chr14	49586580	49586878	7SL	6029	HGNC:10038	ENSG00000276168	NR_002715	qPCR, Western blot, ChIP, Luciferase reporter assay etc.	differential expression	In this study, we detected that over-expression of FOXP3 repressed the transcription of 7SL RNA and contributed to inhibiting tumor growth. Knock down of FOXP3 in MCF-10A normal mammary breast cells up-regulated the transcription of 7SL RNA. Chromatin Immuno-precipitation (ChIP) analysis showed that FOXP3 directly bound to the Forkhead/HNF-3 domain DNA binding sites (-789 to -795) relative to the transcription start site. Meanwhile, Luciferase analysis showed that FOXP3 repressed the full-length 7SL promoter activity, but this suppressive effect was reversed after mutation of the FOXP3 binding site. Further studies showed that FOXP3 promoted the expression of P53 at translational levels through repressing 7SL RNA.	26718402	2016	Tumor FOXP3 represses the expression of long noncoding RNA 7SL.	0	0	0
NA	NA	NA	91H	NA	NA	NA	NA	qPCR, RNAi, ChIP, Cell proliferation assay etc.	up-regulated	Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. 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. 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.	27780718	2017	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications.	0	0	0
NA	NA	NA	AC026904.1	NA	NA	NA	NA	Microarray, qPCR, RIP, Luciferase reporter assay etc.	up-regulated	We observed that TGF-B induced genome-wide changes in lncRNA levels in breast cancer cells, among which AC026904.1 and UCA1 were highly expressed in metastatic breast cancer and closely associated with poor prognosis.	29774079	2018	Long non-coding RNAs AC026904.1 and UCA1: a ¡°one-two punch¡± for TGFB-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer	0	0	1
chr2	168846243	168846834	AF251187	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr4	7754090	7778928	AFAP1-AS1	84740	HGNC:28141	ENSG00000272620	NR_026892	qPCR	up-regulated	both genes were significantly down-regulated in Ki-67 negative tumor samples. The observed up-regulation of AFAP1-AS1 in tumor samples compared with ANCTs implies its involvement in breast cancer pathogenesis and potentiates it as a biomarker or therapeutic target.	29439313	2018	Expression analysis of AFAP1-AS1 and AFAP1 in breast cancer.	0	0	0
chr4	7754090	7778928	AFAP1-AS1	84740	HGNC:28141	ENSG00000272620	NR_026892	qPCR,etc.	up-regulated	Up-regulated lncRNA AFAP1-AS1 indicates a poor prognosis in breast cancer patients and regulated the breast cancer cells proliferation, apoptosis and metastasis. AFAP1-AS1 knockdown can inhibit the proliferation,metastasis and promote apoptosis of MCF-7. However,the AFAP1 expression and actin filament integrity was not affected after AFAP1-AS1 knockdown.The Kaplan¨CMeier method was used to estimate survival curves,the log-rank test wasused to compare between groups. 	29974352	2018	Up-regulated lncRNA AFAP1-AS1 indicates a poor prognosis and promotes carcinogenesis of breast cancer.	0	0	1
chr2	111036776	111523376	AK001796	541471	HGNC:35163	ENSG00000172965	NR_015395	qPCR etc.	up-regulated	Here, we identify a lncRNA, LINC00978, which is upregulated in breast cancer cell lines and tissues compared with corresponding controls. Furthermore, LINC00978 expression is negatively associated with hormone receptor (HR) status in 195 breast cancer patients studied.	27897214	2016	LINC00978 predicts poor prognosis in breast cancer patients.	0	0	1
chr9	19409059	19452020	AK024898	340485	HGNC:23675	ENSG00000177076	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
chr8	37597480	37599858	AK025743	NA	NA	ENSG00000254290	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
chr6	33867506	33896914	AK057709	100507584	HGNC:48991	ENSG00000249346	NR_038989	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
NA	NA	NA	AK090603	647946	HGNC:44332	NA	NR_024391	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
chr15	92592579	92596142	AK096780	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
chr9	5832649	5835435	AK123408	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr19	20220597	20222169	AK124454	NA	NA	NA	NA	microarray, qPCR, RNAi, Cell proliferation assay, Cell invasion assay etc.	up-regulated	lncRNAs HIF1A-AS2 and AK124454 could promote cell proliferation and invasion, and attenuate G2-M arrest, which might contribute to paclitaxel resistance in TNBC cells.	26921339	2016	Transcriptome Analysis of Triple-Negative Breast Cancer Reveals an Integrated mRNA-lncRNA Signature with Predictive and Prognostic Value.	0	0	1
chr18	76615212	76625940	AK127565	NA	NA	ENSG00000266256	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr8	123523808	123525468	AL832444	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr8	22679015	22684009	AL833160	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
NA	NA	NA	ANAC	NA	NA	NA	NA	qPCR, Western blot, Luciferase reporter assay etc.	down-regulated	We find that lncRNA ANCR participates in TGF-B1-induced EMT. By our ChIP and Real-time PCR assays, we reveal that TGF-B1 down-regulates ANCR expression by increasing HDAC3 enrichment at ANCR promoter region, which decreases both H3 and H4 acetylation of ANCR promoter. In addition, by western blot and transwell assays, we indicate that ectopic expression of ANCR partly attenuates the TGF-B1-induced EMT. Downstream, ANCR inhibits breast cancer cell migration and breast cancer metastasis by decreasing RUNX2 expression in vitro and in vivo. Thus, our study identifies ANCR, as a new TGF-B downstream molecular, is essential for TGF-B1-induced EMT by decreasing RUNX2 expression. These results implicate that ANCR might become a prognostic biomarker and an anti-metastasis therapy target for breast cancer. These results demonstrate that ANCR is down-regulated during the TGF-B1-induced EMT in MCF10A cells. 	28978036	2017	LncRNA ANCR down-regulation promotes TGF-B-induced EMT and metastasis in breast cancer.	0	0	0
chr3	50337511	50338300	ANRASSF1	102060282	HGNC:49091	ENSG00000281358	NR_109831	RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc.	up-regulated	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. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region.	23990798	2013	The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation.	1	0	1
chr3	50337511	50338300	ANRASSF1	102060282	HGNC:49091	ENSG00000281358	NR_109831	qPCR etc.	up-regulated	In this study, we analyzed expression of four long noncoding RNAs (lncRNAs) namely SOX2OT, PTPRG-AS1, ANRASSF1, and ANRIL in 38 breast cancer tissues and their adjacent noncancerous tissues (ANCTs). ANRASSF1 expression was not detected in any noncancerous tissue. All lncRNAs showed significant overexpression in tumor tissues compared with ANCTs.	26409453	2016	Expression analysis of four long noncoding RNAs in breast cancer.	0	0	0
chr9	21994778	22121097	ANRIL	100048912	HGNC:34341	ENSG00000240498	NR_003529	microarray, qPCR etc.	up-regulated	Expression level of these 3 lncRNAs was determined in plasma samples of 60 patients with BC and 40 healthy individuals by performing real-time PCR. As expected, the relative expression of ANRIL, HIF1A-AS2, and UCA1 was significantly higher in patients with TNBC than in patients with NTNBC, which was consistent with the results of microarray analysis.	28248879	2017	A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers.	0	1	1
chr9	21994778	22121097	ANRIL	100048912	HGNC:34341	ENSG00000240498	NR_003529	qPCR etc.	up-regulated	In breast cancer, the rs11515 CG genotype is more frequent and associated with a more aggressive tumor that could be due to increased ANRIL and reduced p16 (INK4a) expression. Compared to the CC genotype, the CG genotype was associated with lower expression of CDKN2A/p16INK4a, and higher expression of ANRIL.	26835415	2016	The rs11515 Polymorphism Is More Frequent and Associated With Aggressive Breast Tumors with Increased ANRIL and Decreased p16 (INK4a) Expression.	0	0	0
chr9	21994778	22121097	ANRIL	100048912	HGNC:34341	ENSG00000240498	NR_003529	qPCR etc.	up-regulated	In a series of 12 breast tumor tissues showing a wide range of p14/ARF, p16/ CDKN2A, and p15/CDKN2B mRNA levels, we also observed a stronger positive correlation of ANRIL with p14/ARF than with p16/ CDKN2A or p15/CDKN2B. This study points to the existence of a new gene within the p15/CDKN2B-p16/CDKN2A-p14/ARF locus putatively involved in melanoma-NST syndrome families and in melanoma-prone families with no identified p16/CDKN2A mutations as well as in somatic tumors.	17440112	2007	Characterization of a germ-line deletion, including the entire INK4/ARF locus, in a melanoma-neural system tumor family: identification of ANRIL, an antisense noncoding RNA whose expression coclusters with ARF.	0	0	0
chr9	21994778	22121097	ANRIL	100048912	HGNC:34341	ENSG00000240498	NR_003529	qPCR etc.	up-regulated	In this study, we analyzed expression of four long noncoding RNAs (lncRNAs) namely SOX2OT, PTPRG-AS1, ANRASSF1, and ANRIL in 38 breast cancer tissues and their adjacent noncancerous tissues (ANCTs). ANRASSF1 expression was not detected in any noncancerous tissue. All lncRNAs showed significant overexpression in tumor tissues compared with ANCTs.	26409453	2016	Expression analysis of four long noncoding RNAs in breast cancer.	0	0	0
chr11	69475567	69481545	AP000439.3	NA	NA	ENSG00000255980	NA	qPCR etc.	up-regulated	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. This fnding revealed lncRNAs may serve as important effectors of ER in regulation of gene expression and cell phenotype in breast cancer.	29048636	2017	Genome-wide study of ER-regulated lncRNAs shows AP000439.3 may function as a key regulator of cell cycle in breast cancer	0	0	0
chr21	17611744	17633199	ASBEL	110806272	HGNC:53145	ENSG00000280594	NR_149073	qPCR, Western blot etc.	down-regulated	LncRNA ASBEL has been identified as an anti-sense transcript of BTG3 (B cell translocation gene 3) gene, which encodes an anti-proliferation protein. Remarkable down-regulation of BTG3 has been reported in triple-negative breast cancer (TNBC). In the present study, a number of single-stranded modified anti-sense DNA oligonucleotides (antago) were designed, synthesized and screened for specific lncRNA ASBEL knockdown. We showed here that anti-ASBEL antago played a significant tumor suppressive role in TNBC by effective down-regulation of lncRNA ASBEL, which in turn led to increased BTG3 expression. The obtained data suggest lncRNA ASBEL as a novel therapeutic target in TNBC. antago3 has a great potential to be an useful therapeutic tool for TNBC treatment through targeting lncRNA ASBEL-related pathway.	28552529	2017	Targeting long non-coding RNA ASBEL with oligonucleotide antagonist for breast cancer therapy	0	1	1
chr14	19284653	19337730	ASHGA5P014632	NA	NA	ENSG00000244306	NA	qPCR, RNAi etc.	up-regulated	The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines.	27322459	2016	Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis.	0	0	1
NA	NA	NA	AX747207	NA	NA	NA	NA	qPCR etc.	down-regulated	Compared to the MCF-7 cells, 8,892 lncRNAs were differentially expressed in MCF/ADR cells (absolute fold-change >2.0). A total of 32 lncRNAs were selected for RT-qPCR by fold-change filtering, standard  Student's t-test, and multiple hypothesis testing. Among the dysregulated lncRNAs, AX747207 was prominent because its associated gene RUNX3 was previously  reported to be relative to malignant tumor chemoresistance. In addition, the study identified the lncRNA AX747207, and its potential targeted gene RUNX3, may be related to chemoresistance in breast cancer. 	29749447	2018	Chemoresistance-related long non-coding RNA expression profiles in human breast cancer cells.	0	0	0
chr9	69296682	69311111	BANCR	100885775	HGNC:43877	ENSG00000278910	NR_047671	qPCR,Western blot, in vitro knockdown etc.	up-regulated	LncRNA BANCR is highly expressed in breast cancer, which is significantly correlated with the prognosis of patients; moreover, it can promote the growth, invasion and metastasis of ovarian cancer cells. The down-regulation of BANCR can inhibit the proliferation, invasion and metastasis capacities of MCF-7 cells.	29565494	2018	Long non-coding RNA BANCR indicates poor prognosis for breast cancer and promotes cell proliferation and invasion.	0	0	1
chr9	69296682	69311111	BANCR	100885775	HGNC:43877	ENSG00000278910	NR_047671	qPCR etc.	up-regulated	In conclusion, BANCR overexpression could promote the clinical progression, metastasis and proliferation of BC and indicate poor prognosis of patients with BC.	29805676	2018	Long non-coding RNA BRAF-regulated lncRNA 1 promotes lymph node invasion, metastasis and proliferation, and predicts poor prognosis in breast cancer	0	0	1
chr1	68496676	68538627	BC016787	NA	NA	ENSG00000234264	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr11	106674027	106676271	BC036599	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr3	42770612	42773635	BC038366	729083	HGNC:53019	ENSG00000225611	NR_122070	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr2	74940258	74942670	BC038580	NA	NA	ENSG00000230836	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr6	6724886	6725300	BC039678	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr8	90646441	90646633	BC040572	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr3	116921431	116932238	BC040587	100506724	HGNC:40352	ENSG00000242385	NR_121607	qPCR etc.	down-regulated	It showed that BC040587 expression was down regulated both in BC samples and in BC cell lines compared with corresponding normal control. BC040587 expression was correlated with menopausal status and tumor differentiation. Furthermore, expression of BC040587 was significantly associated with worse prognosis and was shown to be an independent prognostic marker breast cancer.	25435812	2014	Role of BC040587 as a predictor of poor outcome in breast cancer.	0	0	1
chr21	42599280	42615058	BC041455	101928233	HGNC:52459	ENSG00000225431	NR_131192	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. Overexpression of BC041455 prevented ERK1/2 phosphorylation. The effects of BC041455 on hormone-dependent MAPK signalling were observed in both MCF-7 and T-47D cells.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	1	1	1
chr2	47335315	47335514	BC200	618	HGNC:1022	ENSG00000236824	NR_001568	qPCR etc.	up-regulated	BC200 expression was substantially upregulated in brain and elevated expression was also observed in testes, small intestine and ovary. Expression in  cultured tumour cells was dramatically higher than corresponding normal tissue; however, expression in cultured primary cells was similar to that in immortalized and cancer cell lines. BC200 knockdown resulted in a dramatic loss of viability through growth arrest and induction of apoptosis that could be partially rescued  by overexpression of wild-type BC200 but not an siRNA-resistant sequence mutant. Upon release from cell cycle arrest, BC200 expression was recovered as cells entered S-phase, but did not follow a periodic expression pattern during synchronized progression through the cell cycle. This elevated expression was critical for the survival of proliferating cancerous and non-cancerous cells, but is dispensable upon senescence or cell cycle arrest. Our knock-down assays challenge reports that BC200 knockdown confers a survival advantage, as we clearly demonstrate growth arrest and induction of apoptosis in a broad spectrum of both cancer and normal primary cells. For the first time, we show that BC200 expression is greatly reduced in senescent and arrested cells and is elevated upon resumption of the cell cycle, suggesting the possibility of a distinct role for this long non-coding RNA outside of the nervous system.	28651607	2017	The long non-coding RNA BC200 (BCYRN1) is critical for cancer cell survival and proliferation.	0	0	1
chr2	47335315	47335514	BC200	618	HGNC:1022	ENSG00000236824	NR_001568	qPCR, ChIP etc.	up-regulated	In this study, we show that BC200 is upregulated in breast cancer; among breast tumor specimens there is a higher level of BC200 in estrogen receptor (ER) positive than in ER-negative tumors. Further experiments show that activation of estrogen signaling induces expression of BC200.	27277684	2016	Regulation of alternative splicing of Bcl-x by BC200 contributes to breast cancer pathogenesis.	1	0	1
chr2	47335315	47335514	BC200	618	HGNC:1022	ENSG00000236824	NR_001568	microarray, ISH etc.	up-regulated	We here report that BC200 RNA is expressed at high levels in invasive carcinomas of the breast. In normal breast tissue or in benign tumors such as fibroadenomas, in contrast, we found that the RNA is not detectable at significant levels. The difference in expression levels between invasive carcinomas and normal/benign tissue was statistically highly significant.	15240511	2004	BC200 RNA in invasive and preinvasive breast cancer.	0	0	0
chr2	47335315	47335514	BC200	618	HGNC:1022	ENSG00000236824	NR_001568	Northern hybridization, ISH etc.	up-regulated	BC200 RNA was expressed in carcinomas of the breast, cervix, oesophagus, lung, ovary, parotid, and tongue, but not in corresponding normal tissues.	9422992	1997	Expression of neural BC200 RNA in human tumours.	0	0	0
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	microarray, qPCR, RNAi etc.	differential expression	As BCAR4 expression in cell lines did not change the sensitivity to different chemotherapeutic agents, the increased sensitivity to lapatinib is not due to a general mechanism of drug resistance. Also in our BCAR4-expressing cell models, the combination of lapatinib and antioestrogens was more potent in inhibiting cell growth than lapatinib alone; indicating that blocking the ERBB2 pathway with lapatinib re-sensitises BCAR4-expressing cells to antioestrogens. BCAR4 expression strongly sensitised ZR-75-1 and MCF7 breast cancer cells to the combination of lapatinib and antioestrogens.	22892392	2012	BCAR4 induces antioestrogen resistance but sensitises breast cancer to lapatinib.	1	0	1
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	qPCR etc.	up-regulated	Forced expression of BCAR4 in human ZR-75-1 and MCF7 breast cancer cells resulted in cell proliferation in the absence of estrogen and in the presence of various antiestrogens. Inhibition of estrogen receptor 1 (ESR1) expression with small interfering RNA (siRNA), implied that the BCAR4-induced mechanism of resistance is independent of ESR1. BCAR4 is a strong transforming gene causing estrogen-independent growth and antiestrogen resistance, and induces tumor formation in vivo. Due to its restricted expression, BCAR4 may be a good target for treating antiestrogen-resistant breast cancer.	21506106	2011	Characterization of BCAR4, a novel oncogene causing endocrine resistance in human breast cancer cells.	1	0	1
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	qPCR, Western blot etc.	up-regulated	Multivariate analyses established high BCAR4 mRNA levels as an independent predictive factor for poor PFS after start of tamoxifen therapy for recurrent disease. BCAR4 may have clinical relevance for tumour aggressiveness and tamoxifen resistance. Our cell model suggests that BCAR4-positive breast tumours are driven by ERBB2/ERBB3 signalling. Patients with such tumours may benefit from ERBB-targeted therapy.	20859285	2010	Relevance of BCAR4 in tamoxifen resistance and tumour aggressiveness of human breast cancer.	1	0	1
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	qPCR etc.	up-regulated	We showed that ectopic expression of this gene, designated as breast cancer antiestrogen resistance 4 (BCAR4), caused OH-TAM resistance and anchorage-independent cell growth in ZR-75-1 cells and that the intact open reading frame was required for its function. We conclude that retroviral transfer of cDNA libraries into human breast cancer cells is an efficient method for identifying genes involved in tamoxifen resistance.	16778085	2006	Functional screen for genes responsible for tamoxifen resistance in human breast cancer cells.	1	0	1
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	1
chr16	11819829	11828845	BCAR4	400500	HGNC:22170	ENSG00000262117	NR_024049	qPCR, Western blot, Cell proliferation assay etc.	up-regulated	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.	26317614	2015	Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells.	1	0	1
