1|P53|TRP53	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02594	expression association
Epithelial ovarian cancer	MEG3	GDF15	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130513	NA	55384	9518	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	GDF-15|MIC-1|MIC1|NAG-1|PDF|PLAB|PTGFB	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02595	expression association
Epithelial ovarian cancer	MEG3	RB1	positively-E	RNAi	downregulation	qPCR	NA	NA	cell proliferation(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000139687	NA	55384	5925	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	OSRC|PPP1R130|RB|p105-Rb|pRb|pp110	Promoter hypermethylation influences the suppressive role of maternally expressed 3, a long non-coding RNA, in the development of epithelial ovarian cancer.In contrast to normal ovarian tissues, the expression of MEG3 was absent or decreased in most EOC tissues as well as in human EOC cell lines, and the promoter of the MEG3 gene was highly methylated in both cancer tissues and cell lines. Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. In addition, ectopic expression of MEG3 suppressed the proliferation and growth of OVCAR3 cells and promoted apoptosis. Finally, MEG3 activated p53 in OVCAR3 cells. In conclusion, our data suggest that MEG3 is epigenetically silenced in EOC due to promoter hypermethylation, which may contribute to the development of EOC.In vitro study indicated that over-expression of MEG3 in OVCAR3 cells inhibited proliferation and promoted apoptosis by promoting p53, GDF15 and RB1 expression	24859196	RID02596	expression association
Ovarian cancer	AB073614	AKT1	positively-E	RNAi	upregulation	qPCR;microarray	GSE18521;GSE38666	GSE18521.zip;GSE38666.zip	cell proliferation(+);prognosis(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Ovarian cancer	lncRNA	PCG	NA	GRCh38_3:149173591-149175492	ENSG00000142208	NA	NA	207	NA	AKT|CWS6|PKB|PKB-ALPHA|PRKBA|RAC|RAC-ALPHA	A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts (P < 0.01). Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway.	26299803	RID02597	expression association
Ovarian cancer	XIST	XIAP	positively-E	RNAi	downregulation	qPCR;microarray	NA	NA	apoptosis process(+);chemoresistance(-)	NA	association	NA	cisplatin	NA	Evading Apoptosis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000101966	NA	7503	331	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	API3|BIRC4|IAP-3|ILP1|MIHA|XLP2|hIAP-3|hIAP3	The charm of the results by Silver's and Xiao's researches raise the interesting that communication between BRCA1 and Xist-coated Xi may be a reflection of a larger role for BRCA1 in maintaining heterochromatin structure or function. Of note, Mechanistic investigations found that down-regulation of Xist might increase the expression level of X-linked inhibitor of apoptosis (XIAP) and block Taxol-induced apoptosis to cause resistance phenotype, suggesting that Xist may be a potential marker for chemotherapeutic responses in ovarian cancer.Down-regulated expression of XIAP has been shown to induce apoptosis in chemoresistant human ovarian cancer cells (24). Down-regulation of XIST might increase the expression level of XIAP and block drug-induced apoptosis to cause resistance phenotype.	12492109	RID02598	expression association
Lung adenocarcinoma	MALAT1	AURKB	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000178999	NA	378938	9212	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AIK2|AIM-1|AIM1|ARK-2|ARK2|AurB|IPL1|PPP1R48|STK-1|STK12|STK5|aurkb-sv1|aurkb-sv2	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02599	expression association
Lung adenocarcinoma	MALAT1	LAYN	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000204381	NA	378938	143903	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02600	expression association
Lung adenocarcinoma	MALAT1	HMMR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000072571	NA	378938	3161	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD168|IHABP|RHAMM	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02601	expression association
Lung adenocarcinoma	MALAT1	SLC26A2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000155850	NA	378938	1836	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	D5S1708|DTD|DTDST|EDM4|MST153|MSTP157	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02602	expression association
Lung adenocarcinoma	MALAT1	CCT4	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115484	NA	378938	10575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CCT-DELTA|Cctd|SRB	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02603	expression association
Lung adenocarcinoma	MALAT1	PTBP3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119314	NA	378938	9991	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ROD1	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02604	expression association
Lung adenocarcinoma	MALAT1	CTHRC1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164932	NA	378938	115908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02605	expression association
Lung adenocarcinoma	MALAT1	FHL1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell motility(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000022267	NA	378938	2273	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	FCMSU|FHL-1|FHL1A|FHL1B|FLH1A|KYOT|RBMX1A|RBMX1B|SLIM|SLIM-1|SLIM1|SLIMMER|XMPMA	MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes. The down-regulated genes in MALAT-1 KD cells included genes previously implicated in extracellular matrix and cytoskeleton regulation, such as LAYN, HMMR, SLC26A2, CCT4, CTHRC1 and FHL1. Tano et al. established a link between MALAT1 and transcriptional and/or post-transcriptional modulation of genes regulating cell motility, including AIM1, LAYN, HMMR, SLC26A2, CCT4, ROD1, CTHRC1, and FHL1. Schmidt then demonstrated that siRNA-mediated knockdown of MALAT1 significantly impaired migration and invasion in vitro.	20937273;29739426	RID02606	expression association
Non-small cell lung cancer	MALAT1	CXCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000163735	NA	378938	6374	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENA-78|SCYB5	MALAT1 is an oncogenic long non-coding RNA associated with tumor invasion in non-small cell lung cancer regulated by DNA methylation. Here we showed that the expression of MALAT1 was upregulated in non-small cell lung cancer cells (NSCLCs) or tissues as compared with the normal lung cell or tissues. Thus, the knockdown of MALAT1 led to decreased cell migration and invasion. Next we also found that CXCL5 as a downstream gene of MALAT1 regulated cell migration and invasion.	26884862	RID02607	expression association
Breast cancer	MALAT1	ELAVL1	interact	RIP;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	The Ribonucleic Complex HuR-MALAT1 Represses CD133 Expression and Suppresses Epithelial-Mesenchymal Transition in Breast Cancer. In this study, we show that a ribonucleoprotein complex including the long noncoding RNA MALAT1 and the RNA-binding protein HuR (ELAVL1) binds the CD133 promoter region to regulate its expression. In conclusion, our findings suggest that the failure of a repressive complex to form or stabilize in breast cancer promotes CD133 upregulation and an EMT-like program, providing new mechanistic insights underlying the control of prometastatic processes.	27197265	RID02608	interact with protein
Colon cancer	PTEN	MALAT1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	PCG	lncRNA	ENSG00000171862	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5728	378938	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02609	expression association
Colon cancer	MALAT1	EPCAM	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119888	NA	378938	4072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02610	expression association
Colon cancer	MALAT1	ITGB4	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132470	NA	378938	3691	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD104|GP150	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02611	expression association
Breast cancer	PTEN	MALAT1	positively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000171862	NA	ENSG00000251562	GRCh38_11:65497688-65506516	5728	378938	10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|TEP1	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02612	expression association
Breast cancer	MALAT1	EPCAM	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000119888	NA	378938	4072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DIAR5|EGP-2|EGP314|EGP40|ESA|HNPCC8|KS1/4|KSA|M4S1|MIC18|MK-1|TACSTD1|TROP1	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;29739426	RID02613	expression association
Breast cancer	MALAT1	ITGB4	negatively-E	RNA pull-down assay;luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000132470	NA	378938	3691	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD104|GP150	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. We identified the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) as a target of PTEN and find that this regulation is conserved in both human and mouse as well as with both chronic and acute PTEN dysregulation Recent work by Kwok et al. unveiled a tumor suppressive role of MALAT1 in BC and colorect cancer, where MALAT1 was induced by the tumor suppressor PTEN and negatively affected the expression of genes implicated in migration and invasion, such as EpCAM and ITGB4	29574704;30349115;29739426	RID02614	expression association
Cervical cancer	MALAT1	miR-375	negatively-F	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	sponge	binding/interaction	RNA-RNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.	27658300	RID02615	ceRNA or sponge
Cervical cancer	MALAT1	CDH2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(-)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170558	NA	378938	1000	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD325|CDHN|CDw325|NCAD	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.	27658300	RID02616	expression association
Endometrial carcinoma	PCDH10	MALAT1	negatively-E	RNAi	upregulation	qPCR;microarray	NA	NA	Wnt/beta-catenin signaling pathway(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Endometrial cancer	PCG	lncRNA	ENSG00000138650	NA	ENSG00000251562	GRCh38_11:65497688-65506516	57575	378938	OL-PCDH|PCDH19	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	A novel wnt regulatory axis in endometrioid endometrial cancer.MALAT1 as a downstream target of the protocad herin10 (PCDH10) gene, a Wnt pathway negative regulatory element, shedding light on a novel targetable PCDH10-Wnt/beta-catenin-MALAT1 axis. Gene expression profiling revealed as part of the transcriptomic changes induced by PCDH10 a reduction in levels of MALAT1, a long noncoding RNA, that mediated tumor suppression functions of PCDH10 in EEC cells. We found that MALAT1 transcription was regulated by Wnt/beta-catenin signaling via TCF promoter binding and PCDH10 decreased MALAT1 by modulating this pathway.	25085246	RID02617	expression association
Hepatocellular carcinoma	MALAT1	CCAR2	interact	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000158941	NA	378938	57805	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DBC-1|DBC1|KIAA1967|NET35|p30 DBC|p30DBC	Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation. The interaction between MALAT1 and depleted in breast cancer 1 (DBC1) was validated using RNA pull-down and RNA immunoprecipitation. Further mechanistic studies reveal that MALAT1 binding competes with the interaction between sirtuin1 (SIRT1) and DBC1, which then releases SIRT1 and enhances its deacetylation activity. Consequently, the deacetylation of p53 reduces the transcription of a spectrum of its downstream target genes, promotes cell proliferation and inhibits cell apoptosis. Our results uncover a novel mechanism by which MALAT1 regulates the activity of p53 through the lncRNA-protein interaction.	28973437	RID02618	interact with protein
Hepatocellular carcinoma	MALAT1	TP53	negatively-E	RNA pull-down assay;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	histone modification	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000141510	NA	378938	7157	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCC7|BMFS5|LFS1|P53|TRP53	Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation. The interaction between MALAT1 and depleted in breast cancer 1 (DBC1) was validated using RNA pull-down and RNA immunoprecipitation. Further mechanistic studies reveal that MALAT1 binding competes with the interaction between sirtuin1 (SIRT1) and DBC1, which then releases SIRT1 and enhances its deacetylation activity. Consequently, the deacetylation of p53 reduces the transcription of a spectrum of its downstream target genes, promotes cell proliferation and inhibits cell apoptosis. Our results uncover a novel mechanism by which MALAT1 regulates the activity of p53 through the lncRNA-protein interaction.	28973437	RID02619	epigenetic regulation
Esophagus squamous cell carcinoma	MALAT1	CDH1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell stemness(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	In vitro studies revealed that knock-down of MALAT1 reduced cell proliferation, migration and number of tumor spheres representing putative stem cell-like cells, along with increasing cell apoptosis. Moreover, MALAT1 downregulation induced a decrease of beta-catenin, Lin28, EZH2 and EMT stem genes as OCT4, while promoted E-cadherin expression. Of note, EZH2 overexpression completely reverted repression of Beta-catenin and Lin28 induced by MALAT1-targeting siRNAs, thus supporting EZH2-dependent activity of MALAT1 in ESCC.	29739426	RID02620	expression association
Esophagus squamous cell carcinoma	MALAT1	MIA2	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000150527	NA	378938	4253	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CTAGE5|MEA6|MGEA|MGEA11|MGEA6|TALI	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02621	expression association
Esophagus squamous cell carcinoma	MALAT1	HNF4G	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164749	NA	378938	3174	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NR2A2|NR2A3	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02622	expression association
Esophagus squamous cell carcinoma	MALAT1	ROBO1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000169855	NA	378938	6091	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	DUTT1|SAX3	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02623	expression association
Esophagus squamous cell carcinoma	MALAT1	CCT4	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000115484	NA	378938	10575	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CCT-DELTA|Cctd|SRB	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02624	expression association
Esophagus squamous cell carcinoma	MALAT1	CTHRC1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000164932	NA	378938	115908	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Interestingly, tumor suppressor miR-101 and miR-217 acted as post-transcriptional regulators of MALAT1, whose silencing induced cell cycle arrest by p21 and p27 upregulation, and b-MYB inhibition. miR-101 and miR-217 overexpression or MALAT1 knockdown via miRNA mimics and siRNAs respectively, inhibited migration and invasion capabilities of ESCC cells, and were accompanied by deregulation of MALAT1 downstream metastasis-associated genes MIA2, HNF4G, ROBO1, CCT4, and CTHRC1	25538231	RID02625	expression association
Gastric cancer	MALAT1	IGF1R	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000140443	NA	378938	3480	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD221|IGFIR|IGFR|JTK13	Moreover, knock-down of MALAT1 in GC cells inhibited cell proliferation, cell cycle progression, migration and invasion, and promoted apoptosis. Mechanistically, miR-122-IGF-1R signaling was found involved in dysregulated MALAT1 expression. Indeed, enforced miR-122 expression inhibited, whereas miR-122 inhibitor increased MALAT1 in GC cell lines. miR-122-mediated regulation of MALAT1 involved IGF-1R, a target of miR-122, whose expression positively correlated with MALAT1 in GC cell lines	27486823;29739426	RID02626	expression association