NA	NA	NA	BORG	NA	NA	NA	NA	qPCR etc.	up-regulated	Through in silico and biological analyses, we identifed a novel lncRNA, BMP/OP-Responsive Gene (BORG), whose expression directly correlates with aggressive breast cancer phenotypes, as well as with metastatic competence and disease recurrence in multiple clinical cohorts. Mechanistically, BORG elicits the metastatic outgrowth of latent breast cancer cells by promoting the localization and transcriptional repressive activity of TRIM28, which binds BORG and induces substantial alterations in carcinoma proliferation and survival. Moreover, inhibiting BORG expression in metastatic breast cancer cells impedes their metastatic colonization of the lungs of mice, implying that BORG acts as a novel driver of the genetic and epigenetic alterations that underlie the acquisition of metastatic and recurrent phenotypes by breast cancer cells.	28983112	2017	The lncRNA BORG Drives Breast Cancer Metastasis and Disease Recurrence	0	1	1
chr10	118046279	118210153	CASC2	255082	HGNC:22933	ENSG00000177640	NR_026939	qPCR, Western blot, in vitro knockdown etc.	down-regulated	Overexpression of lncRNA CASC2 significantly repressed proliferation and metastasis while caused cell cycle arrest and much more early apoptosis of breast cancer.The inactivation of TGF-signal pathway was involved in the function of lncRNA CASC2.lncRNA CASC2 was a key factor in the tumorigenesis and malignancy of breast cancer, thereby possibly was a potential therapy target for the treatment of breast cancer. 	29523222	2018	Up-regulation of lncRNA CASC2 suppresses cell proliferation and metastasis of breast cancer via inactivating of the TGF-signaling pathway. 	0	0	0
NA	NA	NA	CASIMO1	NA	NA	NA	NA	in vitro knockdown etc.	up-regulated	CASIMO1 RNA is overexpressed predominantly in hormone receptor-positive breast tumors. Its knockdown leads to decreased proliferation in multiple breast cancer  cell lines. Its loss disturbs the organization of the actin cytoskeleton, leads to inhibition of cell motility, and causes a G0/G1 cell cycle arrest. The proliferation phenotype upon overexpression is observed only with CASIMO1 protein expression, but not with a non-translatable mutant attributing the effects to the sORF-derived protein rather than a lncRNA function. CASIMO1 microprotein interacts with squalene epoxidase (SQLE), a key enzyme in cholesterol synthesis and a known oncogene in breast cancer. Overexpression of CASIMO1 leads to SQLE protein accumulation without affecting its RNA levels and increased lipid droplet clustering, while knockdown of CASIMO1 decreased SQLE protein abundance and ERK phosphorylation downstream of SQLE. Importantly, SQLE knockdown mimicked the CASIMO1 knockdown phenotype and in turn SQLE overexpression fully rescued the effect of CASIMO1 knockdown.	29765154	2018	The cancer-associated microprotein CASIMO1 controls cell proliferation and interacts with squalene epoxidase modulating lipid droplet formation.	0	0	0
chr8	127207382	127219268	CCAT1	100507056	HGNC:45128	ENSG00000247844	NR_108049	qPCR etc.	up-regulated	Expression levels of lncRNA CCAT1 in BC tissues were significantly higher than those in adjacent normal tissues. High expression of lncRNA CCAT1 was associated with differentiation grade, TNM stage, and lymph node metastases. Kaplan-Meier analysis with the log-rank test indicated that high expression of lncRNA CCAT1 had a decreased overall survival and progression-free survival. Multivariable analysis was further identified high expression of lncRNA CCAT1 as an independent prognosis factor for overall survival and progression-free survival.	26464701	2015	Overexpression of long non-coding RNA CCAT1 is a novel biomarker of poor prognosis in patients with breast cancer	0	0	1
chr8	127207382	127219268	CCAT1	100507056	HGNC:45128	ENSG00000247844	NR_108049	qPCR, Luciferase reporter assay, RIP	up-regulated	CCAT1 was up-regulated and miR-148b was down-regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues.CCAT1 down-regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation. Moreover, CCAT1 could negatively regulate miR-148b expression. Furthermore, overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown.	29024383	2017	Down-regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR-148b in breast cancer.	0	0	1
chr8	127400399	127402150	CCAT2	101805488	HGNC:47044	ENSG00000280997	NR_109834	qPCR	down-regulated	significant inverse correlations were found between CCAT2 expression and stage, as well as lymph node involvement. Besides, a significant inverse correlation was found between the relative MYC expression in tumor tissues compared with their corresponding ANCTs and disease stage.CCAT2 expression level was suggested as a predictor of metastasis and poor survival for a particular subgroup of breast cancer patients. 	28480695	2017	Expression Study and Clinical Correlations of MYC and CCAT2 in Breast Cancer Patients	0	0	1
chr8	127400399	127402150	CCAT2	101805488	HGNC:47044	ENSG00000280997	NR_109834	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	The expression level of CCAT2 in breast cancer tissues was significantly increased. The expression level of CCAT2 in breast cancer without metastasis was decreased compared with breast cancer metastasis. Meanwhile, down-regulation of CCAT2 inhibited the proliferation, invasion and migration in breast cancer cells. Furthermore, 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-B, Smad2 and a-SMA in breast cancer cells.	28272713	2017	Long non-coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-B signaling pathway.	0	0	0
chr8	127400399	127402150	CCAT2	101805488	HGNC:47044	ENSG00000280997	NR_109834	qPCR, Western blot, RIP, ChIP etc.	up-regulated	Moreover, when CCAT2 silencing, the cell cycle relative protein CyclinD1, CyclinE1 and CDK4 expression were downregulated, but p15 was up-regulated in MCF7 and MDA-MB-231 cells.CCAT2 expression levels in tumor tissues were markedly increased than that in adjacent normal tissues. higher CCAT2 expression was closely correlated with shorter over survival (OS) time in patients. CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells. In vivo, the tumor growth was inhibited after knockdown of CCAT2.	28531944	2017	Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer.	0	0	1
chr8	127400399	127402150	CCAT2	101805488	HGNC:47044	ENSG00000280997	NR_109834	qPCR, RNAi, Western blot etc.	up-regulated	We first confirmed the high expression level of CCAT2 in breast cancer tissues and breast cancer cell lines by reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay, and we further analyzed the relationship between CCAT2 expression and clinical prognostic factors. Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo. Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway.	26442763	2015	Long noncoding RNA CCAT2 promotes breast tumor growth by regulating the Wnt signaling pathway	0	1	1
chr8	127400399	127402150	CCAT2	101805488	HGNC:47044	ENSG00000280997	NR_109834	microarray, qPCR, RNAi etc.	up-regulated	Although, after dividing the tumors at the median in groups containing a low or high percentage of invasive tumor cells, CCAT2 RNA levels were significantly higher in the group of tumors with high invasive tumor cells.	24077681	2013	CCAT2, a novel long non-coding RNA in breast cancer: expression study and clinical correlations.	1	0	0
chr12	69239537	69274358	CPSF6	NA	NA	ENSG00000111605	NA	qPCR, Western blot etc.	up-regulated	Aggressive breast cancer cells require CPSF6 for viability and tumorigenesis. CPSF6 and paraspeckles core proteins are associated with poor outcome in breast cancer. Prolactin hormone reprograms cells to suppress CPSF6 interaction with paraspeckles and ADAR1, A-I RNA editing machinery. CPSF6 and all core paraspeckles proteins to be overexpressed in human breast cancer cases and their expression to correlate with poor patient outcomes. the important role and contribution of CPFS6 to survival and tumor formation of aggressive breast cancer cells. 	28673861	2017	CPSF6 is a Clinically Relevant Breast Cancer Vulnerability Target: Role of CPSF6 in Breast Cancer.	0	0	1
NA	NA	NA	CR592608	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
NA	NA	NA	CR593775	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. These results suggest that CR593775 is involved in mediating the downstream effects of oestrogen signalling on breast cancer cell proliferation, including possible interactions with mechanisms of DNA synthesis regulation. Cell cycle analysis in synchronized cells indicates that disruption of CR593775 expression did not affect cell cycle progression.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
NA	NA	NA	CR610499	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	down-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
NA	NA	NA	CR612213	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
NA	NA	NA	CRALA	NA	NA	NA	NA	qPCR etc.	up-regulated	CRALA is upregulated in chemoresistant breast cancer cell lines compared to their parental lines. Silencing of CRALA in chemoresistant breast cancer cells resensitizes the cells to chemotherapy in vitro. Furthermore, univariate and multivariate analysis showed that higher CRALA expression was significantly associated with poor prognosis in 144 breast cancer patients.	28834648	2017	Long non-coding RNA CRALA is associated with poor response to chemotherapy in primary breast cancer	1	0	1
chr16	54845189	54929189	CRNDE	NA	NA	ENSG00000245694	NA	qPCR	up-regulated	CRNDE expression is remarkably up-regulated in BC tissue specimens and cell lines in comparison to corresponding normal tissues and normal human breast epithelial cells. Up-regulated CRNDE expression was greatly associated with larger tumor size, advanced TNM stage and unfavorable prognosis of BC patients. 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 B-catenin, c-myc and cyclinD1.	28469804	2017	Long noncoding RNA CRNDE activates Wnt/B-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer	0	0	1
chr4	52712404	52720351	DANCR	57291	HGNC:28964	ENSG00000226950	NR_024031	qPCR, Western blot, RIP, RNA pull-down assay, Cell proliferation assay etc.	down-regulated	We also uncover ANCR is an important player in breast cancer progression and metastasis mainly through decreasing EZH2 stability. More specifically, we initially found that ANCR level was lower in breast cancer tissues and breast cancer cell lines, in contrast to their normal counterparts. We then demonstrated that knockdown of ANCR induced an EMT program and promoted cell migration and invasion in MCF10A (epithelial cells), whereas ectopic expression of ANCR repressed breast cancer cells migration and invasion.	27716745	2017	The degradation of EZH2 mediated by lncRNA ANCR attenuated the invasion and metastasis of breast cancer.	0	0	0
chr21	40383083	40385358	DSCAM-AS1	100506492	HGNC:40197	ENSG00000235123	NR_038896	RNA-seq, qRT-PCR, Western blot, in vitro knockdown, RNAi	up-regulated	By the analysis of H3K27ac enrichment in hormone-deprived MCF-7 cells, we defined a set of Super Enhancers (SEs) occupied by apoERa, including one mapped in proximity of the DSCAM-AS1 lncRNA gene.This represents a paradigm of apoERa activity since its expression is largely unaffected by estrogenic treatment,despite the fact that E2 increases ERa binding on DSCAM-AS1 promoter. We validated the enrichment of apoERa, p300, GATA3, FoxM1 and CTCF at both DSCAM-AS1 TSS and at its associated SE by ChIP-qPCR. Furthermore, by analyzing MCF-7 ChIA-PET data and by 3C assays, we confirmed long range chromatin interaction between the SE and the DSCAM-AS1 TSS. Interestingly, CTCF and p300 binding showed an enrichment in hormone-depleted medium and in the presence of ERa, elucidating the dynamics of the estrogen-independent regulation of DSCAM-AS1 expression.The most significant down-regulated lncRNAs were RP11-68L18.1, MIR9-3HG, and LINC01016, whereas NKILA, AC144831.1, and LINC00657 were the most significant up-regulated lncRNAs	29462945	2018	Luminal lncRNAs Regulation by ERa-Controlled Enhancers in a Ligand-Independent Manner in Breast Cancer Cells.	MCF-7	0	0
chr21	40383083	40385358	DSCAM-AS1	100506492	HGNC:40197	ENSG00000235123	NR_038896	RNA-seq, qPCR, RNAi, ChIP, Cell proliferation assay etc.	up-regulated	The most abundant AER-lncRNA, DSCAM-AS1, is expressed in ERa+ breast carcinoma, but not in pre-neoplastic lesions, and correlates inversely with EMT markers. Down-regulation of DSCAM-AS1 recapitulated, in part, the effect of silencing ERa, i.e. growth arrest and induction of EMT markers.	26621851	2016	Luminal long non-coding RNAs regulated by estrogen receptor alpha in a ligand-independent manner show functional roles in breast cancer.	0	0	0
chr21	40383083	40385358	DSCAM-AS1	100506492	HGNC:40197	ENSG00000235123	NR_038896	RNA-seq, qPCR, RNAi, RIP, ChIP, Cell proliferation assay etc.	up-regulated	Among the luminal breast cancers, DSCAM-AS1 is expressed significantly higher in luminal B, a clinical subtype containing most of the clinically aggressive ER-positive breast cancers. We demonstrate that DSCAM-AS1 mediates tumour progression and tamoxifen resistance and identify hnRNPL as an interacting protein involved in the mechanism of DSCAM-AS1 action.	27666543	2016	The lncRNA landscape of breast cancer reveals a role for DSCAM-AS1 in breast cancer progression.	1	0	0
chr21	40383083	40385358	DSCAM-AS1	100506492	HGNC:40197	ENSG00000235123	NR_038896	qPCR, Northern blot, ISH etc.	up-regulated	M41 mRNA is expressed at a statistically significantly higher level in human breast cancer specimens than in normal human breast and benign lesions. In carcinomas, its up-regulation is associated with the development of the malignant cell.	12177779	2002	Identification of mRNAs differentially-expressed between benign and malignant breast tumour cells.	0	0	0
chr14	19294785	19337674	DUXAP10	NA	NA	NA	NA	qPCR, RNAi etc.	up-regulated	The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines.	27322459	2016	Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis.	0	0	1
chr1	155078872	155087538	EFNA3	1944	HGNC:3223	ENSG00000143590	NA	qPCR, RIP etc.	up-regulated	We demonstrate that sustained expression of both Ephrin-A3 and novel EFNA3 lncRNAs increased the metastatic potential of human breast cancer cells, possibly by increasing the ability of tumor cells to extravasate from the blood vessels into surrounding tissue. In agreement, we found a strong correlation between high EFNA3 expression and shorter metastasis-free survival in breast cancer patients. hypoxia could contribute to metastatic spread of breast cancer via HIF-mediated induction ofEFNA3lncRNAs and subsequent Ephrin-A3 protein accumulation.	25023702	2014	EFNA3 long noncoding RNAs induced by hypoxia promote metastatic dissemination.	0	0	1
chr3	4749192	4751590	EGOT	100126791	HGNC:37129	ENSG00000235947	NR_004428	qPCR etc.	down-regulated	EGOT expression was lower in breast cancer compared with the adjacent noncancerous tissues, and low levels of EGOT expression were significantly correlated with larger tumor size, more lymph node metastasis, and higher Ki-67 expression. Moreover, patients with low levels of EGOT expression showed significantly worse prognosis for overall survival. Multivariate analysis suggested that low levels of EGOT were a poor independent prognostic predictor for breast cancer patients	26159853	2015	Downregulation of the long noncoding RNA EGOT correlates with malignant status and poor prognosis in breast cancer	0	0	1
chr3	2110409	2144241	ENSG00000227588	100873976	HGNC:39986	ENSG00000227588	NR_046555	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr1	248691760	248716755	ENSG00000229703	NA	NA	ENSG00000229703	NA	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr9	3526723	3691814	ENSG00000232104	101929302	HGNC:51197	ENSG00000232104	NR_121586	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr2	558204	578145	ENSG00000233633	NA	NA	ENSG00000233633	NA	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr3	1008135	1012934	ENSG00000235158	NA	NA	ENSG00000235158	NA	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr13	113926514	113928844	ENSG00000260910	100861555	HGNC:43709	ENSG00000260910	NR_047495	qPCR, SNP array etc.	differential expression	qPCR was used to selectively validate lincRNA-associated CNVs showing a predicted recurrence within 7 pairs. Of 33 qPCR reaction assays for 6 lincRNAs, 28 (85%) were in agreement with the prediction from Nexus. All six calls for sample BC-4 were detected while five calls for BC-5 were not detected.	23267367	2012	Identifying putative breast cancer-associated long intergenic non-coding RNA loci by high density SNP array analysis.	0	0	0
chr16	52258564	52280638	ENST00000515084	NA	HGNC:50627	ENSG00000260887	NA	qPCR, Luciferase reporter assay, Cell viability assay, Transient transfection etc.	up-regulated	We found that the C allele of the rs12325489C>T polymorphism in the exonic regions of lincRNA-ENST00000515084 was associated with a significantly increased risk of breast cancer, compared with the rs12325489TT genotype. Biochemical analysis demonstrated that the C to T base change at rs12325489C>T disrupts the binding site for miRNA-370, thereby influencing the transcriptional activity of lincRNA-ENST00000515084 in vitro and in vivo, and affecting cell proliferation and tumor growth.	24879036	2014	A polymorphism rs12325489C>T in the lincRNA-ENST00000515084 exon was found to modulate breast cancer risk via GWAS-based association analyses.	0	0	0
chr5	112419583	112420978	EPB41L4A-AS2	NA	NA	ENSG00000278921	NA	qPCR, Flow cytometry assay etc.	down-regulated	we investigated the expression of EPB41L4A-AS2 in breast cancer tissues and evaluated its relationship with the clinicopathological features and prognosis of patients with breast cancer. This entailed conducting a meta-analysis and prognosis validation study using two cohorts from the Gene Expression Omnibus (GEO). In addition, we assessed EPB41L4A-AS2 expression and its relationship with the clinicopathological features of renal and lung cancers using the Cancer Genome Atlas cohort and a GEO dataset. We also clarified the role of EPB41L4A-AS2 expression in mediating cancer cell proliferation in breast, renal, and lung cancer cell lines transfected with an EPB41L4A-AS2 expression vector. We found that high EPB41L4A-AS2 expression is associated with favorable disease outcomes. Gene ontology enrichment analysis revealed that EPB41L4A-AS2 may be involved in processes associated with tumor biology. Finally, overexpression of EPB41L4A-AS2 inhibited tumor cell proliferation in breast, renal, and lung cancer cell lines	26980733	2016	The long non-coding RNA EPB41L4A-AS2 inhibits tumor proliferation and is associated with favorable prognoses in breast cancer and other solid tumors	0	0	1
NA	NA	NA	EPIC1	NA	NA	NA	NA	qPCR, Western blot, in vitro knockdown, RIP etc.	up-regulated	Overexpression of EPIC1 is associated with poor prognosis in luminal B breast cancer patients and enhances tumor growth in vitro  and in vivo. Mechanistically, EPIC1 promotes cell-cycle progression by interacting with MYC through EPIC1's 129-283 nt region. EPIC1 knockdown reduces the occupancy of MYC to its target genes (e.g., CDKN1A, CCNA2, CDC20, and CDC45). MYC depletion abolishes EPIC1's regulation of MYC target and luminal breast cancer tumorigenesis in vitro and in vivo. 	29622465	2018	lncRNA Epigenetic Landscape Analysis Identifies EPIC1 as an Oncogenic lncRNA that Interacts with MYC and Promotes Cell-Cycle Progression in Cancer.	0	0	1
NA	NA	NA	ESRPS-AS	NA	NA	NA	NA	qPCR, RNA-seq, western blot etc.	up-regulated	ESRPs were shown previously to have a dual role in carcinogenesis. Both gain and loss have been associated with poor prognosis in human cancers, but the mechanisms regulating expression are not known. Indepth analyses indicate that coordinate overexpression of Esrp2 and Esrp2-as inversely correlates with DNA methylation. Using the Kaplan¨CMeier plotter survival analysis tool,we could confirm that high ESRP2 mRNA levels reduce the fraction of relapse-free survival, overall survival, and distant metastasis-free survival of breast cancer cases analyzed together or when cases were subdivided into breast cancer subtypes.	28759043	2017	Genome-wide screen for differentially methylated long noncoding RNAs identifies Esrp2 and lncRNA Esrp2-as regulated by enhancer DNA methylation with prognostic relevance for human breast cancer	0	0	1
chr1	150515757	150518032	FAL1	100874054	HGNC:43713	ENSG00000228126	NR_051960	qPCR, RNA pull-down assay etc.	up-regulated	We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. 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.	25203321	2014	A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p22 expression in cancer.	0	0	1
chr16	86474529	86509099	FENDRR	400550	HGNC:43894	ENSG00000268388	NR_033925	qPCR, in vitro knockdown etc.	down-regulated	FENDRR inhibits breast cancer cell proliferation and migration and promotes cell apoptosis, while FENDRR knockdown promotes breast cancer cell proliferation and migration and suppresses cell apoptosis. FENDRR overexpression could inhibit tumor growth in a xenograft model. FENDRR inhibits breast cancer cell proliferation, promotes cell apoptosis, and is associated with good prognosis in  breast cancer. 	29559798	2018	Long non-coding RNA FENDRR inhibits cell proliferation and is associated with good prognosis in breast cancer.	0	0	1
chr7	122303658	122310077	FEZF1-AS1	154860	HGNC:41001	ENSG00000230316	NR_036484	qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	FEZF1-AS1 was significantly over-expressed in breast cancer cells, especially in sphere subpopulation compared with parental subpopulation. In summary, our study validate the important role of FEZF1-AS1/miR-30a/Nanog in breast cancer stemness and tumorigenesis, providing a novel insight and treatment strategy for breast cancer.	29797562	2018	Long non-coding RNA FEZF1-AS1 promotes breast cancer stemness and tumorigenesis via targeting miR-30a/Nanog axis	0	0	0
chr13	102394630	102395703	FGF14-AS2	283481	HGNC:44368	ENSG00000272143	NR_036487	qPCR, RIP etc.	down-regulated	In this study, we demonstrated that FGF14 antisense RNA 2 (FGF14-AS2), a novel long non-coding RNA, was significantly down-regulated in breast cancer tissue compared with adjacent normal tissue both in validated cohort and TCGA cohort. Reduced expression of FGF14-AS2 was correlated with larger tumor size, more lymph node metastasis and advanced clinical stage in both cohorts.	26820525	2016	A novel long non-coding RNA FGF14-AS2 is correlated with progression and prognosis in breast cancer.	0	0	1
chr16	86565145	86567761	FOXC2-AS1	103752587	HGNC:50665	ENSG00000260944	NR_125795	qPCR, Western blot etc.	up-regulated	Cyclin D1 Cyclin D2, and Cyclin D3 were all partly positively modulated by FOXC2-AS1 in BC. FOXC2-AS1 may serve as a promising prognostic biomarker and therapeutic target for BC patients. FOXC2-AS1 significantly suppressed the proliferation ability and flow cytometric analysis illustrated the influence of FOXC2-AS1 on cell cycle and apoptosis rate. 	29562954	2018	Long non-coding RNA FOXC2-AS1 predicts poor survival in breast cancer patients and promotes cell proliferation	0	0	1
chr2	27392784	27393367	FTH1P3	NA	NA	ENSG00000213453	NA	qPCR,Flow cytometry assay,Western blot,Luciferase reporter assay,etc.	up-regulated	Bioinformatics tools and luciferase reporter assay validated that,FTH1P3 promoted ABCB1 protein expression through targeting miR-206,acting as,a miRNA sponge. In summary,our results reveal the potential regulatory mechanism ,of FTH1P3 on breast cancer paclitaxel resistance through miR-206/ABCB1,providing a novel insight for the breast cancer chemoresistance. However,the occurrence of chemoresistance causes the poor prognosis,high recurrence rate and low 5-year survival rate.In the present study,we investigate the role of lncRNA FTH1P3 in breast cancer paclitaxel resistance and explore the underlying mechanism for the drug resistance generation.	29971911	2018	Long non-coding RNA FTH1P3 activates paclitaxel resistance in breast cancer through miR-206/ABCB1.	1	0	1
chr2	16050427	16085801	GACAT3	104797537	HGNC:50847	ENSG00000236289	NR_126559	qPCR, Luciferase activity assay, etc.	up-regulated	GACAT3 promotes breast cancer malignancy by sponging miR-497, leading to the enhancement of its endogenous target CCND2. 	29945347	2018	LncRNA GACAT3 predicts poor prognosis and promotes cell proliferation in breast cancer through regulation of miR-497/CCND2.	0	0	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR, RNAi, Western blot, ISH, MTT assay etc.	down-regulated	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. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor.	23933812	2013	Negative regulation of lncRNA GAS5 by miR-21.	0	0	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR etc.	down-regulated	GAS5 down-regulation can suppress many aspects of DNC anti-cancer effects in breast cancer cells, it seems that co-treatment with DNC and GAS5 over-expression may provide a clinically useful tool for drug-resistance breast cancer cells.	29655698	2018	Down-regulation of lncRNA, GAS5 decreases chemotherapeutic effect of dendrosomal  curcumin (DNC) in breast cancer cells.	1	1	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR etc.	down-regulated	GAS5 transcript was abundant in HUVEC and normal breast epithelial cells (MCF10 cell line), but barely detectable in all tested breast and prostate cancer cells.	27922078	2016	MALAT1 and HOTAIR Long Non-Coding RNAs Play Opposite Role in Estrogen-Mediated Transcriptional Regulation in Prostate Cancer Cells.	0	0	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR etc.	down-regulated	Analysis in the 39 paired preoperative and postoperative plasma samples showed that lower GAS5 levels appeared in the patients with a high Ki67 proliferation index before surgery and the patients with a positive lymph node metastasis state after surgery. Plasma lncRNA GAS5 may have the potential to assess the surgical effects and prognosis for BC patients	26662314	2015	Circulating long noncoding RNA GAS5 as a potential biomarker in breast cancer for assessing the surgical effects	0	1	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR, RNAi etc.	down-regulated	In this preclinical study, the consequences of decreased GAS5 expression for breast cancer cell survival following treatment with chemotherapeutic agents are addressed. 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.	24789445	2014	Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy.	0	0	1
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR etc.	down-regulated	We have found that, in some cell lines, GAS5 expression induces growth arrest and apoptosis independently of other stimuli. GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues.	18836484	2009	GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer.	0	0	1
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	microarray, qPCR etc.	down-regulated	Expression of the lncRNA GAS5 was decreased in SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. Inhibition of GAS5 promoted SKBR-3 cell proliferation, and GAS5 knockdown partially reversed lapatinib-induced inhibition of SKBR-3/Tr cell proliferation. 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.	27034004	2016	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer	trastuzumab	0	1
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR, RNAi, Western blot, Cell proliferation assay etc.	down-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly. High level of Notch-1 provided a poor prognosis in breast cancer. Interference of Notch-1 significantly suppressed proliferation of T47D cell, and significantly increased the level of GAS5.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	1
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR	differential expression	The expression levels of both genes was lower in the overweight-obese (BMI ¡Ý 25) subgroup than that in the normal BMI (BMI < 25) subgroup (GAS5 P = .019, LSINCT5 P = .036). Moreover, the expression level of GAS5 was negatively correlated with BMI (r: _x0001_.170, P: .041). The expression level of GAS5 was higher in women with late menarche (>13 years) than that with early menarche (¡Ü13 years; P = .017). 	29785740	2018	Expression levels of breast cancer-related GAS5 and LSINCT5 lncRNAs in cancer-free breast tissue: Molecular associations with age at menarche and obesity	0	0	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qPCR, Western blot	down-regulated	Here, we show that levels of the lncRNA, growth arrest-specific transcript 5 (GAS5), are decreased in TNBC tissues, and this down-regulation of GAS5 is associated with an aggressive tumor phenotype in patients, affecting clinical stage, lymph node metastasis and overall survival.  These data suggest that GAS5 can suppress TNBC progression by competitively binding miR-196a5p, therefore GAS5 may be a prognostic biomarker of TNBC.	29793177	2018	Long noncoding RNA GAS5 suppresses triple negative breast cancer progression through inhibition of proliferation and invasion by competitively binding miR-196a-5p	0	0	1
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	qRT-PCR, RIP, Luciferase reporter assay, Western blot assay ect.	down-regulated	GAS5 levels were frequently decreased in breast cancer tissues and cell lines, and its relatively low expression was closely related to a larger tumour size, advanced tumour-node-metastasis (TNM) stage and estrogen receptor-negative (ER-) breast cancer tissues. More importantly, we found that GAS5 promoted autophagy, with enhanced autophagosome formation after GAS5 overexpression. GAS5 was found to act as a microRNA sponge in a pathway that included miR-23a and its target gene ATG3. The GAS5-miR-23a-ATG3 axis significantly regulated autophagy in vivo and in vitro.	30007957	2018	Effect of the LncRNA GAS5-MiR-23a-ATG3 Axis in Regulating Autophagy in Patients with Breast Cancer.	0	0	0
chr1	173863900	173868882	GAS5	60674	HGNC:16355	ENSG00000234741	NR_002578	Microarray, qPCR, Western blot, RIP, luciferase reporter assay, Flow cytometry assay, etc.	down-regulation	Collectively, our study demonstrates that GAS5 enhances the efficacy of tamoxifen in the treatment of breast cancer and could be a novel prognostic biomarker. Tamoxifen is a frequently used drug for hormonal therapy in patients with breast cancer, however, development of resistance to tamoxifen remains a serious clinical problem.Kaplan-Meier survival analysis was used to analyze the relationship between the expression of GAS5 and survival rate. P < 0.05 indicates a significant difference. Moreover, GAS5 increased sensitivity of breast cancer cells to tamoxifen by serving as a molecular sponge for miR-222, contributing to suppression of phosphatase and tensin homologs (PTEN) (one endogenous target of miR-222).	29969658	2018	Downregulation of lncRNA GAS5 confers tamoxifen resistance by activating miR-222 in breast cancer.	1	0	1
chr7	148987527	148989432	GHET1	102723099	HGNC:49425	ENSG00000281189	NR_130107	qPCR, western blot etc.	up-regulated	Our results demonstrated that GHET1 was up-regulated in breast cancer tissues and cell lines, and promoted breast cancer cell proliferation, invasion and migration by affecting EMT.	29843220	2018	up-regulated	0	0	1
chr1	67832303	68202987	GNG12-AS1	100289178	HGNC:43938	ENSG00000232284	NR_040077	qPCR, RNAi, ChIP etc.	down-regulated	We report that GNG12-AS1 is coexpressed with DIRAS3 in several tissues and coordinately downregulated with DIRAS3 in breast cancers. In breast cancer cell lines with loss of DIRAS3 imprinting, DIRAS3 and GNG12-AS1 are silenced in cis and the remaining GNG12-AS1 transcripts are predominantly monoallelic.	23871723	2013	Imprinted chromatin around DIRAS3 regulates alternative splicing of GNG12-AS1, a long noncoding RNA.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	up-regulated	Network analysis revealed the existence of five genes related with H19,including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS). The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 	29693231	2018	LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness.	0	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	up-regulated	Furthermore, H19 knockdown decreases PDK1 xpression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo.Reprogramming is referred to as the conversion of differentiated cells to a stem-like state. Ectopic expression of four transcription factors (Oct4, Klf4, Sox2 and c-Myc) reprograms various types of somatic cells to induced pluripotent stem cells. Accordingly, H19 and PDK1 expression exhibits strong correlations in primary breast carcinomas. H19 acting as a competitive endogenous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1a, leading to an increase in PDK1 expression. Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. 	29106390	2017	Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia.	aspirin	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc.	up-regulated	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.	26353930	2015	H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, microarray, RIP, Western blotting etc.	up-regulated	H19 might be exploited as a biomarker for metastatic cells within breast tumors and perhaps as a therapeutic target to prevent metastasis.	28611183	2017	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	down-regulated	We identified 2 SNPs significantly associated with breast cancer risk in stage I (P<0.05), but not significantly replicated in stage II. We combined the data from stage I and stage II, and found that, compared with the rs2071095 CC genotype, AA and CA+AA genotypes were associated with significantly decreased risk of breast cancer (adjusted OR 0.83, 95% CI 0.69-0.99; adjusted OR 0.88, 95%  CI 0.80-0.98, respectively). Stratified analyses showed that rs2071095 was associated with breast cancer risk in estrogen receptor (ER)-positive patients (P=0.002), but not in ER-negative ones (P=0.332). Expression levels of H19 in breast cancer cases with AA genotype were significantly lower than those with CC  genotype. rs2071095 CA and AA genotypes were found to be significantly associated with decreased expression of H19 in breast cancer patients compared with the CC genotype (P = 0.027 and P < 0.001, respectively).	29737472	2018	SNP rs2071095 in LincRNA H19 is associated with breast cancer risk.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	Microarray, qPCR, Western blot	differential expression	Microarray data derived from Huaier-treated breast cancer cells identified H19 as a potential target. Huaier extract reduced the expression of H19. Collectively, the data demonstrate that Huaier extract reduces viability and induces apoptosis in breast cancer cells via H19-miR-675-5p-CBL axis regulation.	29145193	2017	Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway	Huaier	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	Microarray, qPCR, Western blot, RNAi etc.	up-regulated	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. Moreover, we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression, and a high tumor CUL4A expression was associated with low survival in breast cancer patients treated with chemotherapy. A similar trend was observed in ER-positive breast cancer patients treated with chemotherapy although it was not statistically significant in overall survival due to a small sample size 	29190892	2017	LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway.	Doxorubicin (Dox) and cisplatin (CDDP)	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	up-regulated	In our study, we confirmed that the T variant of rs217727 was consistently associated with an increased risk of BC in the codominant model.Another previous study by Yang et al32 found that the rs217727 CT + TT genotypes were correlated with significantly increased gastric cancer risk (OR 1.32, 95% CI 1.01¨C1.71), while in functional assay analysis, the rs217727 CT, TT, or CT + TT genotypes were found not to affect H19 mRNA expression levels compared with the CC genotype, suggesting the C/T mutation might potentially change translational efficiency and lead to a transformation in H19 structure, thereby influencing the function of H19.	28919786	2017	Genetic variants in long noncoding RNA H19 contribute to the risk of breast cancer in a southeast China Han population.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	up-regulated	The results revealed that the expression of H19 was significantly increased in BC tissues and plasma compared with healthy controls, and plasma H19 levels were significantly correlated with estrogen receptor, progesterone receptor, c-erbB-2 and lymph node metastasis. Furthermore, plasma H19 levels were significantly decreased in postoperative samples than preoperative samples.	27540977	2016	Circulating lncRNA H19 in plasma as a novel biomarker for breast cancer.	0	1	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Western blot, RIP, ChIP etc.	up-regulated	In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERa-positive breast cancer cells, but not in ERa-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.	27845892	2016	LncRNA H19 confers chemoresistance in ERa-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK.	1	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	RNA-CISH etc.	up-regulated	HOTAIR, H19 and KCNQ1OT1 had significantly higher expression levels in IBC than NA, and HOTAIR and H19 were both expressed more strongly in IBC than in DCIS tissues.	26323944	2015	Long non-coding RNA chromogenic in situ hybridisation signal pattern correlation with breast tumour pathology.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, ChIP etc.	differential expression	Additionally, blocking ERa decreased H19 expression in the luminal progenitors and led to the development of smaller luminal colonies. We further showed that knocking down the H19 gene in the luminal progenitors significantly decreased the colony-forming potential of the luminal progenitors, and this phenotype could not be rescued by the addition of estrogen. Lastly, we explored the clinical relevance of the estrogen-H19 signaling axis in breast tumors and found that ERa(+) tumors exhibited a higher expression of H19 as compared with ERa(-) tumors and that H19 expression showed a positive correlation with ERa expression in those tumors. 	25944846	2015	Estrogen regulates luminal progenitor cell differentiation through H19 gene expression.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	differential expression	Only rs2107425 near H19 was significantly associated with shorter MFS in uni- and multi-variate analysis, with the more aggressive minor allele displaying a recessive trait.	21748294	2012	Correlation of breast cancer susceptibility loci with patient characteristics, metastasis-free survival, and mRNA expression of the nearest genes.	0	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	up-regulated	The role of H19 in transformation is addressed using a knockdown approach and shows that down-regulation of H19 significantly decreases breast and lung cancer cell clonogenicity and anchorage-independent growth. In addition, c-Myc and H19 expression shows strong association in primary breast and lung carcinomas. This work indicates that c-Myc induction of the H19 gene product holds an important role in transformation.	16707459	2006	The c-Myc oncogene directly induces the H19 noncoding RNA by allele-specific binding to potentiate tumorigenesis.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Northern blot etc.	differential expression	H19 RNA and insulin-like growth factor II mRNA were up-regulated significantly in non-neoplastic WAP-CRD-BP mammary tissue. WAP-CRD-BP mice are a novel model for mammary neoplasia and might provide insights into human breast cancer biology.	14729626	2004	Mammary tumor induction in transgenic mice expressing an RNA-binding protein.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Northern blot etc.	up-regulated	Here, we demonstrate, using a proteomic approach, that an H19 overexpression in human cancerous mammary epithelial cells stably transfected with genomic DNA containing the entire H19 gene is responsible for positively regulating at the post-transcriptional level the thioredoxin, a key protein of the cellular redox metabolism. Interestingly, this protein accumulates in many cancerous tissues, such as breast carcinomas in which we have also demonstrated an overexpression of the H19 gene.	11896592	2002	Thioredoxin post-transcriptional regulation by H19 provides a new function to mRNA-like non-coding RNA.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, ISH etc.	up-regulated	An overload of H19 transcript is associated with cells exhibiting higher tumorigenic phenotypes and therefore we conclude that the H19 gene has oncogenic properties in breast epithelial cells.	12419837	2002	Overexpression of an ectopic H19 gene enhances the tumorigenic properties of breast cancer cells.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	Immunohistochemical Staining, ISH etc.	up-regulated	In 72.5% of studied breast adenocarcinomas an overall H19 gene expression is increased when compared with healthy tissues. The H19 gene is generally overexpressed in stromal cells (92.2%) and rarely in epithelial cells (2.9% only). An up-regulation of the H19 gene is significantly correlated with the tumor values and the presence of both estrogen and progesterone receptors, and at the cellular level, the H19 gene demonstrates an independent expression versus accumulation of both the p53 protein and the Ki-67/MIB-1 cell-cycle marker.	