Gastric cancer	MALAT1	miR-122	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);cell migration(+);cell invasion(+);apoptosis process(-)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Moreover, knock-down of MALAT1 in GC cells inhibited cell proliferation, cell cycle progression, migration and invasion, and promoted apoptosis. Mechanistically, miR-122-IGF-1R signaling was found involved in dysregulated MALAT1 expression. Indeed, enforced miR-122 expression inhibited, whereas miR-122 inhibitor increased MALAT1 in GC cell lines. miR-122-mediated regulation of MALAT1 involved IGF-1R, a target of miR-122, whose expression positively correlated with MALAT1 in GC cell lines	27486823;29739426	RID02627	expression association
Pancreatic ductal adenocarcinoma	MALAT1	ELAVL1	interact	RNA pull-down assay;RIP;western blot	upregulation	qPCR	NA	NA	cell autophagy(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000066044	NA	378938	1994	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ELAV1|HUR|Hua|MelG	Long Noncoding RNA MALAT1 Promotes Aggressive Pancreatic Cancer Proliferation and Metastasis via the Stimulation of Autophagy.Mechanistically, we found that MALAT1 interacted with RNA binding protein HuR, and silencing of MALAT1 greatly enhanced the posttranscriptional regulation of TIA-1 and had further effects on inhibiting autophagy. MALAT1 was speculated to regulate tumorigenesis via HuR-TIA-1-mediated autophagic activation.	27371730	RID02628	interact with protein
Pancreatic ductal adenocarcinoma	MALAT1	TIA1	negatively-E	RNA pull-down assay;western blot	upregulation	qPCR	NA	NA	cell autophagy(+)	NA	association	NA	NA	NA	Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000116001	NA	378938	7072	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	TIA-1|WDM	Long Noncoding RNA MALAT1 Promotes Aggressive Pancreatic Cancer Proliferation and Metastasis via the Stimulation of Autophagy.Mechanistically, we found that MALAT1 interacted with RNA binding protein HuR, and silencing of MALAT1 greatly enhanced the posttranscriptional regulation of TIA-1 and had further effects on inhibiting autophagy. MALAT1 was speculated to regulate tumorigenesis via HuR-TIA-1-mediated autophagic activation.	27371730	RID02629	expression association
Pancreatic cancer	MALAT1	LATS1	positively-E	western blot;IHC	upregulation	qPCR	NA	NA	Hippo/YAP signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000131023	NA	378938	9113	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	WARTS|wts	Study on mechanism about long noncoding RNA MALAT1 affecting pancreatic cancer by regulating Hippo-YAP signaling. The microarray analysis determined that lncRNA MALAT1 in pancreatic cancer was highly expressed. LncRNA MALAT1 presented an extremely high expression level in pancreatic cancer tissues and cells. After transfected with si-MALAT1, the proliferation of AsPC-1 cells decreased, induce apoptosis of AsPC-1 cells, and migration and invasion ability were reduced. The tendency of LATS1 expression level was down-regulated and YAP1 show the opposite trend in the Hippo-YAP signaling. The in vivo assay was found that the tumor to be small in size and volume, and the expression of Ki-67 was decreased. High expression of lncRNA MALAT1 in PC disorder the proliferation, apoptosis, and migration and invasion ability via influence Hippo-YAP signaling pathway.	29215734	RID02630	expression association
Pancreatic cancer	MALAT1	YAP1	negatively-E	western blot;IHC	upregulation	qPCR	NA	NA	Hippo/YAP signaling pathway(+);cell proliferation(-);cell migration(-);cell invasion(-);apoptosis process(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis;Evading Apoptosis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000137693	NA	378938	10413	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	COB1|YAP|YAP2|YAP65|YKI	Study on mechanism about long noncoding RNA MALAT1 affecting pancreatic cancer by regulating Hippo-YAP signaling. The microarray analysis determined that lncRNA MALAT1 in pancreatic cancer was highly expressed. LncRNA MALAT1 presented an extremely high expression level in pancreatic cancer tissues and cells. After transfected with si-MALAT1, the proliferation of AsPC-1 cells decreased, induce apoptosis of AsPC-1 cells, and migration and invasion ability were reduced. The tendency of LATS1 expression level was down-regulated and YAP1 show the opposite trend in the Hippo-YAP signaling. The in vivo assay was found that the tumor to be small in size and volume, and the expression of Ki-67 was decreased. High expression of lncRNA MALAT1 in PC disorder the proliferation, apoptosis, and migration and invasion ability via influence Hippo-YAP signaling pathway.	29215734	RID02631	expression association
Osteosarcoma	MALAT1	CDH1	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	histone modification	regulation	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID02632	interact with protein
Osteosarcoma	TGFB1	MALAT1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Osteosarcoma	PCG	lncRNA	ENSG00000105329	NA	ENSG00000251562	GRCh38_11:65497688-65506516	7040	378938	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2; lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin; MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown	28388584	RID02633	expression association
Osteosarcoma	MALAT1	RHOA	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+)	NA	association	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067560	NA	378938	387	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ARH12|ARHA|RHO12|RHOH12	Long noncoding RNA MALAT1 as a potential therapeutic target in osteosarcoma.Furthermore, MALAT1 knockdown delayed tumor growth in an osteosarcoma xenograft model. Specifically, we found that administration of MALAT1 siRNA decreased the protein levels of RhoA and its downstream effectors Rho-associated coiled-coil containing protein kinases (ROCKs). We observed that MALAT1 expression was up-regulated in human osteosarcoma cell lines and tissues.	26575981	RID02634	expression association
Osteosarcoma	MALAT1	ROCK1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000067900	NA	378938	6093	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	P160ROCK|ROCK-I	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.Furthermore, we confirmed that MALAT1 and ROCK1/ROCK2 which were targeted by microRNA-144-3p (miR-144-3p) shared the same miR-144-3p combining site. Furthermore, the constructed luciferase assay verified that MALAT1 was a target of miR-144-3p.Finally, we affirmed that an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overly expressed in osteosarcoma.	28938647;26575981	RID02635	ceRNA or sponge
Osteosarcoma	MALAT1	ROCK2	positively-E	RNAi	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+);cell proliferation(+)	ceRNA(miR-144-3p)	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000134318	NA	378938	9475	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ROCK-II	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.Furthermore, we confirmed that MALAT1 and ROCK1/ROCK2 which were targeted by microRNA-144-3p (miR-144-3p) shared the same miR-144-3p combining site. Furthermore, the constructed luciferase assay verified that MALAT1 was a target of miR-144-3p.Finally, we affirmed that an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overly expressed in osteosarcoma.	28938647;26575981	RID02636	ceRNA or sponge
Peripheral primitive neuroectodermal tumor	SYK	MALAT1	positively-E	RIP;luciferase reporter assay;ChIP;IHC	upregulation	qPCR;microarray	GSE93677	GSE93677.zip	cell proliferation(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Sarcoma	PCG	lncRNA	ENSG00000165025	NA	ENSG00000251562	GRCh38_11:65497688-65506516	6850	378938	p72-Syk	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Identification of a Novel SYK/c-MYC/MALAT1 Signaling Pathway and Its Potential Therapeutic Value in Ewing Sarcoma. Ectopic expression of SYK rescued the cytotoxicity triggered by SYK-depletion associated with the reactivation of both AKT and MYC; MALAT1, was identified to be dependent on SYK-mediated signaling;c-MYC, a SYK-promoted gene, bound to the promoter of MALAT1 and transcriptionally activated MALAT1, which further promoted the proliferation of EWS cells	28336564	RID02637	transcriptional regulation
Colorectal cancer	MALAT1	EZH2	interact	RIP;ChIP;western blot	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	oxaliplatin	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2.MALAT1 is overexpressed in colorectal cancer patients and correlated with tumor metastasis. LncRNA MALAT1 knockdown enhances E-cadherin expression and inhibits oxaliplatin-induced EMT in colorectal cancer cells. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin.	28069878	RID02638	interact with protein
Colon cancer	MALAT1	AKAP9	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000127914	NA	378938	10142	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	AKAP-9|AKAP350|AKAP450|CG-NAP|HYPERION|LQT11|MU-RMS-40.16A|PPP1R45|PRKA9|YOTIAO	Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1. By genome-wide profiling, Yang et al. showed that among 243 genes regulated by MALAT1 in CRC cells, PRKA kinase anchor protein 9 (AKAP-9) was significantly upregulated at both mRNA and protein level. Of note, knockdown of AKAP-9 rescued MALAT1-induced CRC cell proliferation, migration and invasion. MALAT1 was also associated with colon cancer progression by stimulating tumor associated dendritic cells (TADC)-derived production of CCL5; consistently, MALAT1 blockade by siRNAs significantly dampened CCL5-induced migration and invasion of CRC cells	25546229;29739426	RID02639	expression association
Colon cancer	MALAT1	CCL5	positively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Colon cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000271503	NA	378938	6352	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	D17S136E|RANTES|SCYA5|SIS-delta|SISd|TCP228|eoCP	Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1. By genome-wide profiling, Yang et al. showed that among 243 genes regulated by MALAT1 in CRC cells, PRKA kinase anchor protein 9 (AKAP-9) was significantly upregulated at both mRNA and protein level. Of note, knockdown of AKAP-9 rescued MALAT1-induced CRC cell proliferation, migration and invasion. MALAT1 was also associated with colon cancer progression by stimulating tumor associated dendritic cells (TADC)-derived production of CCL5; consistently, MALAT1 blockade by siRNAs significantly dampened CCL5-induced migration and invasion of CRC cells	25546229;29739426	RID02640	expression association
Multiple myeloma	MALAT1	SP1	interact	RIP;ChIP;luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	biomarker;tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Sustained Angiogenesis	Cancer	Myeloma	lncRNA	TF	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000185591	NA	378938	6667	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Activation of LTBP3 gene by a long noncoding RNA (lncRNA) MALAT1 transcript in mesenchymal stem cells from multiple myeloma. Our data suggested that lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1, and recruitment of Sp1 to the promoter.Our knowledge of the role of MALAT1 in cellular transformation is pointing toward its potential use as a biomarker and a target for novel therapeutic approaches in multiple myeloma.Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	25187517;29290968	RID02641	interact with protein
Multiple myeloma	MALAT1	EZH2	interact	ChIP;western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02642	interact with protein
Multiple myeloma	MALAT1	MCL1	negatively-E	western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000143384	NA	378938	4170	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	BCL2L3|EAT|MCL1-ES|MCL1L|MCL1S|Mcl-1|TM|bcl2-L-3|mcl1/EAT	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02643	expression association
Multiple myeloma	MALAT1	CDK6	negatively-E	western blot	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	NA	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000105810	NA	378938	1021	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	MCPH12|PLSTIRE	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02644	expression association
Multiple myeloma	MALAT1	miR-29a	positively-E	RNAi;ChIP	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02645	epigenetic regulation
Multiple myeloma	MALAT1	miR-29b	positively-E	RNAi;ChIP	upregulation	qPCR;microarray	GSE73454;GSE73452	GSE73454.zip;GSE73452.zip	tumor-suppressive function(-)	histone modification	regulation	NA	NA	NA	NA	Cancer	Myeloma	lncRNA	miRNA	ENSG00000251562	GRCh38_11:65497688-65506516	NA	NA	378938	NA	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	NA	Inhibition of EZH2 triggers the tumor suppressive miR-29b network in multiple myeloma. Knock-down of the EZH2-interacting long non-coding RNA MALAT1 also reduced H3K27me3 of miR-29a/b-1 promoter, along with induction of miR-29b and downregulation of miR-29b targets SP1, MCL-1 and CDK6.	29290968	RID02646	epigenetic regulation
Lung adenocarcinoma	HOTAIR	HELLS	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000119969	NA	100124700	3070	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ICF4|LSH|Nbla10143|PASG|SMARCA6	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.LSH (lymphoid-specific helicase), also called HELLS (helicase, lymphoid specific)	26658322	RID02647	interact with protein
Lung adenocarcinoma	HOTAIR	FOXA1	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129514	NA	100124700	3169	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3A|TCF3A	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.	26658322	RID02648	expression association
Lung adenocarcinoma	HOTAIR	FOXA2	negatively-E	RNAi	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000125798	NA	100124700	3170	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HNF3B|TCF3B	The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH.HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties. These data suggest that HOTAIR is an important mediator of the ratio of FOXA1 and FOXA2 and LSH involves in, and suggest that HOTAIR inhibition may represent a promising therapeutic option for suppressing lung ADC progression.	26658322	RID02649	expression association
Lung cancer	STAT3	HOTAIR	positively-E	ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	TF	lncRNA	ENSG00000168610	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6774	100124700	ADMIO|ADMIO1|APRF|HIES	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract.The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression.	25447409	RID02650	transcriptional regulation
Lung cancer	HOTAIR	miR-326	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR.	27186394	RID02651	expression association
Lung cancer	HOTAIR	PHOX2A	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000165462	NA	100124700	401	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ARIX|CFEOM2|FEOM2|NCAM2|PMX2A	MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR.	27186394	RID02652	expression association
Non-small cell lung cancer	HOTAIR	TP53	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	histone modification	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000141510	NA	100124700	7157	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCC7|BMFS5|LFS1|P53|TRP53	A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer.Our results showed that HOTAIR expression was significantly higher in the cancer tissues than that in the adjacent normal tissue, and was negatively correlated with p53 functionality rather than expression. We identified two binding sites of p53 on the promoter region of HOTAIR, where the p53 protein would bind to and suppress the HOTAIR mRNA transcription. Inversely, overexpression of lncRNA HOTAIR inhibited the expression of p53 in A549 cells. Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). Modulation of p53 expression alternated the lncRNA HOTAIR expression and cell invasion in NSCLC cells	27695348	RID02653	epigenetic regulation
Non-small cell lung cancer	TP53	HOTAIR	negatively-E	ChIP	upregulation	qPCR	NA	NA	cell invasion(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	TF	lncRNA	ENSG00000141510	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7157	100124700	BCC7|BMFS5|LFS1|P53|TRP53	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer.Our results showed that HOTAIR expression was significantly higher in the cancer tissues than that in the adjacent normal tissue, and was negatively correlated with p53 functionality rather than expression. We identified two binding sites of p53 on the promoter region of HOTAIR, where the p53 protein would bind to and suppress the HOTAIR mRNA transcription. Inversely, overexpression of lncRNA HOTAIR inhibited the expression of p53 in A549 cells. Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3). Modulation of p53 expression alternated the lncRNA HOTAIR expression and cell invasion in NSCLC cells	27695348	RID02654	transcriptional regulation
Lung cancer	HOTAIR	CTNNB1	negatively-E	RNAi	upregulation	qPCR	NA	NA	apoptosis process(+)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168036	NA	100124700	1499	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CTNNB|EVR7|MRD19|NEDSDV|armadillo	Radiotherapy induced Lewis lung cancer cell apoptosis via inactivating beta-catenin mediated by upregulated HOTAIR.	26339352	RID02655	expression association
Liver cancer	HOTAIR	CHUK	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000213341	NA	100124700	1147	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IKBKA|IKK-alpha|IKK1|IKKA|NFKBIKA|TCF16	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02656	epigenetic regulation
Liver cancer	HOTAIR	IKBKB	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000104365	NA	100124700	3551	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	IKK-beta|IKK2|IKKB|IMD15|IMD15A|IMD15B|NFKBIKB	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02657	epigenetic regulation
Liver cancer	HOTAIR	IKBKG	negatively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	telomerase activity(+)	epigenetic regulation	regulation	NA	NA	CSC	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000269335	NA	100124700	8517	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AMCBX1|EDAID1|FIP-3|FIP3|Fip3p|IKK-gamma|IKKAP1|IKKG|IMD33|IP|IP1|IP2|IPD2|NEMO|ZC2HC9	Inflammatory related gene IKK-alpha, IKK-beta, IKK-gamma cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis. One study found that HOTAIR regulated the functions ofIKK-alpha/IKK-beta/IKK-gamma axis in HCC stem cells, implying that the cooperation of IKK-alpha, IKK-beta, IKK-gamma with HOTAR could be used as a potential novel therapeutic target for HCC treatment.	27367027	RID02658	epigenetic regulation
Hepatocellular carcinoma	HOTAIR	CCND1	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression.	28791413	RID02659	expression association
Hepatocellular carcinoma	HOTAIR	STAT3	positively-E	RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+);chemoresistance(+)	NA	association	NA	cisplatin	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168610	NA	100124700	6774	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADMIO|ADMIO1|APRF|HIES	Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression. Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway.	28791413;29250186	RID02660	expression association
Hepatocellular carcinoma	FOXC1	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Liver cancer	TF	lncRNA	ENSG00000054598	NA	ENSG00000228630	GRCh38_12:53962308-53974956	2296	100124700	ARA|ASGD3|FKHL7|FREAC-3|FREAC3|IGDA|IHG1|IRID1|RIEG3	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues; The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1. FOXC1 binding to the promoter region of HOTAIR was confirmed using a chromatin immunoprecipitation assay	27895772	RID02661	transcriptional regulation
Liver fibrosis	HOTAIR	EZH2	interact	luciferase reporter assay;RIP;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.To confirm the association of Hotair and epigenetic repressor, we performed RIP with an antibody against enhancer of zeste homologue 2 (EZH2, an important subunit of the PRC2 complex) from nuclear extracts of LX-2 cells. We observed significant enrichment of Hotair with the EZH2 antibody, but no enrichment of GAPDH compared with the nonspecific IgG control antibody (Fig. 7A). Using a specific antibody against SUZ12, another member of the PRC2 complex, we found Hotair enrichment, but not GAPDH mRNA enrichment (Fig. 7B).	27979710	RID02662	interact with protein
Liver fibrosis	HOTAIR	SUZ12	interact	luciferase reporter assay;RIP;ChIP	upregulation	qPCR	NA	NA	fibrotic(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Gastrointestinal system disease	Fibrosis	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000178691	NA	100124700	23512	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CHET9|JJAZ1	Hotair facilitates hepatic stellate cells activation and fibrogenesis in the liver. Furthermore, we found that Hotair may act as an endogenous 'sponge' of miR-148b, which regulates expression of the DNMT1/MEG3/p53 pathways in HSCs. Intriguingly, Hotair enhanced polycomb repressive complex 2 (PRC2) occupancy and histone H3K27me3 repressive marks, specifically at the MEG3 promoter region. Finally, we found that Hotair forms an RNA/DNA hybrid and recruits PRC2 to MEG3 promoter.To confirm the association of Hotair and epigenetic repressor, we performed RIP with an antibody against enhancer of zeste homologue 2 (EZH2, an important subunit of the PRC2 complex) from nuclear extracts of LX-2 cells. We observed significant enrichment of Hotair with the EZH2 antibody, but no enrichment of GAPDH compared with the nonspecific IgG control antibody (Fig. 7A). Using a specific antibody against SUZ12, another member of the PRC2 complex, we found Hotair enrichment, but not GAPDH mRNA enrichment (Fig. 7B).	27979710	RID02663	interact with protein
Hepatocellular carcinoma	HOTAIR	ABCB1	positively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	association	NA	cisplatin	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000085563	NA	100124700	5243	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ABC20|CD243|CLCS|GP170|MDR1|P-GP|PGY1	Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway.Together, these findings indicated that knockdown of HOTAIR in Huh7 cells decreased STAT3 activity and ABCB1 expression, and increased chemosensitivity to cisplatin. Thus HOTAIR could serve as a novel potential therapeutic target to reverse multidrug resistance in HCC.	29250186	RID02664	expression association
Prostate cancer	HOTAIR	PRC2	interact	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Infiltrating mast cells enhance prostate cancer invasion via altering LncRNA-HOTAIR/PRC2-androgen receptor (AR)-MMP9 signals and increased stem/progenitor cell population. Mechanism dissection revealed infiltrating mast cells could decrease AR transcription via modulation of the PRC2 complex with LncRNA-HOTAIR at the AR 5' promoter region in PCa cells. The consequences of suppressing AR may then increase PCa cell invasion via increased MMP9 expression and/or increased stem/progenitor cell population.	25895025;28082728	RID02665	interact with protein
Prostate cancer	HOTAIR	MMP9	positively-E	luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Infiltrating mast cells enhance prostate cancer invasion via altering LncRNA-HOTAIR/PRC2-androgen receptor (AR)-MMP9 signals and increased stem/progenitor cell population. Mechanism dissection revealed infiltrating mast cells could decrease AR transcription via modulation of the PRC2 complex with LncRNA-HOTAIR at the AR 5' promoter region in PCa cells. The consequences of suppressing AR may then increase PCa cell invasion via increased MMP9 expression and/or increased stem/progenitor cell population.	25895025;28082728	RID02666	expression association
Prostate cancer	miR-34a	HOTAIR	negatively-F	luciferase reporter assay	upregulation	qPCR;microarray	GSE47657	GSE47657.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-);cell cycle(+) 	sponge	binding/interaction	RNA-RNA	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	miRNA	lncRNA	NA	NA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.miR-34a directly targeted HOTAIR in PCa cells, which showed that genistein inhibited the growth of PCa cells by downregulating oncogenic HOTAIR that was also targeted by the tumor suppressor miR-34a.	23936419	RID02667	ceRNA or sponge
Prostate cancer	HOTAIR	EZH2	interact	luciferase reporter assay;ChIP	upregulation	qPCR;sequencing	TCGA	PRAD.zip	cell proliferation(+);cell migration(+);cell invasion(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development.	29141691;29221985	RID02668	interact with protein
Prostate cancer	HOTAIR	DNMT1	interact	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Prostate cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	HOTAIR-mediated reciprocal regulation of EZH2 and DNMT1 contribute to polyphyllin I-inhibited growth of castration-resistant prostate cancer cells in vitro and in vivo.Our results show that PPI inhibits growth of CRPC cells through inhibition of HOTAIR expression, subsequently; this results in the repression of DNMT1 and EZH2 expressions. The interactions among HOTAIR, DNMT1 and EZH2, and reciprocal regulation of DNMT1 and EZH2 contribute to the overall responses of PPI. This study reveals a novel mechanism for HOTAIR-mediated regulating DNMT1 and EZH2 in response to PPI in inhibition of the growth of CRPC cells.	29221985	RID02669	interact with protein
Breast cancer	RHOC	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	PCG	lncRNA	ENSG00000155366	NA	ENSG00000228630	GRCh38_12:53962308-53974956	389	100124700	ARH9|ARHC|H9|RHOH9	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02670	transcriptional regulation
Breast cancer	MRTFA	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	binding/interaction	protein-DNA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000196588	NA	ENSG00000228630	GRCh38_12:53962308-53974956	57591	100124700	BSAC|MAL|MKL|MKL1|MRTF-A	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02671	transcriptional regulation
Breast cancer	SRF	HOTAIR	positively-E	ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	prognosis(-)	transcriptional regulation	regulation	protein-DNA	NA	NA	NA	Cancer	Breast cancer	TF	lncRNA	ENSG00000112658	NA	ENSG00000228630	GRCh38_12:53962308-53974956	6722	100124700	MCM1	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.	28069441	RID02672	transcriptional regulation
Breast cancer	TGFB1	HOTAIR	positively-E	RNAi	upregulation	qPCR	NA	NA	cell stemness(+);epithelial to mesenchymal transition(+)	NA	regulation	NA	NA	NA	Limitless Replicative Potential;Tissue Invasion and Metastasis	Cancer	Breast cancer	PCG	lncRNA	ENSG00000105329	NA	ENSG00000228630	GRCh38_12:53962308-53974956	7040	100124700	CED|DPD1|IBDIMDE|LAP|TGFB|TGFbeta	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines EMT. contributes to tumor invasion and metastasis in many types of cancer and highly correlates with the acquisition of CSC characteristics. One study found that treatment with transforming growth factor beta 1 (TGF-betea1) increased HOTAIR expression and triggered EMT formation. Conversely, blockade of HOTAIR reversed the TGF-beta1-induced EMT and reduced the colony-forming capacity of breast cancer cells. This result indicated that HOTAIR was involved in multiple signaling pathways in EMT in breast cancer cells	24022994	RID02673	expression association
Breast cancer	HOTAIR	BCL2L2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	ceRNA(miR-206)	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000129473	NA	100124700	599	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL-W|BCL2-L-2|BCLW|PPP1R51	Long Noncoding RNA HOTAIR Modulates MiR-206-mediated Bcl-w Signaling to Facilitate Cell Proliferation in Breast Cancer.Moreover, the levels of HOTAIR were positively associated with those of Bcl-w in clinical breast cancer samples. As expected, we observed that HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. Mechanistically, we found that miR-206 was capable of inhibiting the expression of Bcl-w by directly binding to the 3'UTR of Bcl-w mRNA. Interestingly, HOTAIR could increase the expression of Bcl-w through sequestering miR-206 at post-transcriptional level.	29222472	RID02674	ceRNA or sponge
Colorectal cancer	HOTAIR	miR-545	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	association	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent. High HOTAIR expression levels inhibited miR-545, thereby increasing CRC cell proliferation.Differential expressions of HOTAIR, miR-545, and EGFR were observed in cancerous tissues in comparison to non-cancerous tissues. By expressional management of miR-545, we observed that miR-545 negatively regulated cell proliferation. Also luciferase reporter assay revealed that miR-545 inhibited regulated EGFR expression by affecting its 3'-UTR activity. In addition, miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. Monitoring of tumor growth in mice showed that miR-545 overexpression suppressed LOVO tumor growth. Our data suggested that HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.	28364379	RID02675	expression association
Colorectal cancer	HOTAIR	EGFR	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+)	NA	regulation	NA	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000146648	NA	100124700	1956	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ERBB|ERBB1|HER1|NISBD2|PIG61|mENA	MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent. High HOTAIR expression levels inhibited miR-545, thereby increasing CRC cell proliferation.Differential expressions of HOTAIR, miR-545, and EGFR were observed in cancerous tissues in comparison to non-cancerous tissues. By expressional management of miR-545, we observed that miR-545 negatively regulated cell proliferation. Also luciferase reporter assay revealed that miR-545 inhibited regulated EGFR expression by affecting its 3'-UTR activity. In addition, miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. Monitoring of tumor growth in mice showed that miR-545 overexpression suppressed LOVO tumor growth. Our data suggested that HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.	28364379	RID02676	expression association
Colorectal cancer	HOTAIR	miR-218	negatively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	epigenetic regulation	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02677	epigenetic regulation
Colorectal cancer	HOTAIR	VOPP1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	NA	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000154978	NA	100124700	81552	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ECOP|GASP|WBP1L2	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02678	expression association
Colorectal cancer	HOTAIR	NFKB1	positively-E	luciferase reporter assay;ChIP	upregulation	qPCR	NA	NA	NF-kB signaling pathway(+);chemoresistance(+)	NA	regulation	NA	5-fluorouracil	NA	Sustained Angiogenesis	Cancer	Colorectal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer.Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-kB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC.	28918035	RID02679	expression association
Cervical cancer	HOTAIR	RPS6KB1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell viability(+);apoptosis process(-);cell growth(+)	NA	regulation	NA	propofol	NA	Evading Apoptosis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000108443	NA	100124700	6198	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	PS6K|S6K|S6K-beta-1|S6K1|STK14A|p70 S6KA|p70(S6K)-alpha|p70-S6K|p70-alpha	Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer	26523512	RID02680	expression association
Ovarian cancer	HOTAIR	NFKB1	positively-E	ChIP;luciferase reporter assay;RNAi;luciferase reporter assay	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+);prognosis(-)	transcriptional regulation	regulation	protein-DNA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28118613;29843138;28420874	RID02681	transcriptional regulation
Ovarian cancer	HOTAIR	IL6	positively-E	luciferase reporter assay;RNAi	upregulation	qPCR;sequencing	TCGA	OV.zip	DNA damage(+);chemoresistance(+);senescence(+);NF-kB signaling pathway(+);prognosis(-)	NA	regulation	NA	cisplatin;platinum	NA	Genome Instability and Mutation;Sustained Angiogenesis	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000136244	NA	100124700	3569	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer.To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. We show that HOTAIR regulates activation of NF-kB by decreasing Ik-Ba (NF-kB inhibitor) and establish that by inducing prolonged NF-kB activation and expression of NF-kB target genes during DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity. Our findings suggest that an NF-kB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers.In response to DNA damage, we found that NF-kB directly upregulates HOTAIR expression in OC cell lines. Downregulation of Ik-Ba during DDR induced a NF-kB-HOTAIR signaling positive-feedback loop cascade, and we demonstrate that DDR further induces HOTAIR-mediated expression of p65-NF-kB and NF-kB target genes MMP9 and IL-6 to promote OC cellular senescence and resistance to DNA-damaging agents. Collectively, these results are the first to demonstrate a role for HOTAIR in DNA damage-induced NF-kB signaling pathway.	27041570;28118613;29843138;28420874	RID02682	expression association