9811352	1998	H19 overexpression in breast adenocarcinoma stromal cells is associated with tumor values and steroid receptor status but independent of p53 and Ki-67 expression.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	Immunohistochemical Staining, ISH etc.	up-regulated	H19 gene is generally overexpressed in stromal cells (92.2%) and rarely in epithelial cells (2.9% only), 3) an up-regulation of the H19 gene is significantly correlated with the tumor values and the presence of both estrogen and progesterone receptors, and 4) at the cellular level, the H19 gene demonstrates an independent expression versus accumulation of both the p53 protein and the Ki-67/MIB-1 cell-cycle marker.	9811352	1998	H19 overexpression in breast adenocarcinoma stromal cells is associated with tumor values and steroid receptor status but independent of p53 and Ki-67 expression.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR etc.	differential expression	The expression of H19 RNA in these tumors was increased in 5 tumors, but decreased by < or = 50% in 6 tumors when compared with normal adjacent tissue. H19 imprinting was maintained in all 18 informative fresh-frozen and paraffin-embedded formalin-fixed samples. 	8636375	1996	Imprinting and expression of insulin-like growth factor-II and H19 in normal breast tissue and breast tumor.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Northern blot etc.	up-regulated	We discovered that the mRNA of the H19 gene is overexpressed in MCF-7/AdrVp cells relative to parental MCF-7 cells or drug-sensitive MCF-7/AdrVp revertant cells. H19 is an imprinted gene with an important role in fetal differentiation, as well as a postulated function as a tumor suppressor gene. Another p95-overexpressing multidrug-resistant cell line, human lung carcinoma NCI-H1688, also displays high levels of H19 mRNA.	8674037	1996	H19 gene overexpression in atypical multidrug-resistant cells associated with expression of a 95-kilodalton membrane glycoprotein.	1	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	ISH etc.	up-regulated	In conclusion, it seems that a high H19 expression matches the tumor invasion. Our results suggest that the expression of this gene is concerned by the relationships between epithelial and stromal cells, and can reflect peculiar physiological states of the cells. Furthermore, we discuss results showing an abundant expression of H19 gene in some adenocarcinomas of bad prognosis, in the context of the otherwise established tumor-suppressor role of this gene, or the strictly controlled gene dosage, which could be overridden in these particular cases.	8785513	1995	The H19 gene is expressed within both epithelial and stromal components of human invasive adenocarcinomas.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi, Luciferase reporter assay, ISH etc.	up-regulated	BCSCs express high levels of H19, and ectopic overexpression of H19 significantly promotes breast cancer cell clonogenicity, migration and mammosphere-forming ability. Conversely, silencing of H19 represses these BCSC properties. In concordance, knockdown of H19 markedly inhibits tumor growth and suppresses tumorigenesis in nude mice. 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	2017	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.	0	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi, ChIP, Cell proliferation assay etc.	up-regulated	Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. 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. 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.	27780718	2017	The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, Western blot, Luciferase report assay	up-regulated	In conclusion, H19 promoted proliferation and invasion of breast cancer through the miR-152/DNMT1 axis, providing a novel mechanism about the occurrence and development of breast cancer. 	28544374	2017	Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer  through upregulating DNMT1 expression by sponging miR-152.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi, Western blot etc.	up-regulated	Quantitation of H19 lncRNA in human breast cancer tissues showed that the level of H19 lncRNA was higher in ER-positive than in ER-negative tumor tissues. These results suggest that H19 is an estrogen-inducible gene and plays a key role in cell survival and in estrogen-induced cell proliferation in MCF-7 cells, H19 expression is ER-dependent and induced by estrogen through the traditional genomic pathway of estrogen-ER interaction with the gene.	25846769	2015	H19 lncRNA mediates 17B-estradiol-induced cell proliferation in MCF-7 breast cancer cells.	0	0	1
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi etc.	up-regulated	We identify here a novel transcriptional activity at both the human and the mouse H19/IGF2 imprinted loci. This activity occurs antisense to the H19 gene and has the potential to produce a single 120-kb transcript that we called the 91H RNA. This nuclear and short-lived RNA is not imprinted in mouse but is expressed predominantly from the maternal allele in both mice and humans within the H19 gene region. Moreover, the transcript is stabilized in breast cancer cells and overexpressed in human breast tumors.	18794369	2008	A novel H19 antisense RNA overexpressed in breast cancer contributes to paternal IGF2 expression.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, RNAi, Western blot, Northern blot, ChIP etc.	up-regulated	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. H19 repression by pRb and E2F6 confirms the E2F1-dependent control of the H19 promoter. Consistently, we demonstrate by chromatin immunoprecipitation assays that endogenous E2F1 is recruited to the H19 promoter in vivo. The functionality of E2F promoter sites was further confirmed by gel shift and mutagenesis experiments, revealing that these sites are required for binding and promoter response to E2F1 exogenous expression and serum stimulation. 	15985428	2005	H19 mRNA-like noncoding RNA promotes breast cancer cell proliferation through positive control by E2F1.	0	0	0
chr11	1995176	2001470	H19	283120	HGNC:4713	ENSG00000130600	NR_002196	qPCR, etc.	down-regulation	Our results suggest that the combined let-7a and H19 signature is a novel prognostic factor for breast cancer patients treated with neoadjuvant chemotherapy.H19 is associated with drug-resistance in breast cancer cells.Univariate and multivariate survival analyses were conducted using the Cox proportional hazards regression method. As determined using X-tile, the optimal cutoff value for the risk score to assess progression-free survival (PFS) based on the combined signature was -0.1. Several miRNAs and lncRNAs, including let-7a and H19, provide prognostic information for many cancers.	29963109	2018	Combined Let-7a and H19 Signature: A Prognostic Index of Progression-Free Survival in Primary Breast Cancer Patients.	1	0	1
chr14	61715558	61751097	HIF1A-AS2	100750247	HGNC:43015	ENSG00000258667	NR_045406	microarray, qPCR etc.	up-regulated	Expression level of these 3 lncRNAs was determined in plasma samples of 60 patients with BC and 40 healthy individuals by performing real-time PCR. As expected, the relative expression of ANRIL, HIF1A-AS2, and UCA1 was significantly higher in patients with TNBC than in patients with NTNBC, which was consistent with the results of microarray analysis.	28248879	2017	A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers.	0	1	0
chr14	61715558	61751097	HIF1A-AS2	100750247	HGNC:43015	ENSG00000258667	NR_045406	qPCR, Immunohistochemistry etc.	up-regulated	We found a strong positive association between HIF-1alpha and sHIF-1alpha, sHIF-1alpha and aHIF, and an inverse correlation between HIF-1alpha /sHIF-1alpha and aHIF. aHIF transcript expression was associated with poor disease-free survival in univariate and multivariate analyses in this series of high-risk primary breast carcinomas.	14580258	2003	aHIF but not HIF-1alpha transcript is a poor prognostic marker in human breast cancer.	0	0	1
chr14	61715558	61751097	HIF1A-AS2	100750247	HGNC:43015	ENSG00000258667	NR_045406	microarray, qPCR, RNAi, Cell proliferation assay, Cell invasion assay etc.	up-regulated	lncRNAs HIF1A-AS2 and AK124454 could promote cell proliferation and invasion, and attenuate G2-M arrest, which might contribute to paclitaxel resistance in TNBC cells.	26921339	2016	Transcriptome Analysis of Triple-Negative Breast Cancer Reveals an Integrated mRNA-lncRNA Signature with Predictive and Prognostic Value.	0	1	0
chr5	163483065	163494058	HMMR-AS1	101927813	HGNC:49149	ENSG00000251018	NR_109892	qPCR, RNAi, Luciferase reporter assay etc.	up-regulated	We found that the expression of HMMR was positively correlated with HMMR-AS1 (RP11-80G.1). When HMMR-AS1 (RP11-80G.1) was knocked down, the expression of HMMR markedly reduced. Furthermore, in MDA-MB-231 and MDA-MB-468 breast cancer cells, the proliferation and migration abilities were remarkably suppressed via knocking down HMMR-AS1 (RP11-80G.1) in vitro.	27920576	2016	The HMMR-AS1 expression was markedly higher in BLBCs in contrast to those in non-BLBC subtypes. HMMR antisense RNA 1, a novel long noncoding RNA, regulates the progression of basal-like breast cancer cells.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR etc.	up-regulated	A statistically significant difference was found in HOTAIR expression level between different TNM Stages. being higher in advanced stages, where patients with distant metastasis showed significantly higher HOTAIR expression. In addition, HOTAIR expression was overexpressed in patients with poorly differentiated tumor compared with other grades .Furthermore, plasma HOTAIR was positively correlated with the CEA level  while no signifi- cant association was observed between plasma HOTAIR and age or gender. 	29687854	2018	Plasma long non-coding RNAs (lncRNAs) serve as potential biomarkers for predicting breast cancer.  	0	1	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, TaqMan allelic discrimination assay etc.	differential expression	We found that the CC genotype of HOTAIR rs920778 polymorphism significantly increased the risk of BC in both codominant and recessive inheritance genetic models. Our research also indicated an association between the CC genotype of HOTAIR rs920778 polymorphism and clinicopathologic features of tumor, including advanced tumor-node-metastasis (TNM) stage, larger tumor size, distant metastasis, and poor histological grade. CC genotype of HOTAIR rs920778 polymorphism might play important roles in genetic susceptibility to BC development and aggressiveness in a Turkish population.	25586347	2015	Effect of HOTAIR rs920778 polymorphism on breast cancer susceptibility and clinicopathologic features in a Turkish population.	0	1	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, ChIP, Luciferase reporter assay etc.	up-regulated	We show that expression of HOTAIR is regulated by B-catenin through a LEF1/TCF4-binding site. The dual treatment blocks nuclear expression of B-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of B-catenin rescued HOTAIR expression and cell viability in the presence of both drugs. Upregulation of HOTAIR is associated with TNBC in cell lines and a cohort of primary tumors.	25883211	2015	Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR.	1	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR etc.	up-regulated	We found that total HOTAIR was effectively amplified by most of the primers, suggesting the presence of HOTAIR in serum. The primer pair for 2-1 showed the highest amplification efficiency, and the PCR product was confirmed by gel detection and sequencing	26033707	2015	Circulating DNA of HOTAIR in serum is a novel biomarker for breast cancer.	0	1	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Luciferase reporter assay etc.	up-regulated	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-231and 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	2016	Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer	1	1	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot, CHIP-PCR, Dual-luciferase reporter assay etc.	up-regulated	To explore why miR-7 expression was downregulated in breast cancer cells and BCSCs, we examined HOTAIR expression and found that the downregulation of miR-7 was closely related to the high level of HOTAIR expression in breast cancer patients. HOTAIR inhibits many tumor suppression genes including HoxD10 in MDA-MB-231 cells. We downregulated the expression of HOTAIR by RNA interference in MDA-MB-231 cells and found that the expression of HoxD10 along with miR-7 were enhanced.	25070049	2014	MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	RC-PCR, Western blot, Luciferase reporter assay	up-regulated	Paracrine TGF-B1 was essential for CAFs induced EMT and metastasis in breast cancer cells, which is a crucial mediator of the interaction between stromal and cancer cells. CAF-CM significantly enhanced the HOTAIR expression to promote EMT, whereas treatment with small-molecule inhibitors of TGF-B1 attenuated the activation of HOTAIR. Most importantly, SMAD2/3/4 directly bound the promoter site of HOTAIR, located between nucleotides -386 and -398, -440 and -452, suggesting that HOTAIR was a directly transcriptional target of SMAD2/3/4. Additionally, CAFs mediated EMT by targeting CDK5 signaling through H3K27 tri-methylation.	29325547	2018	Paracrine and epigenetic control of CAF-induced metastasis: the role of HOTAIR stimulated by TGF-1 secretion.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot, ChIP, Luciferase reporter assay etc.	differential expression	We found that, when the RhoC-ROCK signaling was disturbed by specific siRNAs or chemical inhibitors, the expression of HOTAIR would be down-regulated. 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.	28069441	2017	Transcription of HOTAIR is regulated by RhoC-MRTF-A-SRF signaling pathway in human breast cancer cells.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, Cell proliferation assay etc.	up-regulated	HOTAIR is highly upregulated in both CSC-MCF7 and CSC-MB231 populations compared with MCF7 and MB231 populations. By modulating the level of HOTAIR expression, we showed that HOTAIR tightly regulates the proliferation, colony formation, migration and self-renewal capacity of CSCs, which occurs in part through regulation of Sox2 and p53.	28122024	2017	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.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot	up-regulated	The results showed a higher expression of HOTAIR in advanced tumor cells. HOTAIR efficiently enhanced radioresistance in MDA-MB231 breast cancer cells and accelerated proliferation through the Akt pathway by targeting HOXD10.	28454226	2017	Long non-coding RNA HOTAIR enhances radioresistance in MDA-MB231 breast cancer cells	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, Luciferase reporter assay	differential expression	Treatment of mice harboring platinum-resistant ovarian tumor xenografts with pHLIP-PNA constructs suppressed HOTAIR activity, reduced tumor formation and improved survival.	28420874	2017	Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer	1	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot	differential expression	We discovered that knockdown of HOTAIR induced significant decrease in proliferation and increase in apoptosis of MCF-7 cells, and the cell cycles of HOTAIR siRNA transfected cells have been arrested at G1 phase (p < 0.01);	28407576	2017	HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR etc.	up-regulated	The expression levels of HOTAIR were significantly higher in BC tissues and plasma than in the control. The expression levels of plasma HOTAIR were correlated with lymph node metastasis, estrogen receptor, c-erbB-2 and triple positive.	27755794	2016	Circulating long non-coding HOX transcript antisense intergenic ribonucleic acid in plasma as a potential biomarker for diagnosis of breast cancer.	0	1	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	up-regulated	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. The combination of HOTAIR and FOXM1 enables greater discrimination of endocrine therapy responders and non-responders in patients with oestrogen receptor positive breast cancer. Consistent with this, HOTAIR expression is increased in cell-line models of endocrine resistance.	27378691	2016	Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.	1	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	RNA-CISH etc.	up-regulated	HOTAIR, H19 and KCNQ1OT1 had significantly higher expression levels in IBC than NA, and HOTAIR and H19 were both expressed more strongly in IBC than in DCIS tissues.	26323944	2015	Long non-coding RNA chromogenic in situ hybridisation signal pattern correlation with breast tumour pathology.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot, Cell proliferation assay etc.	down-regulated	Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR.	25613518	2015	Calycosin and genistein induce apoptosis by inactivation of HOTAIR/p-Akt signaling pathway in human breast cancer MCF-7 cells.	1	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, ChIP, Dual-luciferase reporter assay etc.	up-regulated	Luciferase assay showed that HOTAIR promoter estrogen-response-elements (EREs) are induced by BPA and DES. Estrogen-receptors (ERs) and ER-coregulators such as MLL-histone methylases (MLL1 and MLL3) bind to the HOTAIR promoter EREs in the presence of BPA and DES, modify chromatin (histone methylation and acetylation) and lead to gene activation. Knockdown of ERs down-regulated the BPA and DES-induced expression of HOTAIR.	24533973	2014	Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR etc.	up-regulated	When compared with MCF-7 cells, MCF-7-TNR cells exhibited an increase in the expression of HOTAIR, which correlated with characteristics of a luminal-like to basal-like transition as evidenced by dysregulated gene expression and accelerated growth. MCF-7-TNR cells exhibited reduced suppressive histone H3 lysine27 trimethylation on the HOTAIR promoter. Inhibition of HOTAIR and EZH2 attenuated the luminal-like to basal-like transition in terms of gene expression and growth in MCF-7-TNR cells.	25328122	2014	Elevated expression of long intergenic non-coding RNA HOTAIR in a basal-like variant of MCF-7 breast cancer cells.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, ChIP, Dual-luciferase reporter assay etc.	up-regulated	Microscopic analysis showed that HOTAIR knockdown has suppressed the growth of MCF7 cells in comparison to the control or scramble-antisense treated cells even at 24 h of post HOTAIR siSENSE transfection. Growth analysis showed that HOTAIR knockdown has suppressed the growth of MCF7 cells significantly in comparison to the control (untreated) or scramble-antisense treated cells. 	23375982	2013	Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol.	estradiol	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc.	up-regulated	Here, we investigated the role of Hotair in the scenario of epithelial-to-mesenchymal transition (EMT) and in the arising and maintenance of cancer stem cells (CSCs). We found that treatment with TGF-B1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-B1, and also the colony-forming capacity of colon and breast cancer cells. Furthermore, we observed that the colon CSC subpopulation (CD133(+)/CD44(+)) presents much higher levels of Hotair when compared with the non-stem cell subpopulation.	24022994	2013	Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR etc.	differential expression	A positive correlation was found between DNA methylation and HOTAIR expression. Methylation was associated with unfavorable disease characteristics, whereas no significant associations were found between HOTAIR expression and clinical or pathologic features. In multivariate, but not in univariate, Cox proportional hazard regression models, patients with high HOTAIR expression had lower risks of relapse and mortality than those with low HOTAIR expression. We found that patients with high levels of HOTAIR expression had lower risks of relapse and death than those with low expression. The results suggest that clinicopathological features and therapy treatments could modify the effect of HOTAIR.	