Ovarian cancer	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	platinum	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02683	interact with protein
Breast cancer	HOTAIR	NFKB1	negatively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000109320	NA	100124700	4790	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CVID12|EBP-1|KBF1|NF-kB1|NF-kappa-B1|NF-kappaB|NFKB-p105|NFKB-p50|NFkappaB|p105|p50	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02684	expression association
Breast cancer	HOTAIR	IL6	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000136244	NA	100124700	3569	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BSF-2|BSF2|CDF|HGF|HSF|IFN-beta-2|IFNB2|IL-6	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02685	expression association
Breast cancer	HOTAIR	MMP9	negatively-E	RNAi	upregulation	qPCR	NA	NA	chemoresistance(+)	NA	regulation	NA	platinum	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000100985	NA	100124700	4318	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CLG4B|GELB|MANDP2|MMP-9	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer. In the current study, we describe a peptide nucleic acids (PNA)-based approach to block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum. Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. Furthermore, the mechanism of action correlated with reduced nuclear factor-kappaB (NF-kB) activation and decreased expression of NF-kB target genes matrix metalloprotease 9 and interleukin 6.	28420874	RID02686	expression association
Head and neck squamous cell carcinoma	HOTAIR	BCL2	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000171791	NA	100124700	596	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Bcl-2|PPP1R50	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02687	expression association
Head and neck squamous cell carcinoma	HOTAIR	BAX	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000087088	NA	100124700	581	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL2L4	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02688	expression association
Head and neck squamous cell carcinoma	HOTAIR	CASP3	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Evading Apoptosis	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000164305	NA	100124700	836	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CPP32|CPP32B|SCA-1	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02689	expression association
Head and neck squamous cell carcinoma	HOTAIR	CYCS	negatively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-)	NA	regulation	NA	NA	NA	Reprogramming Energy Metabolism	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000172115	NA	100124700	54205	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CYC|HCS|THC4	Targeting HOTAIR Induces Mitochondria Related Apoptosis and Inhibits Tumor Growth in Head and Neck Squamous Cell Carcinoma in vitro and in vivo.Mitochondrial calcium uptake 1(MICU1) dependent cell death was induced by HOTAIR depletion. Protein expression analysis indicated that mitochondrial related cell death pathway (Bcl-2, BAX, Caspase-3, Cleaved Caspase-3, Cytochrome c) involved in HOTAIR dependent apoptosis process.	26592246	RID02690	expression association
Oral squamous cell carcinoma	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell invasion(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Oral cavity cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTAIR promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in oral squamous cell carcinoma. Furthermore, significant negative correlation between HOTAIR levels and E-cadherin levels was found in OSCC tissues and cell lines, and HOTAIR contributed to the regulation of E-cadherin through binding to EZH2 and H3K27me3 with the E-cadherin promoter.	25901533	RID02691	interact with protein
Laryngeal squamous cell carcinoma	HOTAIR	miR-21	negatively-E	RNAi	upregulation	qPCR	NA	NA	biomarker	NA	association	NA	NA	NA	NA	Cancer	Larynx cancer	lncRNA	miRNA	ENSG00000228630	GRCh38_12:53962308-53974956	NA	NA	100124700	NA	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	NA	Combined detection of serum exosomal miR-21 and HOTAIR as diagnostic and prognostic biomarkers for laryngeal squamous cell carcinoma.Serum exosomal miR-21 and HOTAIR were significantly correlated with the clinical parameters of laryngeal squamous cell carcinoma (LSCC) and combined evaluation of their serum expressions may be considered a valuable biomarker and promising predicting tool for LSCC.	25099764	RID02692	expression association
Esophagus squamous cell carcinoma	HOTAIR	SNAI1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02693	expression association
Esophagus squamous cell carcinoma	HOTAIR	CTNNB1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000168036	NA	100124700	1499	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	CTNNB|EVR7|MRD19|NEDSDV|armadillo	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02694	expression association
Esophagus squamous cell carcinoma	HOTAIR	CDH1	positively-E	RNAi	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	NA	association	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000039068	NA	100124700	999	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	The expression and significance of HOX transcript antisense RNA and epithelial-mesenchymal transition-related factors in esophageal squamous cell carcinoma.In the 96 ESCC tissues, HOTAIR mRNA expression levels were positively correlated with Snail mRNA and protein expression levels, and were negatively correlated with E-cadherin expression levels. HOTAIR mRNA expression levels were also positively correlated with beta-catenin mRNA expression levels. In conclusion, HOTAIR may be involved in carcinogenesis and metastasis, and may induce the expression of EMT-related factors; detection of these factors may assist in early diagnosis and prognostic prediction.	28260072	RID02695	expression association
Acute myeloid leukemia	HOTAIR	EZH2	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02696	expression association
Acute myeloid leukemia	HOTAIR	KDM1A	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02697	expression association
Acute myeloid leukemia	HOTAIR	DNMT3A	positively-E	RNAi;luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+);prognosis(-)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000119772	NA	100124700	1788	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	DNMT3A2|M.HsaIIIA|TBRS	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172;27748863	RID02698	ceRNA or sponge
Acute myeloid leukemia	HOTAIR	DNMT3B	positively-E	RNAi	upregulation	qPCR	NA	NA	prognosis(-)	NA	association	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000088305	NA	100124700	1789	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ICF|ICF1|M.HsaIIIB	Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls (P<0.05). Compared to patients with low HOTAIR expression, overall survival and event-free survival of patients with high HOTAIR expression was significantly reduced. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR (P<0.05).In conclusion, HOTAIR was closely related with a poor prognosis in AL patients. It may be involved in the development of leukemia by mediating methylation of DNA and histones.	27748863	RID02699	expression association
Acute promyelocytic leukemia	HOTAIRM1	ITGA4	positively-E	RNAi	upregulation	qPCR;microarray	GSE49516	GSE49516.zip	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000115232	NA	100506311	3676	HOXA-AS1|HOXA1-AS1|NCRNA00179	CD49D|IA4	Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.Blockade of HOTAIR myeloid 1 (HOTAIRM1), a human HOXA gene cluster and a novel myeloid-specific lncRNA, resulted in the retained expression of many otherwise all-trans retinoic acid (ATRA)-induced cell cycle and DNA replication genes, abated ATRA induction of cell surface leukocyte activation, defense response, and other maturation-related molecules, all of which were accompanied by the retained expression of the alpha-4-integrin gene (ITGA4) (CD49d) and decreased induction of integrin alpha X (ITGAX) (CD11c) in NB4 acute promyelocytic leukemia cells.	24824789	RID02700	expression association
Acute promyelocytic leukemia	HOTAIRM1	ITGAX	negatively-E	RNAi	upregulation	qPCR;microarray	GSE49516	GSE49516.zip	cell cycle(+)	NA	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000233429	GRCh38_7:27095647-27100265	ENSG00000140678	NA	100506311	3687	HOXA-AS1|HOXA1-AS1|NCRNA00179	CD11C|SLEB6	Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.Blockade of HOTAIR myeloid 1 (HOTAIRM1), a human HOXA gene cluster and a novel myeloid-specific lncRNA, resulted in the retained expression of many otherwise all-trans retinoic acid (ATRA)-induced cell cycle and DNA replication genes, abated ATRA induction of cell surface leukocyte activation, defense response, and other maturation-related molecules, all of which were accompanied by the retained expression of the alpha-4-integrin gene (ITGA4) (CD49d) and decreased induction of integrin alpha X (ITGAX) (CD11c) in NB4 acute promyelocytic leukemia cells.	24824789	RID02701	expression association
Melanoma	LINC00673	MMP9	positively-E	RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000100985	NA	100499467	4318	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	CLG4B|GELB|MANDP2|MMP-9	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02702	expression association
Melanoma	LINC00673	POU4F1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000152192	NA	100499467	5457	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	BRN3A|Oct-T1|RDC-1|brn-3A	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02703	interact with protein
Melanoma	LINC00673	AR	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	TF	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000169083	NA	100499467	367	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AIS|AR8|DHTR|HUMARA|HYSP1|KD|NR3C4|SBMA|SMAX1|TFM	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	RID02704	interact with protein
Non-small cell lung cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Lung cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02705	epigenetic regulation
Non-small cell lung cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02706	interact with protein
Non-small cell lung cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02707	interact with protein
Head and neck cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02708	epigenetic regulation
Head and neck cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02709	interact with protein
Head and neck cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Head and neck cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02710	interact with protein
Ovarian cancer	TARID	TCF21	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	DNA methylation	binding/interaction	RNA-DNA	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	TF	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000118526	NA	100507308	6943	EYA4-AS1	POD1|bHLHa23	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation.	25087872;28747406	RID02711	epigenetic regulation
Ovarian cancer	TARID	GADD45A	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000116717	NA	100507308	1647	EYA4-AS1	DDIT1|GADD45	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02712	interact with protein
Ovarian cancer	TARID	TDG	interact	RIP;ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	tumor-suppressive function(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Ovarian cancer	lncRNA	PCG	ENSG00000227954	GRCh38_6:133502252-133892802	ENSG00000139372	NA	100507308	6996	EYA4-AS1	hTDG	Long noncoding RNA TARID directs demethylation and activation of the tumor suppressor TCF21 via GADD45A.TARID also regulates its antisense gene, TFC21, by guiding GADD45A to the locus and promoting demethylation, which leads to gene activation. TARID and TCF21 are silent and heavily covered by DNA methylation in non-small cell lung cancer (NSCLC), head and neck squamous cell carcinomas (HNSCC) and ovarian cancers (OVC).TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. TARID recruits GADD45A/TDG, thus promoting base excision-mediated demethylation.	25087872;28747406	RID02713	interact with protein
T-cell acute lymphocytic leukemia	LUNAR1	IGF1R	negatively-E	ChIP	upregulation	sequencing	GSE57982	GSE57982.zip	Notch signaling pathway(+);cell growth(+)	transcriptional regulation	regulation	RNA-DNA	NA	NA	Sustained Angiogenesis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	lncRNA	PCG	ENSG00000278090	GRCh38_15:99014526-99031054	ENSG00000140443	NA	104564224	3480	NA	CD221|IGFIR|IGFR|JTK13	Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Finally we have shown that one specific Notch-regulated lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to enhance IGF1R mRNA expression and sustain IGF1 signaling. These results confirm that lncRNAs are important downstream targets of the Notch signaling pathway, and additionally they are key regulators of the oncogenic state in T-ALL.	25083870	RID02714	transcriptional regulation
T-cell acute lymphocytic leukemia	NOTCH1	LUNAR1	negatively-E	ChIP	upregulation	sequencing	GSE57982	GSE57982.zip	Notch signaling pathway(+);cell growth(+)	transcriptional regulation	regulation	protein-DNA	NA	NA	Sustained Angiogenesis;Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Leukemia	PCG	lncRNA	ENSG00000148400	NA	ENSG00000278090	GRCh38_15:99014526-99031054	4851	104564224	AOS5|AOVD1|TAN1|hN1	NA	Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Finally we have shown that one specific Notch-regulated lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to enhance IGF1R mRNA expression and sustain IGF1 signaling. These results confirm that lncRNAs are important downstream targets of the Notch signaling pathway, and additionally they are key regulators of the oncogenic state in T-ALL.	25083870	RID02715	transcriptional regulation
Cancer	TP53COR1	HNRNPK	interact	RNA pull-down assay;RNAi;RIP;ChIP	upregulation	microarray	GSE21761	GSE21761.zip	apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis	Cancer	Cancer	lncRNA	PCG	NA	GRCh38_6:36663392-36667296	ENSG00000165119	NA	102800311	3190	TRP53COR1|linc-p21|lincRNA-p21	AUKS|CSBP|HNRPK|TUNP	A large intergenic noncoding RNA induced by p53 mediates global gene repression in the p53 response. licRNA-p21 in the p53 transcriptional response. Induction of p53 activates the transcription of lincRNA-p21 by binding to its promoter (top left). LincRNA-p21 binds to hnRNP-K, and this interaction imparts specificity to genes repressed by p53 induction. The observed transcriptional repression by lincRNA-p21 is mediated through the physical association with hnRNP-K. This interaction is required for proper genomic localization of hnRNP-K at repressed genes and regulation of p53 mediates apoptosis.	20673990	RID02716	interact with protein
Hepatocellular carcinoma	HOTAIR	EZH2	interact	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition.More recently, it has been proposed that HOTAIR may act as an intermediate factor in the interaction of Snail and EZH2, facilitating Snail recruitment of EZH2 to specific genomic targets repressed by Snail. Thus, HOTAIR appears to be the linking factor of this putative Snail-HOTAIR-EZH2 tripartite epithelial-esenchymal transition (EMT)-promoting repressor switch in HCC.	27452518;29685978	RID02717	interact with protein
Hepatocellular carcinoma	HOTAIR	SNAI1	interact	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	TF	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000124216	NA	100124700	6615	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	SLUGH2|SNA|SNAH|SNAIL|SNAIL1|dJ710H13.1	The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition.More recently, it has been proposed that HOTAIR may act as an intermediate factor in the interaction of Snail and EZH2, facilitating Snail recruitment of EZH2 to specific genomic targets repressed by Snail. Thus, HOTAIR appears to be the linking factor of this putative Snail-HOTAIR-EZH2 tripartite epithelial-esenchymal transition (EMT)-promoting repressor switch in HCC.	27452518;29685978	RID02718	interact with protein