23124417	2012	Association of large noncoding RNA HOTAIR expression and its downstream intergenic CpG island methylation with survival in breast cancer.	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	microarray, qPCR, ISH etc.	up-regulated	Co-expression of HOTAIR and EZH2 trended with a worse outcome. In matched primary and metastatic cancers, both HOTAIR and EZH2 had increased expression in the metastatic carcinomas. This approach offers a method to make observations on lncRNAs that may influence the cancer epigenome in a tissue-based technique.	23133536	2012	Detection of long non-coding RNA in archival tissue: correlation with polycomb protein expression in primary and metastatic breast carcinoma.	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, ChIP etc.	up-regulated	Quantitative PCR showed that HOTAIR is overexpressed from hundreds to nearly two thousand- fold in breast cancer metastases, and HOTAIR level is sometimes high but heterogeneous among primary tumors . We next measured HOTAIR level in an independent panel of 132 primary breast tumors (stage I and II) with extensive clinical follow-up13. Indeed, nearly one third of primary breast tumors overexpress HOTAIR by over 125-fold over normal breast epithelia, the minimum level of HOTAIR overexpression observed in bona fide metastases, and high HOTAIR level is a significant predictor of subsequent metastasis and death.	20393566	2010	Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis.	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot etc.	up-regulated	The level of HOTAIR significantly increases in a time-dependent manner during chronic breast carcinogenesis. Dp treatment down-regulates HOTAIR expression in breast carcinogenesis and breast cancer cells. Furthermore, Dp administration inhibits the growth of xenografted breast tumors in athymic mice, and decreases HOTAIR in vivo. Further studies showed that Dp represses Akt activation, promotes IRF1 expression and increases IRF1 binding to the HOTAIR promoter. Silence of IRF1 expression via transfecting cells with IRF1 siRNAs significantly reduced the effects of Dp on HOTAIR, resulting in decreased cytotoxic effects of Dp on breast cancer cells.	27388461	2016	Delphinidin-3-glucoside suppresses breast carcinogenesis by inactivating the Akt/HOTAIR signaling pathway.	Delphinidin-3-glucoside	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	RNA-seq, qPCR	up-regulated	Elevated overexpression of the lncRNA HOTAIR mediates invasion and metastasis in breast cancer.HOTAIR expression is activated by BRD4 binding to a novel HOTAIR-N promoter in Claudin-low breast cancer cells that are attached to ECM. Induction of HOTAIR is required for invasive growth of Claudin-low breast cancer cells in lrECM 3D culture.	28846832	2017	Induction of a novel isoform of the lncRNA HOTAIR in Claudin-low breast cancer cells attached to extracellular matrix.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Western blot, in vitro knockdown	up-regulated	The expression levels of the lncRNA HOTAIR were upregulated in BC tissues and cells.Knockdown lncRNA HOTAIR inhibited cell propagation and metastasis and facilitated cell apoptosis.MiR-20a-5p was a target of lncRNA HOTAIR and had a negative correlation with lncRNA HOTAIR.MiR-20a-5p overexpression in BC suppressed cell growth,mobility,and invasiveness and facilitated apoptosis.HMGA2 was a target of miR-20a-5p,which significantly induced carcinogenesis of BC.BC cells progression was mediated by lncRNA HOTAIR via affecting miR-20a-5p/HMGA2 in vivo.LncRNA HOTAIR affected cell growth, metastasis,and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.  	29473328	2018	LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the  miR-20a-5p/HMGA2 axis in breast cancer.   	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, Luciferase reporter assay, Western blot	up-regulated	HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. miR-206 was capable of inhibiting the expression of Bcl-w by directly binding to the 3'UTR of Bcl-w mRNA.HOTAIR could increase the expression of Bcl-w through sequestering miR-206 at post-transcriptional level. HOTAIR-induced Bcl-w by miR-206 facilitated the proliferation of breast cancer cells.HOTAIR expression in primary breast tumors was significantly associated with worse prognosis independent of prognostic markers. 	29222472	2017	Long Noncoding RNA HOTAIR Modulates MiR-206-mediated Bcl-w Signaling to Facilitate Cell Proliferation in Breast Cancer.	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	Microarray, qPCR, Western blot	up-regulated	overexpression of JMJD6 increased HOTAIR expression and JMJD6 siRNAs suppressed it in ER+ MCF-7, triple negative MDA-MB-231 and non-breast cancer HEK 293 cells.Therefore, JMJD6  regulates HOTAIR independent of ER status.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	2018	JMJD6 induces HOTAIR, an oncogenic lincRNA, by physically interacting with its proximal promoter.	0	0	1
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RIP, ChIP, ISH etc.	up-regulated	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. Interestingly, this elevated HOTAIR increases ER protein level and thus enhances ER occupancy on the chromatin and potentiates its downstream gene regulation.	26364613	2015	LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer.	tamoxifen 	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	1
chr7	27198575	27207259	HOTTIP	100316868	HGNC:37461	ENSG00000243766	NR_037843	qPCR, Western blot, in vitro knockdown, RNAi	up-regulated	Using gain-and-loss-of experiments in vitro and in vivo, we observed the marked upregulation of HOTTIP/HOXA11 in the breast cancer cell line, MCF-7, and the downregulation of HOTTIP or HOXA11, which might inhibit cell proliferation and migration but promote cell apoptosis in breast cancer MCF-7 cells. In addition, by further rescue experiments with HOXA11 overexpression, we uncovered a novel potential regulatory mechanism between HOTTIP and one of its physical HOXA clusters, HOXA11. Hence, HOTTIP may mediate, at least partly, HOXA11 expression involved in cell growth, migration, and apoptosis of breast cancer MCF-7 cells.	29415429	2018	LncRNA HOTTIP-Mediated HOXA11 Expression Promotes Cell Growth, Migration and Inhibits Cell Apoptosis in Breast Cancer.	Adriamycin	0	0
chr7	27184518	27189293	HOXA11-AS	221883	HGNC:24957	ENSG00000240990	NR_002795	qPCR etc.	up-regulated	The data revealed that the relative transcript level of HOXA11-AS was upregulated in vivo and in vitro in models of breast cancer. Knockdown of HOXA11-AS in MDA-MB-231 and MDA-MB-436 breast cancer cell lines inhibited the formation of cell colonies and arrested the cell cycle at the G0/G1 phase. Depletion of HOXA11-AS using two specific short interfering (si)RNAs against HOXA11-AS (siHOXA11-AS-1 and siHOXA11-AS-2) additionally suppressed the cell proliferative rate. Furthermore, transwell assays and wound-healing analysis revealed that siRNA transfection inhibited cell migration and invasion by ~50% in the two cell lines. The results of the present study demonstrated the oncogenic role of HOXA11-AS in breast cancer, providing novel clues for the future clinical diagnosis and treatment of early stage breast cancer patients.	28791375	2017	Long non-coding RNA HOXA11-AS promotes cell proliferation and metastasis in human breast cancer	0	0	0
chr7	27184518	27189293	HOXA11-AS	221883	HGNC:24957	ENSG00000240990	NR_002795	qPCR, Western blot etc.	up-regulated	HOXA11-AS expression in breast cancer tissue of 50 patients was relatively higher than that in tissue adjacent to cancer. High expression of lncRNA HOXA11-AS promotes breast cancer invasion and metastasis by affecting EMT, and interfering in lncRAN HOXA11-AS expression provides a theoretical basis and important molecular target for inhibiting the distant metastasis of breast cancer in clinical practice.	28701685	2017	Long Non-Coding RNA (LncRNA) HOXA11-AS Promotes Breast Cancer Invasion and Metastasis by Regulating Epithelial-Mesenchymal Transition.	0	0	0
chr7	27107777	27134302	HOXA-AS2	285943	HGNC:43745	ENSG00000253552	NR_122069	qPCR, Luciferase report assay etc.	up-regulated	HOXA-AS2 was up-regulated in human breast cancer tissues and cell lines and associated with clinicopathological characteristics. HOXA-AS2 may be a potential prognostic and therapeutic target in breast cancer. HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	28545023	2017	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	0	0	0
NA	NA	NA	HTF30525	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	0	0	0
chr6	8435568	9294133	HULC	728655	HGNC:34232	ENSG00000251164	NR_004855	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	HULC expression was increased in TNBC tissues and cell lines and associated with malignant status and poor prognosis of TNBC patients. Furthermore, silencing TNBC expression effectively suppressed TNBC cells metastasis through MMP-2 and MMP-9.	27986124	2016	Long Noncoding RNA Highly Up-regulated in Liver Cancer Predicts Unfavorable Outcome and Regulates Metastasis by MMPs in Triple-negative Breast Cancer.	0	0	1
chr19	46189166	46203083	IGFL2-AS1	645553	HGNC:52559	ENSG00000268621	NR_135234	RNA-seq, qPCR, in vitro knockdown	down-regulated	IGFL2-AS1 was the most significantly decreased. Our results indicate that this lncRNA plays a role in downregulating its nearest neighbor, IGFL1, and affects migration of breast cancer cells.	28488769	2017	Selective expression of long non-coding RNAs in a breast cancer cell progression  model.	0	0	0
chr20	31721507	31723409	INXS	103021294	HGNC:49667	ENSG00000281376	NR_131907	qPCR, RACE-PCR etc.	down-regulated	Tumor cell lines from kidney, liver, breast and prostate showed an endogenous INXS expression that was 5- to 9-fold lower compared with non-tumor cell lines derived from the same tissues.	24992962	2014	Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis.	0	0	0
chr15	98645863	98651221	IRAIN	104472848	HGNC:50365	NA	NR_126453	qPCR etc.	down-regulated	In breast cancer tissues, we found that IRAIN lncRNA was transcribed from an intronic promoter in an antisense diretcion as compared to the IGF1R coding mRNA. Unlike the IGF1R coding RNA, this non-coding RNA was imprinted, with monoallelic expression from the paternal allele. IRAIN was aberrantly imprinted in both tumours and peripheral blood leucocytes, exhibiting a pattern of allele-switch: the allele expressed in normal tissues was inactivated and the normally imprinted allele was expressed.	25465188	2014	Aberrant allele-switch imprinting of a novel IGF1R intragenic antisense non-coding RNA in breast cancers.	0	1	0
chr21	44921051	44929678	ITGB2-AS1	100505746	HGNC:44304	ENSG00000227039	NR_038311	Western blot, Flow cytometry, etc.	down-regulated	The results of biological function experiments showed that ITGB2-AS1 could promote the migration and invasion of breast cancer. Furthermore, ITGB2-AS1 increased the mRNA and protein expression of ITGB2. LncRNA ITGB2-AS1 could promote the migration and invasion of breast cancer cells by up-regulating ITGB2.higher expression group had a poorer overall survival rate.	29941860	2018	LncRNA ITGB2-AS1 Could Promote the Migration and Invasion of Breast Cancer Cells through Up-Regulating ITGB2.	0	0	1
chr11	2608328	2699994	KCNQ1OT1	10984	HGNC:6295	ENSG00000269821	NR_002728	RNA-CISH etc.	up-regulated	HOTAIR, H19 and KCNQ1OT1 had significantly higher expression levels in IBC than NA, and HOTAIR and H19 were both expressed more strongly in IBC than in DCIS tissues.	26323944	2015	Long non-coding RNA chromogenic in situ hybridisation signal pattern correlation with breast tumour pathology.	0	0	0
chr15	87576929	87579866	LINC00052	145978	HGNC:26455	ENSG00000259527	NR_026869	microarray, qPCR, RNAi, Western blot, ISH etc.	up-regulated	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. Importantly, neutralization of HER3 signaling with HER3 targeting monoclonal antibodies blocked LINC00052 mediated cancer cell proliferation in vitro and tumor growth in vivo, suggesting LINC00052 promoting cancer growth through HER3 signaling.	28036286	2017	HER3 and LINC00052 interplay promotes tumor growth in breast cancer	0	0	0
chr2	87454781	87636740	LINC00152	112597	HGNC:28717	ENSG00000222041	NR_024204	qPCR, Western blot	differential expression	linc00152 was confirmed to promote the proliferation, migration and invasion in MDA-MB-231, SGC-7901 and 786-O.	29268251	2017	Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer	0	0	0
chr2	87454781	87636740	LINC00152	112597	HGNC:28717	ENSG00000222041	NR_024204	qPCR, Western blot etc.	up-regulated	The results showed that Linc00152 was highly expressed in the breast cancer tissues compared to their adjacent normal tissues, and Linc00152 was also  up-regulated in the breast cancer cell lines compared to normal cell lines. Knock-down of Linc00152 by using siRNAs in breast cancer cell lines (MDA-MB-231 and MCF-7) significantly suppressed cell viability, cell growth, cell invasion and migration as measured by the CCK-8, colony formation, transwell invasion, and migration assays. The qRT-PCR and Western blot results showed that knock-down of  Linc00152 suppressed epithelial-mesenchymal transition in breast cancer cell lines. In addition, CCK-8 assay showed that knock-down of Linc00152 in MCF-7/ADR  cells reversed the chemo-resistance to doxorubicin. 	29863253	2018	Down-regulation of lncRNA Linc00152 suppressed cell viability, invasion, migration, and epithelial to mesenchymal transition, and reversed chemo-resistance in breast cancer cells.	1	0	0
chr21	34157724	34190244	LINC00310	114036	HGNC:16414	ENSG00000227456	NR_027266	qRT-PCR, Western blot analysis	up-regulated	LINC00310 was increased as breast cancer progressed, and the deregulation of LINC00310 was significantly associated with patients' survival. LINC00310 promoted cell proliferation by regulating c-Myc expression in?vitro. LINC00310 KO significantly suppressed tumour growth in?vivo. serum LINC00310 expression was significantly up-regulated in patients with breast cancer, LINC00310 had a powerful capability of distinguishing patients with breast cancer from healthy individuals	29993199	2018	The oncogenic potentials and diagnostic significance of long non-coding RNALINC00310 in breast cancer.	0	1	1
chr6	71344344	71420769	LINC00472	79940	HGNC:21380	ENSG00000233237	NR_121612	qPCR, Cell proliferation assay, Cell migration assay etc.	down-regulated	Our qPCR results showed that high LINC00472 expression was associated with less aggressive breast tumors and more favorable disease outcomes. Patients with high expression of LINC00472 had significantly reduced risk of relapse and death compared to those with low expression. Cell culture experiments showed that up-regulation of LINC00472 expression could suppress breast cancer cell proliferation and migration.	25865225	2015	Prognostic and predictive values of long non-coding RNA LINC00472 in breast cancer.	0	0	1
chr6	10429255	10434874	Linc00518	221718	HGNC:28626	ENSG00000183674	NR_027793	qRT-PCR, Western blot assays, Luciferase reporter assays, RIP	up-regulated	linc00518 expression increased nearly 2 fold and MRP1 level elevated about 2.5 fold in breast cancer tissues as compared to that in adjacent normal tissues. miR-199a inhibitor conferred chemoresistance to ADR, VCR and PTX in MCF-7/ADR cells, and suppressing miR-199a reversed multi-drug susceptibility induced by linc00518 knockdown. Furthermore, 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	30001527	2018	Linc00518 Contributes to Multidrug Resistance Through Regulating the MiR-199a/MRP1 Axis in Breast Cancer.	1	0	0
chr14	55781135	55796688	LINC00520	645687	HGNC:19843	ENSG00000258791	NR_026796	RNA-seq, qPCR, RNAi etc.	up-regulated	LINC00520 is elevated in a subset of human breast carcinomas, with preferential enrichment in the basal-like molecular subtype. ShRNA-mediated depletion of LINC00520 results in decreased cell migration and loss of invasive structures in 3D.	27626181	2016	LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer.	0	0	0
chr1	204368431	204369719	LINC00628	127841	HGNC:27008	ENSG00000280924	NR_027022	qPCR, Western blot, Cell proliferation assay, Cell migration and invasion assay etc.	down-regulated	The relative expression level of LINC00628 in breast cancer tissues and cell lines were significantly decreased. The overexpression of LINC00628 suppressed breast cancer cells proliferation, invasion and migration. Further, with the overexpression of LINC00628, cell cycle was arrested in G0/G1 phase in breast cancer cells and cell apoptosis was promoted. The relative expression of Caspase-3 and Bax protein were significantly increased and the relative expression of Bcl-2 protein was significantly decreased after transfection with LINC00628.	28165561	2017	Long non-coding RNA LINC00628 suppresses the growth and metastasis and promotes cell apoptosis in breast cancer.	0	0	1
chr19	19757366	19776423	LINC00663	284440	HGNC:28609	ENSG00000266904	NR_026956	qPCR etc.	down-regulated	Additionally, LINC00663 was shown to be expressed at low levels in DU-145 and PC3 prostate cancer, HGC-27 stomach carcinoma, CRL-1469 pancreatic carcinoma, A549 lung cancer, MCF7 breast cancer, and BCPAP thyroid cancer cell lines	26743782	2016	A novel variable exonic region and differential expression of LINC00663 non-coding RNA in various cancer cell lines and normal human tissue samples.	0	0	0
chr17	72403322	72592804	LINC00673	100499467	HGNC:44354	NA	NR_036488	RNA-seq, qPCR	up-regulated	We identified lnc00673 (ERRLR01) as a marker of overall survival (OS) in breast cancer patients.ERRLR01 levels were elevated in triple-negative breast cancer (TNBC) as compared with Luminal-A,Luminal-B, and HER2 breast cancer subtypes. ERRLR01 levels were also inversely correlated with breast cancer survival across all breast cancer patients.OS in ERa-tumors correlated with negative overall survival,while in ERa+ tumors,ERRLR01 correlated with positive outcomes.This suggests ERRLR01 is modulated by hormone signaling in breast cancer.ERRLR01 correlated with distinct pathways including epithelial development and cellular differentiation. 	28795861	2017	linc00673 (ERRLR01) is a prognostic indicator of overall survival in breast cancer.	0	0	1
chr10	4650185	4678154	LINC00704	NA	NA	ENSG00000231298	NA	RNA-seq, Western blot, in vitro knockdown etc.	up-regulated	MANCR (mitotically-associated long noncoding RNA; LINC00704), which is upregulated in breast cancer patient specimens and cells. Depletion of MANCR in triple-negative breast cancer cells significantly decreases cell proliferation and viability, with concomitant increases in DNA damage. MANCR expression is highest in mitotic cells by both RT-qPCR and RNA in situ hybridization. Consistent with a role in cell-cycle regulation, MANCR-depleted cells have a lower mitotic index and higher incidences of defective cytokinesis and cell death.MANCR, in genomic stability of aggressive breast cancer, and identify it as a potential therapeutic target	29378907	218	Mitotically-Associated lncRNA (MANCR) Affects Genomic Stability and Cell Division in Aggressive Breast Cancer.	1	0	1
NA	NA	NA	LINC00894-002	NA	NA	NA	NA	qPCR, Western blot etc.	down-regulated	LINC00894-002 exhibits the most sophisticated network pattern and is the most downregulated lncRNA in MCF-7/TamR cells. Moreover,LINC00894-002 is directly upregulated by ERa.Knocking down LINC00894-002 downregulates expression of miR-200a-3p and miR-200b-3p, upregulates the expression of TGF-B2 and ZEB1,and finally contributes to TamR.Herein, we report the first case of an inhibitory lncRNA against TamR through the miR-200-TGF-B2-ZEB1 signaling pathway. 	29738694	2018	Downregulation of LINC00894-002 Contributes to Tamoxifen Resistance by Enhancing the TGF-B Signaling Pathway.	tamoxifen	0	0
chr12	121795267	121803906	LINC01089	338799	HGNC:27886	ENSG00000212694	NR_002809	microarray, qPCR, RNAi, Cell migration and invasion assay etc.	down-regulated	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.	27485121	2016	LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.	0	0	1
chr14	19062316	19131167	LINC01296	NA	HGNC:32188	ENSG00000225210	NA	qRT-PCR, Western blot assays, ect.	up-regulated	LINC01296 is up-regulated in both BC tissue samples and cells. silencing of LINC01296 inhibited BC cell growth in vitro and in vivo. Also, cell apoptosis was enhanced after LINC01296 silenced. Moreover, cell migration and invasion potential were both abrogated in the si-LINC01296 groups.	29981416	2018	Overexpression of long noncoding RNA LINC01296 indicates an unfavorable prognosis and promotes tumorigenesis in breast cancer.	0	0	1