Urinary bladder cancer	MALAT1	CDH2	negatively-E	RNA pull-down assay;RNAi	upregulation	qPCR	NA	NA	cell metastasis(+)	NA	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000170558	NA	378938	1000	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	CD325|CDHN|CDw325|NCAD	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;malat1 is associated with suppressor of zeste 12 (suz12), and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression.	24449823	RID02719	expression association
Urinary bladder cancer	MALAT1	CDH1	negatively-E	RNA pull-down assay;RNAi;ChIP	upregulation	qPCR	NA	NA	cell metastasis(+)	epigenetic regulation	regulation	NA	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000039068	NA	378938	999	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	Arc-1|BCDS1|CD324|CDHE|ECAD|LCAM|UVO	TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12;TGF-beta induces malat1 expression and EMT in bladder cancer cells;malat1 knockdown inhibits TGF-beta-induced EMT;targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGF-beta;These data suggest that malat1 is an important mediator of TGF-beta-induced EMT	24449823	RID02720	epigenetic regulation
Chronic lymphocytic leukemia	MIAT	POU5F1	positively-E	RNAi	upregulation	qPCR	NA	NA	cell survival(+)	NA	regulation	NA	NA	NA	Self Sufficiency in Growth Signals;Evading Apoptosis	Cancer	Leukemia	lncRNA	TF	ENSG00000225783	GRCh38_22:26646411-26676475	ENSG00000204531	NA	440823	5460	C22orf35|GOMAFU|LINC00066|NCRNA00066|RNCR2|lncRNA-MIAT	OCT3|OCT4|OTF-3|OTF3|OTF4|Oct-3|Oct-4	Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias.Sattari et al. found that MIAT is upregulated in aggressive forms of chronic lymphocytic leukaemia (CLL). The study also revealed that MIAT is involved in a positive regulatory feedback loop with Oct4, as suppression of one led to reduced expression of the other Furthermore, we show that MIAT constitutes a regulatory loop with OCT4 in malignant mature B cell, as was previously reported in mouse pulripotent stem cell, and that both molecules are essential for cell survival.	27527866;29685978	RID02721	expression association
Lung adenocarcinoma	CRNDE	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	radioresistance(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000106462	NA	NA	2146	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression;the mechanistic investigations showed that CRNDE could interact with PRC2 and recruit its core component EZH2 to p21 (CDKN1A) promoter regions and repress its transcription;	28550688	RID02722	interact with protein
Cholangiocarcinoma	SNHG1	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE76297	GSE76297.zip	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000106462	NA	23642	2146	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma;SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A;SNHG1 knockdown extensively inhibited CCA cell migration as well as proliferation in vitro and in vivo	29970899	RID02723	interact with protein
Cholangiocarcinoma	PVT1	EZH2	interact	RIP	upregulation	qPCR;microarray	GSE26566	GSE26566.zip	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Non-coding RNA PVT1 Promotes Cell proliferation and Migration by Silencing ANGPTL4 Expression in Cholangiocarcinoma. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth,migration, and apoptosis progression.PVT1 Binds with EZH2 to Coregulate Target Genes, Especially ANGPTL4.	30388624	RID02724	interact with protein
Colorectal cancer	SNHG1	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR;microarray	GSE9348;GSE8671;GSE29621	GSE9348.zip;GSE8671.zip;GSE29621.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000255717	GRCh38_11:62851984-62855953	ENSG00000106462	NA	23642	2146	LINC00057|NCRNA00057|U22HG|UHG|lncRNA16	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long noncoding RNA SNHG1 regulates colorectal cancer cell growth through interactions with EZH2 and miR-154-5p.Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus. SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084	RID02725	interact with protein
Colorectal cancer	CRNDE	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245694	GRCh38_16:54845189-54929189	ENSG00000106462	NA	NA	2146	CRNDEP|LINC00180|NCRNA00180|PNAS-108|lincIRX5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA CRNDE promotes colorectal cancer cell proliferation via epigenetically silencing DUSP5/CDKN1A expression;RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development	28796262	RID02726	interact with protein
Hepatocellular carcinoma	TUG1	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.RIP with rabbit monoclonal anti-EZH2, anti-SUZ12, anti-SNRNP70 and preimmune IgG from HepG2 and Hep3B cell extracts. RNA levels in immunoprecipitates were determined by qPCR. Expression levels of TUG1 RNA were presented as fold enrichment in EZH2 and SUZ12 relative to IgG immunoprecipitates.	26336870	RID02727	interact with protein
Hepatocellular carcinoma	TUG1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000178691	NA	55000	23512	LINC00080|NCRNA00080|TI-227H	CHET9|JJAZ1	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.RIP with rabbit monoclonal anti-EZH2, anti-SUZ12, anti-SNRNP70 and preimmune IgG from HepG2 and Hep3B cell extracts. RNA levels in immunoprecipitates were determined by qPCR. Expression levels of TUG1 RNA were presented as fold enrichment in EZH2 and SUZ12 relative to IgG immunoprecipitates.	26336870	RID02728	interact with protein
Non-small cell lung cancer	LUCAT1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000248323	GRCh38_5:91054834-91314547	ENSG00000106462	NA	100505994	2146	SCAL1|SCAT5	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression.we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues.We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation.LUCAT1 functions as a tumor activator by epigenetically regulating p21 and p57 expression which are required to target EZH2 occupancy.	28423699	RID02729	interact with protein
Esophagus squamous cell carcinoma	CCAT1	EZH2	interact	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000106462	NA	100507056	2146	CARLO5|CARLo-5|onco-lncRNA-40	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.The existence of independent binding sites for EZH2 and SUV39H1 on CCAT1 suggests that CCAT1 may bridge EZH2 and SUV39H1. EZH2 IP retrieved SUV39H1, and SUV39H1 IP retrieved EZH2 in turn from Eca-109. Knockdown CCAT1 (ASO) of the IP abrogated the interaction between EZH2 and SUV39H1, suggesting that CCAT1 is required to bridge this interaction.	27956498	RID02730	interact with protein
Esophagus squamous cell carcinoma	CCAT1	SUV39H1	interact	RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Esophageal cancer	lncRNA	PCG	NA	GRCh38_8:127207382-127219268	ENSG00000101945	NA	100507056	6839	CARLO5|CARLo-5|onco-lncRNA-40	H3-K9-HMTase 1|KMT1A|MG44|SUV39H	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.Mechanistic investigations found that CCAT1 could serve as a scaffold for two distinct epigenetic modification complexes (5 domain of CCAT1 binding Polycomb Repressive Complex 2 (PRC2) while 3 domain of CCAT1 binding SUV39H1) and modulate the histone methylation of promoter of SPRY4 (sprouty RTK signaling antagonist 4) in nucleus.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo.The existence of independent binding sites for EZH2 and SUV39H1 on CCAT1 suggests that CCAT1 may bridge EZH2 and SUV39H1. EZH2 IP retrieved SUV39H1, and SUV39H1 IP retrieved EZH2 in turn from Eca-109. Knockdown CCAT1 (ASO) of the IP abrogated the interaction between EZH2 and SUV39H1, suggesting that CCAT1 is required to bridge this interaction.	27956498	RID02731	interact with protein
Lung cancer	MEG3	JARID2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	TF	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000008083	NA	55384	3720	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	JMJ	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID02732	interact with protein
Lung cancer	MEG3	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000106462	NA	55384	2146	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-beta (TGF-beta)-induced EMT of human lung cancer cell lines. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. After TGF-beta treatment, we could observe the significant increase of tri-methylated H3K27 (H3K27me3), the enhanced recruitment of EZH2, a catalytic subunit of PRC2, and the substantial decrease of transcriptionally active H3K4me3 marks on the regulatory regions of CDH1, miR-200b/200a/429, and miR-200c/141 genes in A549 and LC-2/ad cells (Fig. 4, A-C and E-G).	27852821	RID02733	interact with protein
Clear cell renal cell carcinoma	MRCCAT1	EZH2	interact	RIP;ChIP;RNA pull-down assay;western blot	upregulation	microarray	GSE88948	GSE88948.zip	cell metastasis(+);P38/MAPK signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Evading Apoptosis;Insensitivity to Antigrowth Signals;Reprogramming Energy Metabolism;Self Sufficiency in Growth Signals;Sustained Angiogenesis	Cancer	Kidney cancer	lncRNA	PCG	ENST00000237853	GRCh38_5:95885098-95962071	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 and activating p38-MAPK signaling. The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway.To test this, we performed RIP assay with an antibody against EZH2 (an important subunit of the PRC2 complex), and found a significant enrichment of MRCCAT1 with EZH2, compared with IgG control.	28659173	RID02734	interact with protein
Non-small cell lung cancer	TUG1	EED	interact	ChIP;RIP	downregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000074266	NA	55000	8726	LINC00080|NCRNA00080|TI-227H	COGIS|HEED|WAIT1	Long noncoding RNA TUG1 is downregulated in non-small cell lung cancer and can regulate CELF1 on binding to PRC2. Knockdown of TUG1 significantly promoted the proliferation of NSCLC cells. The results demonstrated that TUG1 RNA was bound to enhancer of zeste protein 2/embryonic ectoderm development (EZH2/EED), which is essential for PRC2. Finally, our designed ChIP assay revealed that the EZH2/EED was bound to the promotor region of CELF1 within 992 bp upstream of the transcript start site.	27485439	RID02735	interact with protein
Gastric cancer	LINC00668	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000106462	NA	400643	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.Moreover, we also found that LINC00668 plays a key role in the gastric cancer cell cycle by epigenetically silencing CDK inhibitors by binding to PRC2, which could in part account for LINC00668-mediated cell growth regulation.RNA immunoprecipitation (RIP) assays showed that the endogenous LINC00668 was enriched in the anti-EZH2 RIP fraction relative to the input compared to the IgG fraction. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that LINC00668 was enriched in the anti-SUZ12 RNA-IP fraction.	27036039	RID02736	interact with protein
Gastric cancer	LINC00668	SUZ12	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000265933	GRCh38_18:6919496-6929966	ENSG00000178691	NA	400643	23512	NA	CHET9|JJAZ1	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs.Moreover, we also found that LINC00668 plays a key role in the gastric cancer cell cycle by epigenetically silencing CDK inhibitors by binding to PRC2, which could in part account for LINC00668-mediated cell growth regulation.RNA immunoprecipitation (RIP) assays showed that the endogenous LINC00668 was enriched in the anti-EZH2 RIP fraction relative to the input compared to the IgG fraction. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that LINC00668 was enriched in the anti-SUZ12 RNA-IP fraction.	27036039	RID02737	interact with protein
Gastric cancer	TUG1	EZH2	interact	ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. endogenous TUG1 was enriched in the anti-EZH2 RIP fraction relative to the input compared with the IgG fraction both in AGS and BGC-823 cell lines. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous TUG1 was obviously enriched in the anti-SUZ12 RNA-IP fraction.	26913601	RID02738	interact with protein
Gastric cancer	TUG1	SUZ12	interact	ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000178691	NA	55000	23512	LINC00080|NCRNA00080|TI-227H	CHET9|JJAZ1	Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57.In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. endogenous TUG1 was enriched in the anti-EZH2 RIP fraction relative to the input compared with the IgG fraction both in AGS and BGC-823 cell lines. Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous TUG1 was obviously enriched in the anti-SUZ12 RNA-IP fraction.	26913601	RID02739	interact with protein
Hepatocellular carcinoma	CDKN2B-AS1	EZH2	interact	RNAi;RIP	upregulation	qPCR;microarray	GSE45435;GSE56140	GSE45435.zip;GSE56140.zip	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000106462	NA	100048912	2146	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID02740	interact with protein
Hepatocellular carcinoma	CDKN2B-AS1	SUZ12	interact	RNAi;RIP	upregulation	qPCR;microarray	GSE45435;GSE56140	GSE45435.zip;GSE56140.zip	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000178691	NA	100048912	23512	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHET9|JJAZ1	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.We also found that ANRIL could epigenetically repress KLF2 transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. We also found that Sp1 could regulate the expression of ANRIL.Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell apoptosis by epigenetic silencing of KLF2. ANRIL expression was upregulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. We also found that ANRIL could epigenetically repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to the KLF2 promoter region.We also found that SP1 could regulate the expression of ANRIL.	27391317;25966845	RID02741	interact with protein
Cancer	RASSF1-AS1	SUZ12	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE5823;GSE11118;GSE10879;GSE12056;GSE13471	GSE5823.zip;GSE11118.zip;GSE10879.zip;GSE12056.zip;GSE13471.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Cancer	lncRNA	PCG	ENSG00000281358	GRCh38_3:50337511-50338300	ENSG00000178691	NA	102060282	23512	ANRASSF1	CHET9|JJAZ1	The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation.ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region.We demonstrated that ANRASSF1 formed an lncRNA/DNA hybrid, which mediated the recruitment of SUZ12, a member of PRC2, to the RASSF1A promoter.	23990798	RID02742	interact with protein
Gastric cancer	HOXA-AS2	EZH2	interact	RIP;RNAi	upregulation	qPCR;microarray	GSE15459	GSE15459.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000106462	NA	285943	2146	HOXA3as	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression.Furthermore, HOXA-AS2 could epigenetically repress the expression of P21, PLK3, and DDIT3 via binding with EZH2 (enhaner of zeste homolog 2), a key component of PRC2; ChIP assays demonstrated that EZH2 could directly bind to the promoter of P21, PLK3 and DDIT3, inducing H3K27 trimethylated.	26384350	RID02743	interact with protein
Non-small cell lung cancer	LINC00511	EZH2	interact	RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72290091-72640472	ENSG00000106462	NA	400619	2146	LCAL5|onco-lncRNA-12	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Intergenic Noncoding RNA 00511 Acts as an Oncogene in Non-small-cell Lung Cancer by Binding to EZH2 and Suppressing p57. We found LINC00511 was upregulated and associated with oncogenesis, tumor size, metastasis, and poor prognosis in NSCLC. LINC00511 affected cell proliferation, invasiveness, metastasis, and apoptosis in multiple NSCLC cell lines. Mechanistically, LINC00511 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), a highly conserved protein complex that regulates gene expression by methylating lysine 27 on histone H3), and acted as a modular scaffold of EZH2/PRC2 complexes, coordinated their localization, and specified the histone modification pattern on the target genes, including p57, and consequently altered NSCLC cell biology.	27845772	RID02744	interact with protein
Breast cancer	NBAT1	EZH2	interact	RIP;RNAi	downregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Breast cancer	lncRNA	PCG	ENSG00000260455	GRCh38_6:22133205-22147193	ENSG00000106462	NA	729177	2146	CASC14|NBAT-1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2. ectopic NBAT1 inhibits migration and invasion of breast cancer cells. Mechanistic study shows that NBAT1 is associated with PRC2 member EZH2 and regulates global gene expression profile. Among them, DKK1 (dickkopf WNT signaling pathway inhibitor 1) is found to be regulated by NBAT1 in a PRC2 dependent manner, and is responsible for NBAT1's effects in inhibiting migration and invasion of breast cancer cells.	26378045	RID02745	interact with protein
Gastric cancer	CDKN2B-AS1	SUZ12	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000178691	NA	100048912	23512	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	CHET9|JJAZ1	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans (controlling the targets--mTOR and CDK6/E2F1 pathway) by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.Long noncoding RNA ANRIL promotes non-small cell lung cancer cell proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. Our previous study showed that ANRIL was significantly upregulated in gastric cancer, and it could promote cell proliferation and inhibit cell apoptosis by silencing of miR99a and miR449a transcription.Moreover, using an antibody specific to SUZ12, another member of the PRC2 complex, we also observed that endogenous ANRIL was obviously enriched in the anti-SUZ12 RNA-IP fraction.	24810364;25504755	RID02746	interact with protein
Glioblastoma	APTR	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000106462	NA	100505854	2146	RSBN1L-AS1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. APTR is present in immunoprecipitates of EZH2 or SUZ12, but not of ORC2 (negative control protein). An unrelated RNA, GAPDH mRNA was also not precipitated with EZH2 or SUZ12.	24748121	RID02747	interact with protein
Glioblastoma	APTR	SUZ12	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000214293	GRCh38_7:77657659-77696267	ENSG00000178691	NA	100505854	23512	RSBN1L-AS1	CHET9|JJAZ1	A new lncRNA, APTR, associates with and represses the CDKN1A/p21 promoter by recruiting polycomb proteins. APTR is present in immunoprecipitates of EZH2 or SUZ12, but not of ORC2 (negative control protein). An unrelated RNA, GAPDH mRNA was also not precipitated with EZH2 or SUZ12.	24748121	RID02748	interact with protein
Pancreatic cancer	HOTTIP	WDR5	interact	RIP	upregulation	qPCR	NA	NA	cell stemness(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Limitless Replicative Potential	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000196363	NA	100316868	11091	HOXA-AS6|HOXA13-AS1|NCRNA00213	BIG-3|CFAP89|SWD3	LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9; HOTTIP mediated HOXA9 to enhance the Wnt/beta-catenin pathway by binding to WDR5 in PCSCs;the HOTTIP/WDR5/HOXA9/Wnt axis contributes to PCSC stemness and is a potential therapeutic target for PDAC.	28947139	RID02749	interact with protein
Urinary bladder cancer	LINC00958	WDR5	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000251381	GRCh38_11:12961541-12989597	ENSG00000196363	NA	100506305	11091	BLACAT2	BIG-3|CFAP89|SWD3	Long noncoding RNA BLACAT2 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. we demonstrate that BLACAT2 epigenetically upregulation VEGF-C expression by directly associating with WDR5, a core subunit of human H3K4 methyltransferase complexes.	29355840	RID02750	interact with protein
Gastric cancer	HOXA11-AS	WDR5	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000196363	NA	221883	11091	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	BIG-3|CFAP89|SWD3	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID02751	interact with protein
Gastric cancer	HOXA11-AS	STAU1	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell cycle(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000124214	NA	221883	6780	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	PPP1R150|STAU	Over-expressed long noncoding RNA HOXA11-AS promotes cell cycle progression and metastasis in gastric cancer. Mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote beta-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1.These findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating beta-catenin and KLF2.	28441948	RID02752	interact with protein
Osteosarcoma	FOXP4-AS1	KDM1A	interact	ChIP;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000004487	NA	101060264	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID02753	interact with protein
Osteosarcoma	FOXP4-AS1	EZH2	interact	ChIP;RNAi	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000234753	GRCh38_6:41494853-41548621	ENSG00000106462	NA	101060264	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2;upregulation FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells	29859193	RID02754	interact with protein
Pancreatic cancer	DUXAP8	KDM1A	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE16515;GSE15932;GSE15471	GSE16515.zip;GSE15932.zip;GSE15471.zip	cell proliferation(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000004487	NA	503637	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID02755	interact with protein
Pancreatic cancer	DUXAP8	EZH2	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE16515;GSE15932;GSE15471	GSE16515.zip;GSE15932.zip;GSE15471.zip	cell proliferation(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Self Sufficiency in Growth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000106462	NA	503637	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	DUXAP8, a pseudogene derived lncRNA, promotes growth of pancreatic carcinoma cells by epigenetically silencing CDKN1A and KLF2.Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.Pancreatic cancer tissues had significantly higher DUXAP8 levels than paired adjacent normal tissues. These data indicated that DUXAP8 could function as a scaffold by binding to EZH2 and LSD1, thus epigenetically silencing CDKN1A and KLF2 in pancreatic cancer cells.	30367681	RID02756	interact with protein
Pre-eclampsia	HOXA11-AS	KDM1A	interact	RIP;ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000004487	NA	221883	23028	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	AOF2|BHC110|CPRF|KDM1|LSD1	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID02757	interact with protein
Pre-eclampsia	HOXA11-AS	EZH2	interact	RIP;ChIP;RNA pull-down assay	downregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cardiovascular system disease	Eclampsia	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Downregulated lncRNA HOXA11-AS Affects Trophoblast Cell Proliferation and Migration by Regulating RND3 and HOXA7 Expression in PE.Mechanistic analyses showed that HOXA11-AS could recruit Ezh2 and Lsd1 protein and regulate RND3 mRNA expression in the nucleus	30195759	RID02758	interact with protein
Renal cell carcinoma	HOTTIP	KDM1A	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000004487	NA	100316868	23028	HOXA-AS6|HOXA13-AS1|NCRNA00213	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID02759	interact with protein
Renal cell carcinoma	HOTTIP	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Kidney cancer	lncRNA	PCG	ENSG00000243766	GRCh38_7:27198575-27207259	ENSG00000106462	NA	100316868	2146	HOXA-AS6|HOXA13-AS1|NCRNA00213	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HOTTIP is upregulation in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2.The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	30021349	RID02760	interact with protein
Non-small cell lung cancer	FEZF1-AS1	KDM1A	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000004487	NA	154860	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID02761	interact with protein
Non-small cell lung cancer	FEZF1-AS1	EZH2	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000106462	NA	154860	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA FEZF1-AS1 enhances epithelial-mesenchymal transition (EMT) through suppressing E-cadherin and regulating WNT pathway in non-small cell lung cancer (NSCLC);we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells	28858731	RID02762	interact with protein
Lung adenocarcinoma	CYTOR	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000106462	NA	112597	2146	C2orf59|LINC00152|NCRNA00152	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression.LINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. EZH2 was shown to bind the promoter region of IL24, while LINC00152 knockdown reduced the histone H3 lysine 27 trimethylation (H3K27me3) occupancy of the IL24 promoter locus (Fig. 5h). However, LSD1 did not bind the IL24 promoter locus (Additional file 5: Figure S3d). These results indicated that LINC00152 repression of target IL24 expression occured, at least partially, through interaction with EZH2.	28109288	RID02763	interact with protein
Glioblastoma	HOTAIR	KDM1A	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	CSC	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Brain glioma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000004487	NA	100124700	23028	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	AOF2|BHC110|CPRF|KDM1|LSD1	Magnetofection based on superparamagnetic iron oxide nanoparticle-mediated low lncRNA HOTAIR expression decreases the proliferation and invasion of glioma stem cells.CD133+ human glioma stem cells express a high level of HOTAIR. An in-depth mechanistic analysis showed that downregulation of HOTAIR expression reduced the recruitment of downstream molecules, EZH2 and LSD1, thereby activating the expression of PDCD4 at the transcriptional level. In conclusion, downregulation of HOTAIR expression effectively promoted the expression of PDCD4, thereby inhibiting the proliferation, invasion and in vivo tumorigenicity of human GSCs.	27277755	RID02764	interact with protein
Non-small cell lung cancer	AGAP2-AS1	KDM1A	interact	RIP;ChIP	upregulation	qPCR;microarray	GSE18842;GSE19188	GSE18842.zip;GSE19188.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000004487	NA	100130776	23028	PUNISHER	AOF2|BHC110|CPRF|KDM1|LSD1	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID02765	interact with protein
Non-small cell lung cancer	AGAP2-AS1	EZH2	interact	RIP;ChIP	upregulation	qPCR;microarray	GSE18842;GSE19188	GSE18842.zip;GSE19188.zip	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000106462	NA	100130776	2146	PUNISHER	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription.	27195672	RID02766	interact with protein
Non-small cell lung cancer	LINC00673	KDM1A	interact	RIP;RNA pull-down assay;ChIP	upregulation	qPCR;microarray	GSE18842	GSE18842.zip	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000004487	NA	100499467	23028	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AOF2|BHC110|CPRF|KDM1|LSD1	Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer.We identified an oncogene, linc00673, whose expression level was upregulated by bioinformatics analyses and qRT-PCR analyses in NSCLC. Further mechanistic analyses indicated that the oncogenic activity of linc00673 is partially attributable to its repression of NCALD through association with the epigenetic repressor LSD1, Histone demethylase lysine specific demethylase 1.	27027352	RID02767	interact with protein
Non-small cell lung cancer	LINC01133	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000106462	NA	100505633	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID02768	interact with protein
Non-small cell lung cancer	LINC01133	KDM1A	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000224259	GRCh38_1:159958035-159984750	ENSG00000004487	NA	100505633	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 is previously found to be over-expressed in lung squamous cell cancer (LSCC) and knockdown its expression inhibits LSCC cells invasion. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription.	26840083	RID02769	interact with protein
Non-small cell lung cancer	DUXAP8	EZH2	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000106462	NA	503637	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02770	interact with protein
Non-small cell lung cancer	DUXAP8	KDM1A	interact	ChIP;RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000271672	GRCh38_22:15826566-15827187	ENSG00000004487	NA	503637	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion.	28131418	RID02771	interact with protein
Gastric cancer	LINC00673	EZH2	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106462	NA	100499467	2146	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02772	interact with protein
Gastric cancer	LINC00673	KDM1A	interact	ChIP;RIP	upregulation	qPCR;microarray	GSE65801;GSE37023	GSE65801.zip;GSE37023.zip	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000004487	NA	100499467	23028	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	AOF2|BHC110|CPRF|KDM1|LSD1	Long Noncoding RNA LINC00673 Is Activated by SP1 and Exerts Oncogenic Properties by Interacting with LSD1 and EZH2 in Gastric Cancer. In this study, we found that lncRNA LINC00673 is significantly upregulated in gastric cancer. Online transcription factor binding site prediction analysis showed that there are SP1 binding sites in the LINC00673 promoter region. Next, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that SP1 could bind directly to the LINC00673 promoter region and activate its transcription. Moreover, mechanistic investigation showed that CADM4, KLF2, and LATS2 might be the underlying targets of LINC00673 in GC cells, and RNA immunoprecipitation, RNA pull-down, and ChIP assays showed that LINC00673 can interact with EZH2 and LSD1, thereby repressing KLF2 and LATS2 expression. Taken together, these findings show that SP1-activated LINC00673 exerts an oncogenic function that promotes GC development and progression, at least in part, by functioning as a scaffold for LSD1 and EZH2 and repressing KLF2 and LATS2 expression.	28214253	RID02773	interact with protein
Gastric cancer	AGAP2-AS1	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE51575;GSE65801	GSE51575.zip;GSE65801.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000106462	NA	100130776	2146	PUNISHER	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02774	interact with protein
Gastric cancer	AGAP2-AS1	KDM1A	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR;microarray	GSE51575;GSE65801	GSE51575.zip;GSE65801.zip	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000255737	GRCh38_12:57726271-57728356	ENSG00000004487	NA	100130776	23028	PUNISHER	AOF2|BHC110|CPRF|KDM1|LSD1	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.AGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.Taken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.	28209205	RID02775	interact with protein
Gastric cancer	FEZF1-AS1	KDM1A	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000230316	GRCh38_7:122303658-122310119	ENSG00000004487	NA	154860	23028	NA	AOF2|BHC110|CPRF|KDM1|LSD1	LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. ChIP assays demonstrated that LSD1 could directly bind to the promoter of P21, inducing H3K4me2 demethylation. knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis.	28209170	RID02776	interact with protein
Colorectal cancer	HOXA-AS2	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000106462	NA	285943	2146	HOXA3as	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02777	interact with protein
Colorectal cancer	HOXA-AS2	KDM1A	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000253552	GRCh38_7:27107777-27134302	ENSG00000004487	NA	285943	23028	HOXA3as	AOF2|BHC110|CPRF|KDM1|LSD1	Long noncoding RNA HOXA-AS2 represses P21 and KLF2 expression transcription by binding with EZH2, LSD1 in colorectal cancer. The mechanistic investigations showed that HOXA-AS2 could interact with EZH2 (enhancer of zeste homolog 2), LSD1 (lysine specific demethylase 1) and recruit them to p21 (CDKN1A), KLF2 promoter regions to repress their transcription. Furthermore, the rescue experiments demonstrated that HOXA-AS2 oncogenic function is partly through regulating p21. HOXA-AS2 knockdown significantly suppressed proliferation by blocking the G1/S transition and caused apoptosis of CRC cells in vitro and in vivo.	28112720	RID02778	interact with protein
Pancreatic cancer	IRAIN	EZH2	interact	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000106462	NA	104472848	2146	IGF1R-AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02779	interact with protein
Pancreatic cancer	IRAIN	KDM1A	interact	RIP	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000259424	GRCh38_15:98646951-98647371	ENSG00000004487	NA	104472848	23028	IGF1R-AS	AOF2|BHC110|CPRF|KDM1|LSD1	Long non-coding RNA IRAIN suppresses apoptosis and promotes proliferation by binding to LSD1 and EZH2 in pancreatic cancer. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), an enhancer of zeste homolog 2 (EZH2), IRAIN reduced PC tumor cell apoptosis and induced growth arrest by silencing the expression of Kruppel-like factor 2 (KLF2) and P15. Moreover, IRAIN expression was inversely correlated with that of KLF2 and P15 in PC tissues.	27644252	RID02780	interact with protein