chr10	120597949	120600124	linc01561	404216	HGNC:31365	ENSG00000177234	NR_103717	qPCR, Western blot, luciferase reporter assay, etc.	down-regulated	In summary, the findings of this study, based on ceRNA theory, combining the research foundation of miR-145-5p and MMP11, and taking linc01561 as a new study point, provide new insight into molecular-level reversing proliferation and apoptosis of BrCa.	29890225	2018	Mixomics analysis of breast cancer: Long non-coding RNA linc01561 acts as ceRNA involved in the progression of breast cancer.	0	0	0
chr22	27221349	27224727	LINC01638	105372978	HGNC:52425	ENSG00000233521	NA	qRT-PCR, Western blot assay, ChIP, Luciferase reporter assay, RIP	up-regulated	LINC01638 is highly expressed in TNBC tissues and cells.Mechanistically, LINC01638 interacts with c-Myc to prevent SPOP-mediated c-Myc ubiquitination and degradation. C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT. Analysis of the epithelial marker E-cadherin and mesenchymal markers Vimentin and EMT-associated transcription factor Twist1 revealed that LINC01638 knockdown increased E-cadherin and reduced Vimentin and Twist1 expression at the mRNA (Fig. 2g) and protein (Fig. 2h) levels in MDA-MB-231 and BT549 cells, whereas LINC01638 overexpression showed an inverse effect in T47D cells (Fig. 2g, h).	30002443	2018	LINC01638 lncRNA activates MTDH-Twist1 signaling by preventing SPOP-mediated c-Myc degradation in triple-negative breast cancer.	0	0	1
chr20	23985050	23988779	linc-GGTLC1-7	92086	HGNC:16437	ENSG00000149435	NA	RNA-seq, qPCR, RNAi, Western blot etc.	down-regulated	Four out of the five lincRNAs showed statistically significant up- or down-regulation in response to HER2 depletion by RT-qPCR similar to what we observed by RNA-seq analysis. 	25749757	2015	Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer.	0	0	0
NA	NA	NA	LincIN	NA	NA	NA	NA	qPCR, Western blot etc.	up-regulated	High levels of LincIN expression are frequently observed in tumors compared to adjacent normal tissues, and are strongly associated with aggressive breast cancer. 	28558830	2017	LincIN, a novel NF90-binding long non-coding RNA, is overexpressed in advanced breast tumors and involved in metastasis	0	0	0
chr10	32900319	33005792	linc-ITGB1	NA	NA	ENSG00000150093	NA	qPCR etc.	down-regulated	lincITGB1 levels were lower in tumor tissues of BC patients in comparison to adjacent non-cancerous breast tissues (p < 0.001). Linc-ITGB1 expression was significantly associated with lymph node metastasis, pathological differentiation and TNM stage (all p < 0.05).  linc-ITGB1 be a potential biomarker in the prognosis of BC.The present study aimed to determine the relationship between linc-ITGB1 expression and clinicopathological features and survival.	28829502	2017	Expression of long non-coding RNA linc-ITGB1 in breast cancer and its influence on prognosis and survival.	0	0	1
chr10	32900319	33005792	linc-ITGB1	NA	NA	ENSG00000150093	NA	qPCR, RNAi, Western blot, Flow cytometry assay etc.	up-regulated	The expression of linc-ITGB1 was significantly upregulated in both clinical breast cancer tissues and cultured breast cancer cell lines. Linc-ITGB1 depletion caused cell accumulation in the G0/G1 phase. Furthermore, the linc-ITGB1 knockdown decreased the expression of mesenchymal markers N-cadherin and vimentin while increasing the expression of the epithelial marker E-cadherin. Key cell cycle regulators Cdc25C and Cyclin B1 were also decreased by the linc-ITGB1 knockdown. These data suggest that linc-ITGB1 promotes breast cancer progression by inducing cell-cycle arrest and interrupting the epithelial-to-mesenchymal transition (EMT) process.	26601916	2015	Long non-coding RNA linc-ITGB1 promotes cell migration and invasion in human breast cancer.	0	0	0
chr2	104855511	104858574	linc-POU3F3	NA	NA	ENSG00000198914	NA	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	0
NA	NA	NA	linc-PSMD-11	NA	NA	NA	NA	RNA-seq, qPCR, RNAi, Western blot etc.	up-regulated	Four out of the five lincRNAs showed statistically significant up- or down-regulation in response to HER2 depletion by RT-qPCR similar to what we observed by RNA-seq analysis. 	25749757	2015	Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer.	0	0	0
chr19	44926804	44931386	lincRNA-APOC1P1-3	NA	NA	ENSG00000214855	NA	microarray, qPCR, RNAi, RNA pull-down assay etc.	up-regulated	The lincRNA-APOC1P1-3 was overexpressed in breast cancer, which was related to tumor size and hypomethylation in its promoter region. We also found that APOC1P1-3 could directly bind to tubulin to decrease a-tubulin acetylation, to inactivate caspase-3, and to inhibit apoptosis.	27228351	2016	Long intergenic non-coding RNA APOC1P1-3 inhibits apoptosis by decreasing a-tubulin acetylation in breast cancer.	0	0	0
NA	NA	NA	lincRNA-BC2	NA	NA	NA	NA	RNA-seq, qPCR etc.	up-regulated	We analyzed lincRNAs whose expression was significantly different between cancer tissues and adjacent tissues. LincRNA-BC2 and lincRNA-BC5 were consistently up-regulated more than 2-fold (mean¡ÓSD) in cancer samples. Whereas, lincRNA-BC4 and lincRNA-BC8 were down-regulated.They might play important roles in the function of oncogenes or tumor suppressors affecting the development and progression of breast cancer.	25084155	2014	Long intergenic non-coding RNAs (LincRNAs) identified by RNA-seq in breast cancer.	0	0	0
NA	NA	NA	lincRNA-BC4	NA	NA	NA	NA	RNA-seq, qPCR etc.	down-regulated	We analyzed lincRNAs whose expression was significantly different between cancer tissues and adjacent tissues. LincRNA-BC2 and lincRNA-BC5 were consistently up-regulated more than 2-fold (mean¡ÓSD) in cancer samples. Whereas, lincRNA-BC4 and lincRNA-BC8 were down-regulated.They might play important roles in the function of oncogenes or tumor suppressors affecting the development and progression of breast cancer.	25084155	2014	Long intergenic non-coding RNAs (LincRNAs) identified by RNA-seq in breast cancer.	0	0	0
NA	NA	NA	lincRNA-BC5	NA	NA	NA	NA	RNA-seq, qPCR etc.	up-regulated	We analyzed lincRNAs whose expression was significantly different between cancer tissues and adjacent tissues. LincRNA-BC2 and lincRNA-BC5 were consistently up-regulated more than 2-fold (mean¡ÓSD) in cancer samples. Whereas, lincRNA-BC4 and lincRNA-BC8 were down-regulated.They might play important roles in the function of oncogenes or tumor suppressors affecting the development and progression of breast cancer.	25084155	2014	Long intergenic non-coding RNAs (LincRNAs) identified by RNA-seq in breast cancer.	0	0	0
NA	NA	NA	lincRNA-BC8	NA	NA	NA	NA	RNA-seq, qPCR etc.	down-regulated	We analyzed lincRNAs whose expression was significantly different between cancer tissues and adjacent tissues. LincRNA-BC2 and lincRNA-BC5 were consistently up-regulated more than 2-fold (mean¡ÓSD) in cancer samples. Whereas, lincRNA-BC4 and lincRNA-BC8 were down-regulated.They might play important roles in the function of oncogenes or tumor suppressors affecting the development and progression of breast cancer.	25084155	2014	Long intergenic non-coding RNAs (LincRNAs) identified by RNA-seq in breast cancer.	0	0	0
NA	NA	NA	lincRNA-p21	102800311	HGNC:43652	NA	NA	qPCR, Western blot, RIP, ISH, MTT assay etc.	up-regulated	 We found that Linc-RoR was highly expressed in tumor specimens compared to normal tissue. Linc-RoR knockout (KO) suppresses cell proliferation and tumor growth. In particular, Linc-RoR KO causes a significant decrease in c-Myc whereas re-expression of Linc-RoR in the KO cells restores the level of c-Myc. As a result, Linc-RoR may contribute to the increased stability of c-Myc mRNA. Although hnRNP I and AUF1 can interact with many RNA species and regulate their functions, with involvement of Linc-RoR they would be able to selectively regulate mRNA stability of specific genes such as c-Myc.	26656491	2016	Linc-RoR promotes c-Myc expression through hnRNP I and AUF1.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, RNAi, Western blot, ChIP, Flow cytometry assay etc.	up-regulated	Untreated MDA-MB-231 cell lines strongly expressed linc-ROR, but linc-ROR knockdown decreased cell viability and expression of p62 and p53 while increasing apoptosis. Linc-ROR knockdown also increased LC3-II/B-actin, Beclin 1, NOTCH1, and Bcl-2 expression, as well as the number of autophagic vesicles in MDA-MB-231 cells. Linc-ROR negatively regulated miR-34a expression by inhibiting histone H3 acetylation in the miR-34a promoter.	27449099	2016	Large intergenic non-coding RNA-ROR reverses gemcitabine-induced autophagy and apoptosis in breast cancer cells.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, RIP, in vivo knockdown etc.	up-regulated	linc-ROR was upregulated in breast tumor and ectopic overexpression of linc-ROR in immortalized human mammary epithelial cells induced an epithelial-to-mesenchymal transition (EMT) program. Moreover,linc-ROR enhanced breast cancer cell migration and invasion. Linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205. linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs.	24922071	2014	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	Compared with immortalized MCF10A breast epithelial cells, lncRNA-ROR was highly expressed in MCF7 (nonresistant) and MDA-MB-231 (drug-resistant) cell lines. The lncRNA-ROR level was strongly elevated in the MDA-MB-231 cell line as compared to the MCF7 cell line, indicating that lncRNA-ROR can be involved in the development of breast cancer.	28063065	2017	Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205.	1	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR etc.	down-regulated	Among the various tested cancerous tissue samples, three demonstrated overexpression of LINC-ROR including cervical, ovarian, and esophageal cancers. In contrast, the expression in breast, melanoma, colon, and sarcoma tumors was mainly reduced compared to normal controls	26314857	2016	Altered expression of LINC-ROR in cancer cell lines and tissues.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	up-regulated	We present evidence that the human lincRNA-RoR (RoR) is a strong negative regulator of p53. Unlike MDM2 that causes p53 degradation through the ubiquitin-proteasome pathway, RoR suppresses p53 translation through direct interaction with the heterogeneous nuclear ribonucleoprotein I (hnRNP I). Importantly, a 28-base RoR sequence carrying hnRNP I binding motifs is essential and sufficient for p53 repression. We further show that RoR inhibits p53-mediated cell cycle arrest and apoptosis. Finally, we demonstrate a RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression.	23208419	2013	The human long non-coding RNA-RoR is a p53 repressor in response to DNA damage.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, Western blot, RIP etc.	up-regulated	linc-RoR functions as an onco-lncRNA to promote estrogen-independent growth of ER+ breast cancer. Under estrogen deprivation, linc-RoR causes the upregulation of phosphorylated MAPK/ERK pathway which in turn activates ER signaling. Knockout of linc-RoR abrogates estrogen deprivation-induced ERK activation as well as ER phosphorylation, whereas re-expression of linc-RoR restores all above phenotypes. Moreover, we show that the ERK-specific phosphatase Dual Specificity Phosphatase 7 (DUSP7), also known as MKP-X, is involved in linc-RoR KOinduced repression of MAPK/ERK signaling. Interestingly, linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation. Clinical data analysis reveal that DUSP7 expression is lower in ER+ breast cancer samples than that in ER- breast cancer. Moreover, downregulation of DUSP7 expression is associated with poor patient survival.	29041978	2017	Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer	tamoxifen	0	1
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	microarray, qPCR, Western blot etc.	up-regulated	lincRNA-RoR was significant upregulated in DCIS and IDC tumor tissues, showing the highest expression in invasive tumor tissues. Overexpression of the long non-coding RNA, lincRNA-RoR, functions as a competitive endogenous RNA sponge in TNBC. Interestingly, lincRNA-RoR is dramatically upregulated in TNBC and in metastatic disease and knockdown restores miR-145 expression.	25253741	2014	lincRNA-RoR and miR-145 Regulate Invasion in Triple-negative Breast Cancer via Targeting ARF6.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR	up-regulated	Among lncRNAs, large intergenic non-coding RNA regulator of reprogramming (lincRNA-ROR or linc-ROR) is a member of subvariety of lncRNAs, was first discovered in induced pluripotent stem cells (iPSCs), and plays a central role in promoting survival in iPSCs and embryonic stem cells (ESCs) through preventing the activation of cellular stress pathways.And linc-ROR also acts as a ceRNA to increase stemness gene Nanog expression by sponging miR-145 in cancer cells.	28869448	2017	Large intergenic non-coding RNA-ROR as a potential biomarker for the diagnosis and dynamic monitoring of breast cancer	1	1	1
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, RNAi, Western blot, MTT assay etc.	up-regulated	Expression level of linc-ROR messenger RNA (mRNA) in BC tissues was clearly higher than that in adjacent normal tissues, and significant difference was found between expression level of linc-ROR mRNA and lymph node metastasis. Compared with vector cell, overexpressed linc-ROR cell presented decreased sensibility of 5-FU and paclitaxel with decreased E-cadherin expression, increased Vimentin, N-cadherin expression, and invasion ability.	26883251	2016	Linc-ROR induces epithelial-mesenchymal transition and contributes to drug resistance and invasion of breast cancer cells.	1	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR	up-regulated	Plasma lincRNA-ROR levels were associated with estrogen receptors and lymph node metastasis.Plasma lincRNA-ROR may be a potential biomarker for BC diagnosis and a dynamic monitor.LincRNA-ROR is reportedly overexpressed in triple-negative (ER-, PR-, HER2-) breast cancer and could serve as a biomarker or therapeutic target for improving survival.	29090518	2017	Detection and analysis of circulating large intergenic non-coding RNA regulator of reprogramming in plasma for breast cancer.	0	1	1
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR, Western blot etc.	differential expression	These results implied that downregulated long non-coding RNA ROR suppressed BT474 cell proliferation, invasion, and migration and reversed the effect of Tamoxifen on the BT474 cells. These results indicate that inhibition of long non-coding RNA ROR reverses resistance to Tamoxifen by inducing autophagy in breast cancer.	28635401	2017	Inhibition of long non-coding RNA ROR reverses resistance to Tamoxifen by inducing autophagy in breast cancer	Tamoxifen	0	0
NA	NA	NA	linc-TPBG-3	NA	NA	NA	NA	RNA-seq, qPCR, RNAi, Western blot etc.	up-regulated	Four out of the five lincRNAs showed statistically significant up- or down-regulation in response to HER2 depletion by RT-qPCR similar to what we observed by RNA-seq analysis. 	25749757	2015	Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer.	0	0	0
chr14	91965991	92040896	linc-TRIP11	NA	NA	ENSG00000100815	NA	RNA-seq, qPCR, RNAi, Western blot etc.	up-regulated	Four out of the five lincRNAs showed statistically significant up- or down-regulation in response to HER2 depletion by RT-qPCR similar to what we observed by RNA-seq analysis. 	25749757	2015	Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer.	0	0	0
chr1	238480384	238486023	LINK-A	339535	HGNC:27924	ENSG00000215808	NR_015407	Cell transfection, Fluorescence quenching assay, Lipid-RNA pulldown assay etc.	differential expression	LINK-A directly interacts with the AKT pleckstrin homology domain and PIP3 at the single-nucleotide level, facilitating AKT-PIP3 interaction and consequent enzymatic activation. LINK-A-dependent AKT hyperactivation leads to tumorigenesis and resistance to AKT inhibitors. Genomic deletions of the LINK-A PIP3-binding motif dramatically sensitized breast cancer cells to AKT inhibitors.	28218907	2017	The LINK-A lncRNA interacts with PtdIns(3,4,5)P3 to hyperactivate AKT and confer resistance to AKT inhibitors.	0	0	1
chr10	6737382	6739026	LINP1	108570035	HGNC:53170	ENSG00000223784	NR_138480	qPCR, Western blot	up-regulated	LINP1 knockdown mitigated breast cancer cell growth by inducing G1-phase cell cycle arrest and apoptosis. LINP1 also promoted breast cancer cell  metastasis and influenced the expression of epithelial-mesenchymal transition-related markers. We identified p53 as a regulator of LINP1, and LINP1 overexpression could restore the metastatic effects of p53. Furthermore, LINP1 was upregulated in doxorubicin- and 5-fluorouracil-resistant cells and induced chemoresistance. We also observed that LINP1 enrichment played a critical functional role in chemoresistance by inhibiting chemotherapeutics-induced apoptosis. Moreover, LINP1 in tumors was associated with lower overall survival and disease-free survival.	29293402	2018	Long noncoding RNA LINP1 acts as an oncogene and promotes chemoresistance in breast cancer.	doxorubicin	0	1
chr10	6737382	6739026	LINP1	108570035	HGNC:53170	ENSG00000223784	NR_138480	qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc.	up-regulated	LINP1, which is overexpressed in human triple-negative breast cancer. We found that LINP1 enhances repair of DNA double-strand breaks by serving as a scaffold linking Ku80 and DNA-PKcs, thereby coordinating the NHEJ pathway. Importantly, blocking LINP1, which is regulated by p53 and epidermal growth factor receptor (EGFR) signaling, increases the sensitivity of the tumor-cell response to radiotherapy in breast cancer.	27111890	2016	Long noncoding RNA LINP1 regulates repair of DNA double-strand breaks in triple-negative breast cancer.	0	0	0
chr1	6785324	7769706	LncCAMTA1	110841581	HGNC:53020	ENSG00000237436	NR_149049	qPCR, Western blot, Luciferase Reporter Assays	differential expression	Our findings suggested that LncCAMTA1 might promote proliferation and mobility of human breast cancer cell via binding with miR-20b. And VEGF was directly target of miR-20b and regulated activation of MAPK/ERK and JAK/STAT3 signal pathways.	28550685	2017	Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of Human Breast Cancer Cell Line MDA- MB-231 Via Targeting miR-20b	0	0	0
NA	NA	NA	lncFOXO1	NA	NA	NA	NA	microarray, qPCR, Western blot, ChIP, CCK-8 assay etc.	down-regulated	lncFOXO1 is significantly decreased in breast cancer tissues and cell lines and downregulation of lncFOXO1 expression associates with poorer overall survival. Functional assays demonstrated its suppressive role in breast cancer in vivo and in vitro. Mechanistically, lncFOXO1 suppressed the growth of breast cancer by increasing FOXO1 transcription. Moreover, we found that lncFOXO1 associated with BRCA-1-associated protein 1 (BAP1) and regulates its binding and the level of mono-ubiquitinated H2A at K119 (ubH2AK119) at FOXO1 promoter.	28339037	2017	The long non-coding RNA lncFOXO1 suppresses growth of human breast cancer cells through association with BAP1.	0	0	1
NA	NA	NA	lnc-HOST2	642934	HGNC:51354	NA	NR_134505	qPCR, Western blot etc.	up-regulated	Compared with adjacent normal tissues,HOST2 expression was higher but let-7b expression lower in breast cancer tissues. HOST2 expression in breast cancer cells was remarkably increased compared with that in the normal breast epithelial MCF-10A cells.In MCF-7 cells,in comparison with the blank and NC groups,expressions of HOST2 and c-Myc were reduced,but let-7b expression was remarkably elevated in the siHOST2 and let-7b mimic groups,the let-7b inhibitor group exhibited higher expressions of HOST2 and c-Myc but lower let-7b expression.Overexpression of HOST2 could promote cell motility,migration and invasion,thus enhancing the growth of breast cancer tumor. By inhibiting HOST2,opposite trends were found.LncRNA HOST2 promotes cell migration and invasion by inhibiting let-7b in breast cancer  patients. 	29236319	2018	Effects of long non-coding RNA HOST2 on cell migration and invasion by regulating MicroRNA let-7b in breast cancer.	0	0	0
NA	NA	NA	lncRNA00544	NA	NA	NA	NA	Microarray, qPCR	up-regulated	Here, we aim to identify the lncRNAs which are involved in the particular type luminal BC progression. By Gene Chips analysis, we found a novel lncRNA00544, which was highly expressed in the metastatic axillary nodes compared with corresponding luminal BC tissues (fold change=2.26, P=0.043).Many differentially expressed lncRNAs including circulating lncRNA and lncRNA signatures	28959047	2017	Long non-coding RNA00544 serves as a potential novel predictive and prognostic marker for HR+HER2 subtype breast cancer	0	1	1