Hepatocellular carcinoma	MEG3	DNMT1	interact	RIP;RNAi	upregulation	qPCR	NA	NA	cell proliferation(-);prognosis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214548	GRCh38_14:100779410-100861031	ENSG00000130816	NA	55384	1786	FP504|GTL2|LINC00023|NCRNA00023|PRO0518|PRO2160|onco-lncRNA-83|prebp1	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.	25641194	RID02781	interact with protein
Hepatocellular carcinoma	GIHCG	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257698	GRCh38_12:57930115-57936345	ENSG00000106462	NA	100506844	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID02782	interact with protein
Hepatocellular carcinoma	GIHCG	DNMT1	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000257698	GRCh38_12:57930115-57936345	ENSG00000130816	NA	100506844	1786	NA	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. lncRNA-GIHCG is upregulation in HCC and associated with poor survival of patients. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	27380494	RID02783	interact with protein
Non-small cell lung cancer	HOXA11-AS	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID02784	interact with protein
Non-small cell lung cancer	HOXA11-AS	DNMT1	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000130816	NA	221883	1786	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Overexpression of lncRNA HOXA11-AS promotes cell epithelial-mesenchymal transition by repressing miR-200b in non-small cell lung cancer.Our results showed that up-regulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.	28615992	RID02785	interact with protein
Chondrosarcoma	HOTAIR	EZH2	interact	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02786	interact with protein
Chondrosarcoma	HOTAIR	DNMT1	interact	luciferase reporter assay	upregulation	qPCR;microarray	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Chondrosarcoma	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000130816	NA	100124700	1786	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ADCADN|AIM|CXXC9|DNMT|HSN1E|MCMT|m.HsaI	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo.Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	28182000	RID02787	interact with protein
Hepatocellular carcinoma	RB1-DT	DNMT3A	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000231473	GRCh38_13:48296162-48303661	ENSG00000119772	NA	100862704	1788	LINC00441|ncRNA-RB1	DNMT3A2|M.HsaIIIA|TBRS	Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.Here we focused on the bidirectional transcripted long noncoding RNA (Linc00441) with neighbor gene RB1 to investigate whether Linc00441 is involved in the suppression of RB1 in HCC. We found that aberrant upregulation intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement.	28300839	RID02788	interact with protein
Acute myeloid leukemia	HOTAIR	CCND1	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000110092	NA	100124700	595	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	BCL1|D11S287E|PRAD1|U21B31	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID02792	ceRNA or sponge
Acute myeloid leukemia	HOTAIR	MDM2	positively-E	luciferase reporter assay	upregulation	qPCR	NA	NA	oncogenic role(+)	ceRNA(miR-193a)	regulation	NA	NA	NA	NA	Cancer	Leukemia	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000135679	NA	100124700	4193	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ACTFS|HDMX|hdm2	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.Ectopic expression of miR-193a inhibited cell proliferation, facilitated differentiation, and induced apoptosis in AML blasts through directly targeting c-KIT, DNMT3a, CCND1 and MDM2	25979172	RID02793	ceRNA or sponge
Esophagus squamous cell carcinoma	PANTR1	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000233639	GRCh38_2:104656135-104853183	ENSG00000106462	NA	100506421	2146	LINC01158|linc-Brn1a|linc-POU3F3	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Increased levels of the long intergenic non-protein coding RNA POU3F3 promote DNA methylation in esophageal squamous cell carcinoma cells. Levels of a lincRNA encoded by a gene located next to POU3F3 (linc-POU3F3) were significantly higher in ESCC than neighboring nontumor tissues. In RNA immunoprecipitation assays, linc-POU3F3 was associated with the EZH2 messenger RNA (mRNA). Overexpression of linc-POU3F3 in cell lines increased their proliferation and ability to form colonies, and reduced the expression of POU3F3 mRNA, whereas knockdown of linc-POU3F3 increased the levels of POU3F3 mRNA. CpG islands in POU3F3 were densely hypermethylated in cell lines that overexpressed linc-POU3F3; methylation at these sites was reduced by knockdown of linc-POU3F3. Pharmacologic inhibition of EZH2 increased the levels of POU3F3 mRNA and significantly reduced binding of DNA methyltransferase (DNMT)1, DNMT3A, and DNMT3B to POU3F3. Levels of linc-POU3F3 are increased in ESCC samples from patients compared with nontumor tissues. This noncoding RNA contributes to the development of ESCC by interacting with EZH2 to promote methylation of POU3F3, which encodes a transcription factor.	24631494	RID02794	interact with protein
Malignant glioma	HOXB13-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000229637	GRCh38_17:48720802-48724758	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma. Mechanistically, we showed that HOXB13-AS1 overexpression increased DNMT3B-mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP),epigenetically suppressing HOXB13 expression.	30105866	RID02795	interact with protein
Malignant glioma	FAM83H-AS1	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Brain glioma	lncRNA	PCG	ENSG00000203499	GRCh38_8:143734140-143746337	ENSG00000106462	NA	100128338	2146	onco-lncRNA-3	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21).FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A;thereby influencing the cell cycle and proliferation	29870057	RID02796	interact with protein
Hepatocellular carcinoma	SOX21-AS1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cancer progression(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000227640	GRCh38_13:94703454-94803430	ENSG00000106462	NA	100507533	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SOX21-AS1 is associated with progression of hepatocellular carcinoma and predicts prognosis through epigenetically silencing p21;SOX21-AS1 epigenetically silenced p21 via recruiting EZH2 to the promoter of p21;SOX21-AS1 can interact with p21 to affect hepatocellular carcinoma progression	29772433	RID02797	interact with protein
Gastric cancer	SNHG6	EZH2	interact	RIP;ChIP;luciferase reporter assay	upregulation	qPCR	NA	NA	cell proliferation(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p.In this study, we revealed that SNHG6 was overexpressed in gastric cancer tissues and cell lines. Additionally, ChIP, RIP, RNA-pulldown and luciferase reporter assays evidenced that SNHG6 could epigenetically silenced p27 and could competitively sponging miR-101-3p thereby regulating zinc finger E-box-binding homeobox 1 (ZEB1).In summary, our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27.	28683446;30031062	RID02798	interact with protein
Cholangiocarcinoma	NEAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Cholangiocarcinoma	lncRNA	PCG	ENSG00000245532	GRCh38_11:65422774-65445540	ENSG00000106462	NA	283131	2146	LINC00084|NCRNA00084|TncRNA|VINC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells;NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression	29970216	RID02799	interact with protein
T-cell leukemia	CDKN2B-AS1	EZH2	interact	luciferase reporter assay;RNAi	upregulation	qPCR	NA	NA	cell proliferation(+);NF-kB signaling pathway(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Sustained Angiogenesis	Cancer	Leukemia	lncRNA	PCG	ENSG00000240498	GRCh38_9:21994139-22128103	ENSG00000106462	NA	100048912	2146	ANRIL|CDKN2B-AS|CDKN2BAS|NCRNA00089|PCAT12|p15AS	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA ANRIL Supports Proliferation of Adult T-Cell Leukemia Cells through Cooperation with EZH2. In the present study, we show that the expression level of the lncRNA ANRIL was elevated in HTLV-1-infected cell lines and clinical ATL samples. In addition, we observed that the ANRIL/EZH2 complex repressed p21/CDKN1A transcription through H3K27 trimethylation of the p21/CDKN1A promoter. Taken together, our results implicate that the lncRNA ANRIL, by cooperating with EZH2, supports the proliferation of HTLV-1-infected cells, which is thought to be critical for oncogenesis. In this study, we demonstrated that the lncRNA ANRIL was important for maintaining the proliferation of ATL cells in vitro and in vivo ANRIL was shown to activate NF-kB signaling through forming a ternary complex with EZH2 and p65. Furthermore, epigenetic inactivation of p21/CDKN1A was involved in the oncogenic function of ANRIL.	30258009	RID02800	interact with protein
Osteosarcoma	HAGLR	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000224189	GRCh38_2:176164051-176188958	ENSG00000106462	NA	401022	2146	HOXD-AS1|MIR7704HG|Mdgt	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2.our study confirmed that HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis.	30119259	RID02801	interact with protein
Esophagus squamous cell carcinoma	DUXAP10	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Esophageal cancer	lncRNA	PCG	ENSG00000244306	GRCh38_14:19268853-19337730	ENSG00000106462	NA	503639	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA DUXAP10 modulates cell proliferation in esophageal squamous cell carcinoma through epigenetically silencing p21. Results of mechanism experiments suggested that DUXAP10 motivated ESCC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21.	30215547	RID02802	interact with protein
Melanoma	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	tumorigenesis(+);cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma. the lncRNA PVT1 may contribute to the tumorigenesis and metastasis of melanoma through binding to EZH2 and regulating the expression of miR-200c	29286144	RID02803	interact with protein
Glioblastoma	H19	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	tumorigenesis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Brain glioma	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter;by showing that its expression is inversely linked to that of NKD1, a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter	29643989	RID02804	interact with protein
Colorectal cancer	SH3PXD2A-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000280693	GRCh38_10:103745966-103755423	ENSG00000106462	NA	100505839	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer;Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2	29734178	RID02805	interact with protein
Hepatocellular carcinoma	LNCDQ	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_1:155234457-155239960	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of LncDQ is Associated with Poor Prognosis and Promotes Tumor Progression via Epigenetic Regulation of the EMT Pathway in HCC;LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells	29669339	RID02806	interact with protein
Hepatocellular carcinoma	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Liver cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA PVT1 promotes hepatocellular carcinoma progression through regulating miR-214.RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2).	28800314	RID02807	interact with protein
Melanoma	FALEC	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	prognosis(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Melanoma	lncRNA	PCG	ENSG00000228126	GRCh38_1:150515757-150518032	ENSG00000106462	NA	100874054	2146	FAL1|LINC00568|ncRNA-a1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21;we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21	29196104	RID02808	interact with protein
Chordoma	MIR31HG	EZH2	interact	RIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Chordoma	lncRNA	PCG	ENSG00000171889	GRCh38_9:21410969-21559900	ENSG00000106462	NA	554202	2146	LncHIFCAR|hsa-lnc-31	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating miR-31 expression;EZH2 as a binding protein of LOC554202, and it was positively regulated by LOC554202, leading to the reduced expression of miR-31;Our results suggest that LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B via miR-31. NF144B was a target of miR-31	28963737	RID02809	interact with protein
Gastric cancer	DANCR	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	57291	2146	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID02810	interact with protein
Gastric cancer	DANCR	HDAC3	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell migration(-);cell invasion(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000171720	NA	57291	8841	AGU2|ANCR|KIAA0114|SNHG13|lncRNA-ANCR	HD3|KDAC3|RPD3|RPD3-2	LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells;DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion	28951520	RID02811	interact with protein
Melanoma	ILF3-DT	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000267100	GRCh38_19:10651862-10653844	ENSG00000106462	NA	147727	2146	ILF3-AS1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma;we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues	28935763	RID02812	interact with protein
Non-small cell lung cancer	SNHG20	EZH2	interact	RIP;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000106462	NA	654434	2146	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA SNHG20 promotes non-small cell lung cancer cell proliferation and migration by epigenetically silencing of P21 expression;SNHG20 could interact with EZH2 (enhancer of zeste homolog 2), thereby repressing P21 expression	28981099	RID02813	interact with protein
Uveal melanoma	HOXA11-AS	EZH2	interact	RIP;RNA pull-down assay;ChIP	upregulation	qPCR	NA	NA	cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Uveal cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma;we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS.Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression.	28749709	RID02814	interact with protein
Gastric cancer	TRERNA1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell metastasis(+);epithelial to mesenchymal transition(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000231265	GRCh38_20:50040716-50041504	ENSG00000106462	NA	100887755	2146	LINC00651|treRNA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition. TRERNA1 functions as a scaffold to recruit EZH2 to epigenetically silence epithelial-mesenchymal transition marker CDH1 by H3K27me3 of its promoter region;our findings indicated that TRERNA1 serves as a critical effector in GC progression by regulating CDH1 at the transcription level	28918030	RID02815	interact with protein
Osteosarcoma	XIST	EZH2	interact	ChIP;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21;mechanistic analysis revealed that Xist can repress P21 expression to regulate OS cell cycle and proliferation by binding to EZH2	29254174	RID02816	interact with protein
Hepatocellular carcinoma	HOXA11-AS	EZH2	interact	ChIP;RIP;western blot	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000240990	GRCh38_7:27184507-27189298	ENSG00000106462	NA	221883	2146	HOXA-AS5|HOXA11-AS1|HOXA11AS|HOXA11S|NCRNA00076	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Promotion of LncRNA HOXA11-AS on the proliferation of hepatocellular carcinoma by regulating the expression of LATS1;RIP and CHIP experiments showed that HOXA11-AS inhibited the expression of LATS1 genes by binding enhancer of zeste homolog 2 (EZH2) proteins	28829501	RID02817	interact with protein
Cervical cancer	PVT1	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	chemoresistance(-);epithelial to mesenchymal transition(+);cell proliferation(+);cell migration(+)	interact with protein	binding/interaction	RNA-protein	paclitaxel	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells;PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195;PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region;PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells;Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX;Based on these findings, we infer that PVT1 could decrease miR-195 expression via enhancing histone H3K27me3 in the miR-195 promoter region and also via direct sponging of miR-195	28296507;27272214	RID02818	interact with protein
Colorectal cancer	LL22NC03-N64E9.1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colorectal cancer	lncRNA	PCG	NA	GRCh38_22:15796959-15798346	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	A novel lncRNA, LL22NC03-N64E9.1, represses KLF2 transcription through binding with EZH2 in colorectal cancer; Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2;We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2.	28938648	RID02819	interact with protein
Gallbladder cancer	UCA1	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gallbladder cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression;we identified that UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript	28624787	RID02820	interact with protein
Osteosarcoma	ANCR	EZH2	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Osteosarcoma	lncRNA	PCG	ENSG00000226950	GRCh38_4:52712404-52720351	ENSG00000106462	NA	282	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA-ANCR regulates the cell growth of osteosarcoma by interacting with EZH2 and affecting the expression of p21 and p27;Mechanistically, downregulation of lncRNA-ANCR reduced the mRNA level of EZH2 and increased the expression of p21 and p27 at both mRNA and protein levels;LncRNA-ANCR inhibited the cell proliferation, migration, and invasion of OS cells possibly through interacting with EZH2 and regulating the expression of p21 and p27	28679390	RID02821	interact with protein
Breast cancer	CCAT2	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Breast cancer	lncRNA	PCG	ENSG00000280997	GRCh38_8:127400399-127402150	ENSG00000106462	NA	101805488	2146	LINC00873|NCCP1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer;we confirmed that CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells	28531944	RID02822	interact with protein
Colorectal cancer	SNHG6	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000245910	GRCh38_8:66921684-66926398	ENSG00000106462	NA	641638	2146	HBII-276HG|NCRNA00058|U87HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells.	30157475	RID02823	interact with protein
Gastric cancer	UCA1	EZH2	interact	ChIP;RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA UCA1 induced by SP1 promotes cell proliferation via recruiting EZH2 and activating AKT pathway in gastric cancer.This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.	28569779	RID02824	interact with protein
Non-small cell lung cancer	LINC00673	EZH2	interact	RIP;ChIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell metastasis(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Lung cancer	lncRNA	PCG	ENSG00000227036	GRCh38_17:72403322-72592804	ENSG00000106462	NA	100499467	2146	ERRLR01|HI-LNC75|HILNC75|LUCAIR1|SLNCR|SLNCR1	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5	28423732	RID02825	interact with protein
Urinary bladder cancer	AWPPH	EZH2	interact	RIP	downregulation	qPCR	NA	NA	cancer progression(+);cell proliferation(+);cell autophagy(+);cell migration(+);apoptosis process(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Evading Apoptosis;Tissue Invasion and Metastasis	Cancer	Urinary bladder cancer	lncRNA	PCG	ENSG00000172965	GRCh38_2:111195866-111495161	ENSG00000106462	NA	NA	2146	NA	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression.LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.Then, RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2.	29231261	RID02826	interact with protein
Pancreatic cancer	MALAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000251562	GRCh38_11:65497688-65506516	ENSG00000106462	NA	378938	2146	HCN|LINC00047|NCRNA00047|NEAT2|PRO2853	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. RIP and ChIP assays suggest that EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression.	26848980	RID02827	interact with protein
Colon cancer	HULC	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cancer progression(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Colon cancer	lncRNA	PCG	ENSG00000285219	GRCh38_6:8435568-9294133	ENSG00000106462	NA	728655	2146	HCCAT1|LINC00078|NCRNA00078	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HULC promotes colorectal carcinoma progression through epigenetically repressing NKD2 expression. Mechanistically, RNA immunoprecipitation (RIP) and RNA pull-down experiment demonstrated that HULC could simultaneously interact with EZH2 to repress underlying targets NKD2 transcription. In addition, rescue experiments determined that HULC oncogenic function is partly dependent on repressing NKD2.	27496341	RID02828	interact with protein
Non-small cell lung cancer	XIST	EZH2	interact	RNA pull-down assay	upregulation	qPCR	NA	NA	oncogenic role(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Lung cancer	lncRNA	PCG	ENSG00000229807	GRCh38_X:73820649-73852723	ENSG00000106462	NA	7503	2146	DXS1089|DXS399E|LINC00001|NCRNA00001|SXI1|swd66	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression.Mechanistically, RNA immune-precipitation (RIP) and RNA pull-down experiment demonstrated that XIST could simultaneously interact with EZH2 to suppress transcription of its potential target KLF2.	27501756	RID02829	interact with protein
Small cell lung cancer	TUG1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+);cell growth(+)	interact with protein	binding/interaction	RNA-protein	cisplatin;adriamycin;etoposide	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000253352	GRCh38_22:30969245-30979395	ENSG00000106462	NA	55000	2146	LINC00080|NCRNA00080|TI-227H	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA TUG1 is involved in cell growth and chemoresistance of small cell lung cancer by regulating LIMK2b via EZH2.We found that TUG1 was overexpressed in SCLC tissues.We further demonstrated that TUG1 can regulate the expression of LIMK2b (a splice variant of LIM-kinase 2) via binding with enhancer of zeste homolog 2 (EZH2), and then promoted cell growth and chemoresistance of SCLC.After knockdown of TUG1, the IC50 values of H446DDP and H69AR cells significantly decreased with treatment of chemotherapeutic drugs including DDP, ADM or VP-16 (Fig. 4a). Three chemotherapy drugs [Cisplatin (DDP; Shandong, China), Adriamycin (ADM; Jiangsu, China) Etoposide (VP-16; Jiangsu, China),] were used. Furthermore, we conducted ChIP assays and found that knockdown of TUG1 decreased the binding of EZH2 and H3K27me3 levels across the LIMK2b promoter compared to cells transfected with siNC (Fig. 6f). Taken together, these data suggest that TUG1 is required to target EZH2 occupancy and activity to epigenetically modulate the expression of LIMK2b.	28069000	RID02830	interact with protein
Pancreatic ductal adenocarcinoma	HOTAIR	EZH2	interact	ChIP	upregulation	qPCR	NA	NA	cell growth(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma.Loss of miR-34a contributed to EZH2-mediated cell growth in PDAC cells. As HOTAIR was shown to be overexpressed in PDAC.	27594424	RID02831	interact with protein
Pancreatic cancer	HOTAIR	EZH2	interact	RNAi;ChIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	conatumumab;tigatuzumab	NA	NA	Cancer	Pancreatic cancer	lncRNA	PCG	ENSG00000228630	GRCh38_12:53962308-53974956	ENSG00000106462	NA	100124700	2146	HOXAS|HOXC-AS4|HOXC11-AS1|NCRNA00072	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer.These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression.Some TRAIL and DR4/DR5 agonist antibodies, including conatumumab (AMG655, antibody for DR5) and tigatuzumab (CS-1008/TRA-8, antibody for DR5), have also been used for treating several types of cancers	28476883	RID02832	interact with protein
Melanoma	HEIH	EZH2	interact	RIP;RNA pull-down assay	upregulation	qPCR	NA	NA	cell proliferation(+);cell migration(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals;Tissue Invasion and Metastasis	Cancer	Melanoma	lncRNA	PCG	ENSG00000278970	GRCh38_5:180826871-180831605	ENSG00000106462	NA	100859930	2146	HCCAT2|LINC-HEIH|LINC00848|lncRNA-HEIH	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription.lncRNA-HEIH has been reported to interact with enhancer of zeste homologue 2 (EZH2), change the genomic occupation of EZH2 on its target genes' promoters and modulate the expression of EZH2 target genes in HCC. Furthermore, the critical tumour suppressors miR-200b/a/429 have been reported to be EZH2 target genes in cervical cancer and HCC.	28487474	RID02833	interact with protein
Hepatocellular carcinoma	HNF1A-AS1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000241388	GRCh38_12:120941728-120980965	ENSG00000106462	NA	283460	2146	C12orf27|HAS1|NCRNA00262	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines.Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect.Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression.	28292020	RID02834	interact with protein
Hepatocellular carcinoma	SNHG20	EZH2	interact	RIP	upregulation	qPCR	NA	NA	cell invasion(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Liver cancer	lncRNA	PCG	ENSG00000234912	GRCh38_17:77086716-77099902	ENSG00000106462	NA	654434	2146	C17orf86|LINC00338|NCRNA00338|SCARNA16HG	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long non-coding RNA SNHG20 predicts a poor prognosis for HCC and promotes cell invasion by regulating the epithelial-to-mesenchymal transition.In vitro, loss-function assays revealed that knockdown of SNHG20 inhibited cell proliferation and invasion, whereas, gain-of-function promoted cell proliferation and invasion.Mechanistic investigation revealed that SNHG20 could bind to enhancer of zeste homolog 2 (EZH2) and regulated E-cadherin expression.Our results showed that the SNHG20/EZH2/E-cadhein regulator pathway might contribute to the development of novel therapeutic strategies for HCC patients.	28282787	RID02835	interact with protein
Non-small cell lung cancer	PVT1	EZH2	interact	ChIP;luciferase reporter assay;RNA pull-down assay	upregulation	qPCR	NA	NA	apoptosis process(-);cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Evading Apoptosis;Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long Noncoding RNA PVT1 Promotes Non-Small Cell Lung Cancer Cell Proliferation through Epigenetically Regulating LATS2 Expression.Here, we found that PVT1 was upregulated in 105 human NSCLC tissues compared with normal samples.RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription.	26908628	RID02836	interact with protein
Hepatocellular carcinoma	UCA1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell growth(+);cell cycle phase transition (G1/S)(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Self Sufficiency in Growth Signals;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	ENSG00000214049	GRCh38_19:15828206-15836328	ENSG00000106462	NA	652995	2146	CUDR|LINC00178|NCRNA00178|UCAT1|onco-lncRNA-36	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	HBx-upregulated lncRNA UCA1 promotes cell growth and tumorigenesis by recruiting EZH2 and repressing p27Kip1/CDK2 signaling.Further studies show that the upregulated UCA1 promotes cell growth by facilitating G1/S transition through CDK2 in both hepatic and hepatoma cells.More importantly, UCA1 is found to be physically associated with enhancer of zeste homolog 2 (EZH2), which suppresses p27Kip1 through histone methylation (H3K27me3) on p27Kip1 promoter.UCA1 is found to be frequently up-regulated in HBx positive group tissues in comparison with the HBx negative group, and exhibits an inverse correlation between UCA1 and p27Kip1 levels.Our findings demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-UCA1/EZH2-p27Kip1 axis, and a potential target of HCC.	27009634	RID02837	interact with protein
Gastric cancer	CYTOR	EZH2	interact	RIP	upregulation	qPCR;microarray	GSE15459	GSE15459.zip	cell cycle(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	NA	Cancer	Gastric cancer	lncRNA	PCG	ENSG00000222041	GRCh38_2:87454781-87636740	ENSG00000106462	NA	112597	2146	C2orf59|LINC00152|NCRNA00152	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC).Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21.	26799422	RID02838	interact with protein
Thyroid cancer	PVT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000249859	GRCh38_8:127794526-128187101	ENSG00000106462	NA	5820	2146	LINC00079|MIR1204HG|NCRNA00079|onco-lncRNA-100	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR).Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.	26427660	RID02839	interact with protein
Colorectal cancer	BLACAT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell cycle(+);cell proliferation(+);prognosis(-)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Colorectal cancer	lncRNA	PCG	ENSG00000281406	GRCh38_1:205434885-205457091	ENSG00000106462	NA	101669762	2146	LINC00912|linc-UBC1|onco-lncRNA-30	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation.	28277544	RID02840	interact with protein
Hepatocellular carcinoma	SPRY4-IT1	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	epithelial to mesenchymal transition(+);cell proliferation(+);cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis;Insensitivity to Antigrowth Signals	Cancer	Liver cancer	lncRNA	PCG	NA	GRCh38_5:142317636-142318322	ENSG00000106462	NA	100642175	2146	SPRIGHTLY	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Overexpression of the long non-coding RNA SPRY4-IT1 promotes tumor cell proliferation and invasion by activating EZH2 in hepatocellular carcinoma.We found that SPRY4-IT1 was up-regulated in HCC cell lines. our results also indicated that SPRY4-IT1 over-expression significantly promoted the epithelial-mesenchymal transition (EMT) by up-regulating the transcription factor Twist1 and EMT marker Vimentin and inhibited the E-cadherin expression in MHCC97L cell. Mechanisms investigations showed that SPRY4-IT1 interacted with the EZH2 and epigenetically repressed the E-cadherin expression.	27899259	RID02841	interact with protein
Estrogen-receptor positive breast cancer	H19	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	chemoresistance(+)	interact with protein	binding/interaction	RNA-protein	paclitaxel	NA	NA	Cancer	Breast cancer	lncRNA	PCG	ENSG00000130600	GRCh38_11:1995176-2001470	ENSG00000106462	NA	283120	2146	ASM|ASM1|BWS|D11S813E|LINC00008|MIR675HG|NCRNA00008|WT2	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	LncRNA H19 confers chemoresistance in ERalpha-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ERalpha. Altered ERalpha expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ERalpha-H19-BIK signaling axis plays an important role in promoting chemoresistance.	27845892	RID02842	interact with protein
Papillary thyroid carcinoma	BANCR	EZH2	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Thyroid cancer	lncRNA	PCG	ENSG00000278910	GRCh38_9:69296682-69311111	ENSG00000106462	NA	100885775	2146	LINC00586	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.	26323637	RID02843	interact with protein
Cervical cancer	TMPOP2	EZH2	interact	RIP	upregulation	qPCR	NA	NA	cell invasion(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Tissue Invasion and Metastasis	Cancer	Cervical cancer	lncRNA	PCG	ENSG00000262904	GRCh38_16:74667506-74668706	ENSG00000106462	NA	100533619	2146	lncRNA-EBIC	ENX-1|ENX1|EZH2b|KMT6|KMT6A|WVS|WVS2	Long noncoding RNA-EBIC promotes tumor cell invasion by binding to EZH2 and repressing E-cadherin in cervical cancer.Then, we found a specific differentially expressed lncRNA can physically bind to enhancer of zeste homolog2 (EZH2) by using RNA immunoprecipitation. We termed it as EZH2-binding lncRNA in cervical cancer [lncRNA-EBIC]. We also found that the association between lncRNA-EBIC and EZH2 was required for the repression of E-cadherin, which was a key molecular in the metastasis of cervical cancer. Conclusion: These results demonstrated that lncRNA-EBIC was an oncogenic lncRNA, which could promote tumor cell invasion in CC by binding to EZH2 and inhibiting E-cadherin expression.	25007342	RID02844	interact with protein
Lung adenocarcinoma	LUADT1	SUZ12	interact	ChIP;RIP	upregulation	qPCR	NA	NA	cell proliferation(+)	interact with protein	binding/interaction	RNA-protein	NA	NA	Insensitivity to Antigrowth Signals	Cancer	Lung cancer	lncRNA	PCG	ENSG00000196634	GRCh38_6:147158925-147180992	ENSG00000178691	NA	106182249	23512	NA	CHET9|JJAZ1	A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27.Further analysis indicated that LUADT1 may regulate cell cycle progression by epigenetically inhibiting the expression of p27.RNA immunoprecipitation and chromatin immunoprecipitation assays confirmed that LUADT1 binds to SUZ12, a core component of polycomb repressive complex 2, and mediates the trimethylation of H3K27 at the promoter region of p27.	26291312	RID02845	interact with protein