NA	NA	NA	lncRNA-AK058803	NA	NA	NA	NA	qPCR, RNAi, Western blot etc.	up-regulated	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.	26136884	2015	Unregulated long non-coding RNA-AK058003 promotes the proliferation, invasion and metastasis of breast cancer by regulating the expression levels of the ¦Ã-synuclein gene.	0	0	0
NA	NA	NA	lncRNA-ATB	109207222	NA	NA	NA	microarray, qPCR, Western blot, Luciferase reporter assay, MTT assay etc.	up-regulated	We identified long noncoding RNA activated by TGF-B (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients. 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. In addition, we also found that the high level of lnc-ATB was correlated with trastuzumab resistance of breast cancer patients.	25871474	2015	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.	1	0	0
NA	NA	NA	lncRNA-ATB	109207222	NA	NA	NA	qPCR	down-regulated	LncRNA-ATB has been shown to be downregulated in about two third of tumor samples compared with their ANCTs. A significant association has been found between ZEB1 expression and Ki-67 status. In addition, we demonstrated a correlation between expression of lncRNA-ATB and ZEB1 in tumor samples and not in ANCTs.	28598827	2017	Expression analysis of long non-coding ATB and its putative target in breast cancer	0	0	0
NA	NA	NA	lncRNA-BCHE	NA	NA	NA	NA	qPCR, Microarray, etc.	up-regulated	lncRNA-BCHE is an oncogenic lncRNA enhancing the growth and metastatic potential of breast cancer cells. All breast cancer patients were subdivided into ITGB1low and ITGB1 high groups based on their ITGB1 transcript levels, and their distant metastasis-free survival (DMFS) and relapse-free survival (RFS) probability were plotted over time. In all patients, low ITGB1 gene expression was associated with a superior DMFS and RFS probability relative to the corresponding ITGB1 high group, 	29948648	2018	Long non-coding RNA p10247, high expressed in breast cancer (lncRNA-BCHE), is correlated with metastasis.	0	0	1
NA	NA	NA	lncRNA-CTD-2108O9.1	NA	NA	NA	NA	qPCR, Western blot, in vitro knockdown etc.	down-regulated	Long non-coding RNA-CTD-2108O9.1 is downregulated in BC tissues and cells and acts as  a metastatic inhibitor of BC. Mechanistic investigation determined that lncRNA-CTD-2108O9.1 represses metastasis by targeting leukemia inhibitory factor  receptor (LIFR), which is designated as a metastasis suppressor in BC. Our study  characterizes a significant tumor suppressor active in BC metastasis repression through the known metastasis inhibitor LIFR. 	29603493	2017	Long non-coding RNA-CTD-2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor.	1	0	0
chr9	86948699	87002033	lncRNA-Hh	100506834	HGNC:52261	ENSG00000226237	NA	microarray, qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	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. Thus, the mammosphere-formation efficiency (MFE) and the self-renewal capacity in vitro, and oncogenicity in vivo in Twist-positive breast cancer cells are elevated. 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	2016	LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway.	0	0	0
NA	NA	NA	lncRNA-HIT	NA	NA	NA	NA	qPCR, Luciferase reporter assay etc.	up-regulated	The level of expression of lncRNA-HIT in normal breast tissue was low and gradually increased to invasive carcinoma suggesting lncRNA-HIT may play a role in tumor progression in humans. These data further support the findings demonstrating the involvement of lncRNA-HIT in EMT and invasion as observed in NMuMG and 4T1 cells, and suggest that conserved human lncRNA-HIT could play a pivotal role in breast cancer metastasis.	25605728	2015	Long non-coding RNAs regulated by TGFB1 lncRNA-HIT mediated TGFB1-induced epithelial to mesenchymal transition in mammary epithelia.	0	0	0
chr4	128768228	128769948	lncRNA-JADE	101669763	HGNC:48601	ENSG00000280711	NA	microarray, qPCR, RNAi, Western blot, RIP, in vitro knockdown etc.	up-regulated	Markedly higher levels of lncRNA-JADE were observed in human breast tumours in comparison with normal breast tissues. Knockdown of lncRNA-JADE significantly inhibited breast tumour growth in vivo.	24097061	2013	A novel non-coding RNA lncRNA-JADE connects DNA damage signalling to histone H4 acetylation.	0	0	0
chr22	23894004	23895227	lncRNA©MIF	4282	HGNC:7097	ENSG00000240972	NA	qPCR, Luciferase reporter assay etc.	differential expression	In this study, we demonstrate that lncRNA©MIF (Myc inhibitory factor), which is transcribed by c©Myc, is able to reduce c©Myc expression. Mechanistically, lncRNA©MIF competes with coding mRNA Fbxw7 for miR©586 and relieves the inhibitory effect of miR©586 on Fbxw7, thereby leading to increased Fbxw11 expression and decreased c-Myc level.	27317567	2016	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw11-mediated c-Myc degradation	0	0	0
NA	NA	NA	lncRNA-PRLB	NA	NA	NA	NA	Microarray, qPCR, Western blot, RIP etc.	NA	lncRNA-PRLB was upregulated in human breast cancer tissues and breast cancer cell lines.Further evaluation verified that lncRNA-PRLB was positively correlated with the extent of metastasis, and its expression was correlated with shorter survival time of breast cancer patients. We identified microRNA miR-4766-5p as an inhibitory target of lncRNA-PRLB.Both lncRNA-PRLB overexpression and miR-4766-5p knockdown could remarkably enhance cell growth, metastasis, and chemoresistance. We also determined that sirtuin 1 (SIRT1) was an inhibitory target of miR-4766-5p, and that SIRT1 was inhibited by both lncRNA-PRLB knockdown and miR-4766-5p overexpression. The subcellular distribution assay revealed that lncRNA-PRLB is predominately located in the plasma.	29752439	2018	A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer.	anticancer drugs	1	1
NA	NA	NA	LOC284454	NA	NA	NA	NA	RNA-seq, RT-qPCR, Western blot, in vitro knockdown, RIP	down-regulated	Expression of LOC284454 is significantly reduced in breast, prostate, uterus and kidney cancer and also in breast cancer cell lines (MCF7 and T47D). Global gene expression studies upon loss and gain of function of LOC284454 revealed perturbation of genes related to cancer-related pathways. Focal adhesion and cell migration pathway genes are downregulated under overexpression condition, and these genes are significantly upregulated in breast cancer cell lines as well as breast cancer tissue samples suggesting a functional role of LOC284454 lncRNA in breast cancer pathobiology.	29227193	2017	DDX5/p68 associated lncRNA LOC284454 is differentially expressed in human cancers and modulates gene expression.	0	0	0
chr9	21455642	21559669	LOC554202	554202	HGNC:37187	ENSG00000171889	NR_027054	qPCR etc.	down-regulated	Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes.	22289355	2012	miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer.	0	0	0
chr9	21455642	21559669	LOC554202	554202	HGNC:37187	ENSG00000171889	NR_027054	qPCR, RNAi, Western blot etc.	up-regulated	We assay the expression level of lncRNAs-Loc554202 in breast cancer tissues and find that Loc554202 is significantly increased compared with normal control, and associated with advanced pathologic stage and tumor size. Moreover, knockdown of Loc554202 decreased breast cancer cell proliferation, induced apoptosis and inhibits migration/invasion in vitro and impeded tumorigenesis in vivo.	24631686	2014	Long non-coding RNA Loc554202 regulates proliferation and migration in breast cancer cells	0	0	0
NA	NA	NA	LSINCT1	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT10	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT11	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT12	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT2	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT3	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT4	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
chr5	2712591	2715237	LSINCT5	101234261	HGNC:37824	NA	NR_145480	qPCR, Northern blot etc.	up-regulated	LSINCT5 is overexpressed in breast and ovarian cancer cell lines and tumor tissues, relative to their normal counterpart. In addition, knocking down the expression of LSINCT5 in cancer-derived cell lines causes a decrease in cellular proliferation. 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	2011	LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation.	0	0	0
chr5	2712591	2715237	LSINCT5	101234261	HGNC:37824	NA	NR_145480	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
chr5	2712591	2715237	LSINCT5	101234261	HGNC:37824	NA	NR_145480	qPCR	differential expression	The expression levels of both genes was lower in the overweight-obese (BMI ¡Ý 25) subgroup than that in the normal BMI (BMI < 25) subgroup (GAS5 P = .019, LSINCT5 P = .036). Moreover, the expression level of GAS5 was negatively correlated with BMI (r: _x0001_.170, P: .041). The expression level of GAS5 was higher in women with late menarche (>13 years) than that with early menarche (¡Ü13 years; P = .017). 	29785740	2018	Expression levels of breast cancer-related GAS5 and LSINCT5 lncRNAs in cancer-free breast tissue: Molecular associations with age at menarche and obesity	0	0	0
NA	NA	NA	LSINCT6	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT7	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT8	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
NA	NA	NA	LSINCT9	NA	NA	NA	NA	qPCR, Northern blot etc.	up-regulated	Collectively, our results identified a new class of long stress responsive non-coding transcripts, LSINCTs, which have increased expression in response to DNA damage induced by NNK. LSINCTs interestingly also have increased expression in a number of cancer-derived cell lines, indicating that the expression is increased in both, correlating cellular stress and cancer.	20214974	2010	Identification of long stress-induced non-coding transcripts that have altered expression in cancer.	0	0	0
chr15	99014704	99031050	LUNAR1	104564224	HGNC:51199	NA	NR_126487	qPCR, RNAi, Western blot, Cell proliferation assay etc.	down-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	0
chr7	79452877	79471208	MAGI2-AS3	100505881	HGNC:40862	ENSG00000234456	NR_038343	qPCR, Western blot etc.	down-regulated	Our results showed MAGI2-AS3 to be down-regulated in breast cancer tissues compared to normal adjacent tissues. Moreover, MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL).  In conclusion, our data suggest that MAGI2-AS3 expression is decreased in breast  cancer and that MAGI2-AS3 plays an important role as a tumour suppressor by targeting Fas and FasL signalling. 	29679339	2018	Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR	up-regulated	MALAT1 expression was significantly elevated in breast cancer cases compared to controls (P<0.0001). MALAT1 expression level was positively correlated with lymph node status, estrogen receptor (ER), tumor stage and histological grade indicating its possible prognostic value. MALAT1 expression can be used as an accurate marker for diagnosis of breast cancer, in addition it possesses a prognostic value of such disease.	29310836	2017	Circulating long non-coding RNA MALAT1 expression as molecular biomarker in Egyptian patients with breast cancer.	0	1	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Luciferase reporter assay, Western blot	up-regulated	MALAT1 was upregulated in human colon cancer cell lines.miR-129-5p was downregulated in colon cancer cells with a significant increase of HMGB1 expression.miR-129-5p was identified and confirmed as a direct regulator of MALAT1 and miR-129-5p mimics were able to restrain the progression of colon cancer cells. In addition, high motility group box protein 1 (HMGB1), was predicted as a mRNA target of miR-129-5p. MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer.	29130936	2017	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	down-regulated	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin B4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary,we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	29574704	2018	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, Luciferase reporter assay, Immunofluorescent assay etc.	up-regulated	In this study we identified long non-coding RNA (lncRNA) MALAT1 can function as a ceRNA of cell division cycle 42 (cdc42) 3'UTR in inducing migration and invasion of breast cancer cells via miR-1. We found that miR-1 bound both MALAT1 and cdc42 3'UTR directly. Further study showed that MALAT1 induced migration and invasion of breast cancer cells while reduced the level of cdc42. 	26926567	2016	MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, Luciferase reporter assay etc.	down-regulated	The effects of up-regulation of miR-1 were similar to that of silencing K-RAS and MALAT1 in breast cancer cells	26275461	2015	Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, RIP, Luciferase reporter assay etc.	up-regulated	We reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. 	26676637	2015	Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR etc.	up-regulated	The four ncRNAs identified in the serum of patients with breast cancer included let-7a, miR-155, miR-574-5p, and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Analysis based on the risk score showed that the panel of these four ncRNAs could effectively distinguish between patients with breast cancer and the control group. For the training set and the validation set, analysis of the receiver-operating characteristic (ROC) curve showed that the areas under the curve (AUCs) were 0.960 and 0.968, respectively.  Also, the serum expression levels of the four ncRNAs differed in the pre-treatment and the post-treatment patients with breast cancer, with levels of  miR-155 showing a significant decrease following chemotherapy. 	29683112	2018	A Panel of Serum Noncoding RNAs for the Diagnosis and Monitoring of Response to Therapy in Patients with Breast Cancer.	0	1	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qRT-PCR	up-regulated	all three tagging SNPs (rs3200401, rs619586 and rs7927113) in lncRNA MALAT1 were selected for genotyping in 487BCE patients and 489 cancer-free controls in Chinese Han population, and futher experiment of quantitative real-time (qRT) PCR was conducted to examine the relative expression of MALAT1. The results showed that individuals with genotype AG of rs619586 has a decreased risk of BC in codominant model (OR: 0.684, 95%CI: 0.478-0.979), dominant mode (OR: 0.675, 95%CI: 0.479-0.951) and over-dominant model (OR: 0.692, 95%CI: 0484-0.989). Also, qRT-PCR results revealed that the expression for MALAT1 with AG (0.827¡À0.490), GG (0.511¡À0.149) and AG+GG genotypes (0.743¡À0.447) of rs619586 was significantly lower than that with genotype AA (1.511¡À0.737).	29146194	2018	Association analyses of genetic variants in long non-coding RNA MALAT1 with breast cancer susceptibility and mRNA expression of MALAT1 in Chinese Han population.	0	1	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, RIP, ChIP etc.	differential expression	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. VEGFA-dependent expression signatures associate with ID4 expression specifically in basal-like breast cancers carrying TP53 mutations. To evaluate the prognostic value of the signatures, we estimated the patients' survival probability using the Kaplan¨CMeier method. Serum-free media with or without recombinant VEGFA were used as controls.	28652379	2017	The mutant p53-ID4 complex controls VEGFA isoforms by recruiting lncRNA MALAT1.	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, in vitro knockdown	up-regulated	MALAT-1 promotes stem cell-like phenotypes in breast cancer cells. The present data demonstrated that the expression of MALAT-1 was higher in the CSC subpopulation compared with that in the overall MCF7 cell group and that the knockdown of MALAT-1 decreased the proportion of CSCs. The self-renewal assay also demonstrated that knockdown of MALAT-1 decreased the sphere formation rate in vitro. In addition, MALAT-1 is also able to regulate the proliferation, colony formation, migration and invasion of CSCs in vitro.	29434914	2017	Long non-coding RNA MALAT-1 contributes to maintenance of stem cell-like phenotypes in breast cancer cells.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR etc.	up-regulated	MALAT1 was overexpressed in 14% (63/446) of the breast tumours. MALAT1-overexpressed tumour epithelial cells showed marked diffuse nuclear signals and numerous huge nuclear speckles. Screening of the dbEST database led to the identification of ¦¤sv-MALAT1, a major alternatively spliced MALAT1 transcript, with a very different expression pattern compared with FL-MALAT1. This alternative ¦¤sv-MALAT1 transcript was mainly underexpressed (18.8%) in our breast tumour series. Multivariate analysis showed that alternative ¦¤sv-MALAT1 transcript is an independent prognostic factor. ¦¤sv-MALAT1 expression was associated with alterations of the pre-mRNAs alternative splicing machinery, and of the Drosha-DGCR8 complex required for non-coding RNA biogenesis. 	27172249	2016	Prognostic value of a newly identified MALAT1 alternatively spliced transcript in breast cancer	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, RIP, ChIP, RNA-FISH etc.	differential expression	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. The absence of the complex from basal-like cells was attributed to diminished expression of MALAT1, which, when overexpressed, dampened CD133 levels. 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	2016	The Ribonucleic Complex HuR-MALAT1 Represses CD133 Expression and Suppresses Epithelial-Mesenchymal Transition in Breast Cancer.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, in vitro knockdown etc.	up-regulated	We demonstrate that MALAT1 facilitates cell proliferation, tumor progression and metastasis of triple-negative breast cancer (TNBC) cells despite having a comparatively lower expression level than ER or HER2-positive breast cancer cells. Assessment of the prognostic significance of MALAT1 in human breast cancer (n=1992) revealed elevated MALAT1 expression was associated with decreased disease-specific survival in ER negative, lymph node negative patients of the HER2 and TNBC molecular subtypes. Multivariable analysis confirmed MALAT1 to have independent prognostic significance in the TNBC lymph node negative patient subset.	27250026	2016	Functional and prognostic significance of long non-coding RNA MALAT1 as a metastasis driver in ER negative lymph node negative breast cancer.	0	1	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	in vitro knockdown	up-regulated	RUNX1 depletion led to up-regulation of genes associated with chromatin structure and down-regulation of genes related to extracellular matrix biology, as well as NEAT1 and MALAT2 lncRNAs.	27514584	2016	RUNX2 contributes to higher-order chromatin organization and gene regulation in breast cancer cells	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, RNAi, Western blot, Northern blot etc.	up-regulated	Specifically, we looked for the changes of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1), which is found extensively and highly expressed in several kinds of tumor cells, including breast carcinoma. It was observed that proliferation, migration and invasion of breast cells were greatly affected by high concentration E2 treatment and were not affected by low concentration E2 treatment in an ERa independent way. We found that the high concentration E2 treatment largely decreased MALAT-1 RNA level. Interestingly, MALAT-1 decreasing by knocking down showed similar effects on proliferation, migration and invasion.	24525122	2014	17B-estradiol treatment inhibits breast cell proliferation, migration and invasion by decreasing MALAT-1 RNA level.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	This study provided evidence that long non-coding RNA MALAT1 was up-regulated in breast cancer tissues and cell lines. MALAT1 promoted cancer cell invasion through inducing epithelial-mesenchymal transition. Interestingly, we revealed there was a reciprocal repression between MALAT1 and miR-204. ZEB2 was identified as a downstream target of miR-204 and MALAT1 exerted its function mainly through the miR-204/ZEB2 axis. Our findings suggested that MALAT1 may serve as a new diagnostic biomarker and therapy target for breast cancer. Patients with higher levels of MALAT1 expression had poorer overall survival than those with lower levels of MALAT1 expression. 	28675122	2017	MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial-mesenchymal transition in breast cancer.	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	up-regulated	We also found that MALAT1 was increased in most breast cancer cells. In contrast, miR-124 was downregulated in the MCF-7 cells with MALAT1 overexpression. We found that MALAT1 expression had no effect in breast cancer cells treated with the miR-124 mimic or miR-124 inhibitor. Taken together, our results reveal that MALAT1 may act as an endogenous potent regulator that reduces miR-124 expression.	26918449	2016	miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, RNAi, Western blot etc.	up-regulated	KDM5B induces the expression of MALAT1 and its effector metastasis- associated genes in triple negative breast carcinoma cells. KDM5B interacts with MALAT1 to modulate its expression in triple negative breast carcinoma cells and consequently facilitate invasion and associated metastatic activities.	26917489	2016	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR	up-regulated	The expression of MALAT1 in triple negative and Her-2 positive breast cancers was positively correlated to the number of metastatic lymph nodes in patients with breast cancer.MALAT1 promotes proliferation and invasion abilities of breast cancer cells through XBP1 (X-box binding protein 1)-HIF (hypoxia-inducible factor)-1a pathway in MDA-MB-231 and through Her-2 pathway in MDA-MD-435.MALAT1 could possibly be involved in regulation of MYC gene and CD47 (an immune checkpoint gene) in both cell lines.the expression levels of MALAT1 were negatively correlated to OS of patients with triple negative and Her-2 positive patients, but the correlations were not significant.  	29416769	2017	Roles of MALAT1 in development and migration of triple negative and Her-2 positive breast cancer.	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, Luciferase reporter assays etc.	up-regulated	MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p. the ¡°MALAT1-miR-129-5p¡± axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC. patients with high MALAT1 expression had a poor overall survival compared to patients with low MALAT1 expression.	28915533	2017	Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, RNAi, Flow cytometry assay, MTT assay etc.	up-regulated	Results showed that MALAT1 expression was significantly up-regulated in 85.9% (67/78) of cancerous tissues compared with normal counterparts. Further, an elevated MALAT1 expression in BC tissue was significantly associated with lymph metastasis and adverse 5-year disease-free survival. Suppression of lncRNA MALAT1 significantly inhibited BC cells proliferation, migration and invasion, induced apoptosis and cell cycle G1 arrest. In addition, serum MALAT1 levels in BC patients were much higher than levels in patients with benign breast disease.	27466303	2016	Clinical Significance of Long Non-coding RNA MALAT1 Expression in Tissue and Serum of Breast Cancer.	0	1	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR etc.	up-regulated	MALAT1 expression was significantly up-regulated compared with adjacent normal tissues. Furthermore, of 204 breast cancer patients, high MALAT1 expression was associated with positive ER and progesterone receptor (PR) status.	27191888	2016	Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer.	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR etc.	down-regulated	We found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways. Furthermore, lower expression of MALAT1 in breast cancer patients was associated with shorter relapse-free survival	26191181	2015	Downregulation of long noncoding RNA MALAT1 induces epithelial-to-mesenchymal transition via the PI3K-AKT pathway in breast cancer	0	0	1
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	qPCR	up-regulated	Malat1 confers an inhibitory effect on cell growth and migration which is lost following Malat1 KO, but in a Nisch-dependent context. Specifically, Malat1 KO in the background of low Nischarin expression had a limited effect on cell functions, while Malat1 KO in cells with high levels of Nischarin led to significant increases in cell proliferation and migration. Nischarin (Fig 4F) were found to positively correlate with enhanced patient recurrence-free survival.	29912916	2018	Expression of long noncoding RNA MALAT1 correlates with increased levels of Nischarin and inhibits oncogenic cell functions in breast cancer.	0	0	1
chr17	45799390	45895630	MAPT-AS1	100128977	HGNC:43738	ENSG00000264589	NR_024559	qPCR, Western blot, in vitro knockdown	up-regulated	ER-negative patients with younger age (<60), larger tumors (¡Ý2cm), metastatic lymph nodes and stages (III-IV) had higher expression of MAPT-AS1. MAPT-AS1 is correlated with the cell growth, invasiveness and paclitaxel resistance by regulating its natural comparable sense transcripts MAPT in ER-negative breast cancer cells. The result revealed that MAPT-AS1 overexpression could partially protect the MAPT mRNA from degradation, while MAPT-AS1 knockdown decreased the stability of MAPT mRNA. Meanwhile, MAPT knockdown decreased the expression of MAPT-AS1 mRNA. MAPT-AS1 expressed coordinately with MAPT in breast tumor tissues.	29441192	2018	Knockdown of LncRNA MAPT-AS1 inhibites proliferation and migration and sensitizes cancer cells to paclitaxel by regulating MAPT expression in ER-negative breast cancers.	0	0	0
chr14	100779410	100861031	MEG3	55384	HGNC:14575	ENSG00000214548	NR_002766	qPCR, Western blot etc.	down-regulated	Here, we showed that MEG3 was downregulated in breast cancer tissues and cell lines. Collectively, these results suggest that MEG3 might suppress the tumor growth and angiogenesis via AKT signaling pathway and MEG3 may serve as a potential novel diagnostic and therapeutic target of breast cancer.	28635399	2017	Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway	0	0	0
chr14	100779410	100861031	MEG3	55384	HGNC:14575	ENSG00000214548	NR_002766	ChIP, Flow cytometry assay, Cell proliferation assay etc.	down-regulated	we identified the expressing difference of several tumor-related lncRNAs in breast cancer samples and found that, MEG3, which is downregulated in non-small cell lung cancer (NSCLC) tumor tissues, is also downregulated in breast cancer samples compared with adjacent tissues. For figuring out the effect of MEG3 in breast cancer cells MCF7 and MB231, we overexpressed MEG3 in these cells, and found that it resulted the inhibition of proliferation, colony formation, migration and invasion capacities by enhancing p53's transcriptional activity on its target genes, including p21, Maspin and KAI1. MEG3 presented similar effects in MB157, which is a p53-null breast cancer cell line, when functional p53 but not p53R273H mutant, which lacks transcriptional activity, was introduced. 	27166155	2016	Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation, migration and invasion by depending on p53's transcriptional activity	0	0	0
chr14	100779410	100861031	MEG3	55384	HGNC:14575	ENSG00000214548	NR_002766	qPCR etc.	down-regulated	Our findings revealed that the MEG3 expression was significantly decreased in clinical BC tissues compared to adjacent normal tissues. MEG3 level was significantly associated with differentiation grade, TNM stage and lymph nodes metastasis.	28051255	2016	Down-regulation of long non-coding RNA MEG3 serves as an unfavorable risk factor for survival of patients with breast cancer.	0	0	1
chr14	100779410	100861031	MEG3	55384	HGNC:14575	ENSG00000214548	NR_002766	qPCR, Western blot etc.	down-regulated	MEG3 was significantly down-regulated in breast cancer tissues compared to adjacent normal tissues.MEG3/miR-421/E-cadherin regulatory axis may be a novel therapeutic target for breast cancer.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.Survival analysis showed that lower MEG3 predicted a poor DFS and OS for patients. Down-regulation of MEG3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/b-catenin signaling pathway.	28463794	2017	LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer.	1	0	1
chr14	100779410	100861031	MEG3	55384	HGNC:14575	ENSG00000214548	NR_002766	qPCR, ISH etc.	down-regulated	MEG3 mRNA is expressed in the normal human fibroblast cells but is undetectable in human cancer cell lines by Northern blot.	14602737	2003	A pituitary-derived MEG3 isoform functions as a growth suppressor in tumor cells.	0	0	0
chr22	26646428	26676475	MIAT	440823	HGNC:33425	ENSG00000225783	NR_003491	qPCR, Western blot, Luciferase report assay etc.	up-regulated	MIAT expression was upregulated in breast cancer cell lines and tissues.MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients.MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. MIAT was specifically up-regulated in the plasma and aqueous humor of cataract patients.	29100300	2017	Long non-coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p.	0	0	0
chr22	26646428	26676475	MIAT	440823	HGNC:33425	ENSG00000225783	NR_003491	qPCR, Western blot, in vitro knockdown, RNAi	up-regulated	MIAT expression was much higher in high-grade tumors compared to low-grade ones. Unlike P53 positive tumors, MIAT expression was upregulated in ER, PR, Her2 positive tumor tissues. An increase in the expression of mir-302, mir-150, and a decrease in the expression of mir-29c were detected following MIAT silencing. More importantly, knockdown MIAT significantly elevated the expression of p16Ink4A and Cox2, which commitment cellular senescence in breast cancer cells.	29345338	2018	MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line.	0	0	0
chr22	26646428	26676475	MIAT	440823	HGNC:33425	ENSG00000225783	NR_003491	qPCR, Western blot	up-regulated	MIAT was overexpressed in ER-positive breast cancer tissues and ER-positive breast cancer cell line MCF-7	29792859	2018	Long non-coding RNA MIAT is estrogen-responsive and promotes estrogen-induced proliferation in ER-positive breast cancer cells	0	0	0
NA	NA	NA	MVIH	NA	NA	NA	NA	qPCR, RNAi, Flow cytometry assay etc.	up-regulated	Our research revealed that the expression levels of MVIH in breast cancer tissues were higher than in adjacent noncancerous tissues, and high MVIH expression was correlated with Ki67 expression. Moreover, breast cancer patients with high MVIH expression levels showed poor overall survival and disease-free survival. Multivariate analysis results indicated that MVIH was an independent prognostic factor in breast cancer. In addition, upregulated MVIH expression levels promoted cell proliferation and cell cycle, and inhibited cell apoptosis, while reduced MVIH expression showed the converse.	26555546	2015	Long non-coding RNA MVIH is associated with poor prognosis and malignant biological behavior in breast cancer.	0	0	1
chr3	188151206	188154057	MYCLo-5	339929	HGNC:27952	ENSG00000270959	NR_036497	qPCR, Flow cytometry assay, Cell proliferation assay etc.	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.	0	0	0
chr3	188151206	188154057	MYCLo-5	339929	HGNC:27952	ENSG00000270959	NR_036497	qPCR, Flow cytometry assay, Cell proliferation assay etc.	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.	0	0	0
chr6	22134957	22147193	NBAT1	729177	HGNC:49075	ENSG00000260455	NR_034143	microarray, qPCR, Western blot, RIP, ChIP etc.	down-regulated	Here, we report that NBAT1 is down-regulated in various types of cancer. Particularly, reduced NBAT1 in breast cancer is associated with tumor metastasis and poor patient prognosis. In vitro, 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	2015	NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2.	0	0	1
chr12	97430884	97598415	NCRMS	196475	HGNC:29893	ENSG00000255794	NR_024037	qPCR, mmicroarray	down-regulated	RMST played its biological function through regulating the mRNA or protein expression in cytoplasm.RMST could slow down the proliferation of TNBC cells to influence the tumor progression.RMST could enhance cell apoptosis in TNBC. The cell cycle detected by FCM assay indicated that RMST might induce the block of G0/G1 phase thus inhibiting TNBC cell proliferation.RMST overexpression could also restrain the invasion and migration abilities of TNBC cells.	29215701	2017	Long non-coding RNA (LncRNA) RMST in triple-negative breast cancer (TNBC):Expression analysis and biological roles research.	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown	up-regulated	NEAT1 levels were significantly increased in human breast cancer cells including MCF-7, MDA-MB-453, MDA-MB-231, and SKBR3 cells compared to normal mammary epithelial cells MCF-10A while miR-448 was decreased. We found that downregulation of NEAT1 was able to inhibit the growth of breast cancer cells and miR-448 mimic exerted the similar function. Bioinformatics analysis and dual luciferase reporter assays confirmed the negative correlation between NEAT1 and miR-448 in vitro. It was speculated in our study that NEAT1 can serve as a competing endogenous lncRNA (ceRNA) to modulate ZEB1 by sponging miR-448 in breast cancer.	29323713	2018	NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1.	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, RNAi etc.	down-regulated	we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis	27147820	2016	NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, RNAi, ChIP etc.	up-regulated	Our studies show that NEAT1 upregulation resulting from BRCA1 deficiency stimulates in vitro and in vivo breast tumorigenicity. 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. Finally our in silico expression correlation analysis suggests the existence of the BRCA1/NEAT1/miR-129-5p axis in breast cancer.	27556296	2016	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis.	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	in vitro knockdown	up-regulated	RUNX1 depletion led to up-regulation of genes associated with chromatin structure and down-regulation of genes related to extracellular matrix biology, as well as NEAT1 and MALAT1 lncRNAs.	27514584	2016	RUNX1 contributes to higher-order chromatin organization and gene regulation in breast cancer cells	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, ISH etc.	up-regulated	Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival, all of which are hallmarks of increased tumorigenesis.	25417700	2014	Tumor hypoxia induces nuclear paraspeckle formation through HIF-2a dependent transcriptional activation of NEAT1 leading to cancer cell survival.	0	0	1
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, Luciferase reporter assay, Western blot	up-regulated	lncRNA NEAT1 was up-regulated in breast cancer cell lines and tissues.NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance.the EMT-inducer HMGA2 was identified as a down-stream target of miR-211.LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis.breast cancer patients with low levels of NEAT1 expression had better overall survival time than those with high levels. 	28720546	2017	The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer.	5-fluorouracil (5-FU)	0	1
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc.	up-regulated	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.	28034643	2017	The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2.	0	0	0
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, luciferase assay etc.	down-regulated	NEAT1 expression was significantly up-regulated in breast cancer tissues compared to adjacent normal tissues, and higher NEAT1 was positively associated with lymph node metastasis and TNM stage. Patients with higher NEAT1 had a poor prognosis. In addition, NEAT1 promoted cell invasion and proliferation  by negatively regulating miR-218 in breast cancer.MiR-218 is a direct target of NEAT1. Kaplan-Meier analysis and the log-rank test were used to establish the relationship between NEAT1 and overall survival. Recent studies have shown that lncRNAs play a crucial effect in multiple processes in cells by acting as competing endogenous (ceRNAs) to regulate miRNAs. 	28946559	2017	NEAT1 negatively regulates miR-218 expression and promotes breast cancer progression.	0	0	1
chr11	65422774	65445540	NEAT1	283131	HGNC:30815	ENSG00000245532	NR_028272	qPCR, RNAi, Western blot, MTT assay etc.	up-regulated	lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis. MTT and Wound Healing assays showed that suppression of lncRNA NEAT1 could lead to decreased proliferation and metastasis in BC cell lines. Western blot also showed that B-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed.	28338194	2017	lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT.	0	0	1
chr20	57710183	57712780	NKILA	105416157	HGNC:51599	ENSG00000278709	NR_131157	qPCR, Western blot etc.	up-regulated	In this study, we found  that TGF-B activates the NF-kB pathway. Inhibition of NF-kB signaling markedly abrogates TGF-B-induced EMT. By studying the regulatory mechanism of TGF-B-induced NF-kB signaling, we found that lncRNA NKILA was upregulated by TGF-B and was essential for the negative feedback regulation of the NF-kB pathway. Accordingly, overexpression of NKILA significantly reduced TGF-B-induced tumor metastasis in vivo. Consistent with the results from mice, the expression of NKILA was negatively correlated with EMT phenotypes in clinical breast cancer  samples. Collectively, our study findings indicated that the NKILA-mediated negative feedback affects TGF-B-induced NF-kB activation and that NKILA may be a  therapeutic molecule in breast cancer metastasis via inhibition of EMT. 	29761481	2018	LncRNA NKILA Suppresses TGF-B-induced Epithelial-Mesenchymal Transition by Blocking NF-kB Signaling in Breast Cancer.	0	0	1
chr20	57710183	57712780	NKILA	105416157	HGNC:51599	ENSG00000278709	NR_131157	qPCR, RNAi, RIP etc.	down-regulated	Importantly, NKILA is essential to prevent over-activation of NF-£eB pathway in inflammation-stimulated breast epithelial cells. 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-£eB modulators to suppress cancer metastasis.	25759022	2015	A Cytoplasmic NF-£eB Interacting Long Noncoding RNA Blocks I£eB Phosphorylation and Suppresses Breast Cancer Metastasis.	0	0	1
chr5	43571594	43603230	NNT-AS1	100652772	HGNC:49005	ENSG00000248092	NR_073113	qPCR, Western blot etc.	up-regulated	Loss of function assay was carried out to detect the effects of silenced NNT-AS1 on proliferation, metastasis and EMT process of BC cells. Subcellular fractionation assay demonstrated that NNT-AS1 was located in the cytoplasm of BC cells. we found the combination between NNT-AS1 and miR-142-3p through conducting bioinformatics analysis, RIP and luciferase reporter assays. Similarly, the combination between miR-142-3p and ZEB1 was verified. Finally, the recue assays were carried out to demonstrate the effects of NNT-AS1/miR-142-3p/ZEB1 axis on the biological behaviors of BC cells.All the above findings revealed a fact that NNT-AS1 affects breast cancer progression through modulating miR-142-3p/ZEB1 axis. 	29710510	2018	Long non-coding RNA NNT-AS1 affects progression of breast cancer through miR-142-3p/ZEB1 axis.	0	0	1
chr20	36045618	36050960	NORAD	647979	HGNC:44311	ENSG00000260032	NR_027451	qPCR, in vitro knockdown, MTT assay etc.	up-regulated	We found that LINC00657 was upregulated in breast cancer cell lines MCF-7 and MDA-MB-231 cells as compared to non-malignant HMLE cells. LINC00657 knockout significantly suppresses tumor cell growth and proliferation, suggesting that it plays an oncogenic role.	26942882	2016	Long non-coding RNAs as prognostic markers in human breast cancer.	0	0	1
NA	NA	NA	OR3A4	NA	NA	NA	NA	qPCR, Western blot	up-regulated	OR3A4 was over-expressed in human breast cancer tissues and cell lines and associated with clinicopathological characteristics.the silence of OR3A4 suppressed the proliferation of breast cancer cells by influencing cell cycle and apoptosis, and repressed the cell metastasis via EMT.all the functions of OR3A4 in breast cancer were realized in the transcriptional level.OR3A4 played a significant role in BC and might be regarded as a specific biomarker for poor prognosis.  	29031201	2017	Long non-coding RNA OR3A4 promotes proliferation and migration in breast cancer.	0	0	1
chr6	36673621	36675126	PANDAR	101154753	HGNC:44048	ENSG00000281450	NR_109836	qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc.	up-regulated	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 p16INK4A. Moreover, we showed that PANDAR impacted p16INK4A expression by regulating the recruitment Bmi1 to p16INK4A promoter	26927017	2016	LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression	0	0	0
NA	NA	NA	PARTICLE	100630918	HGNC:50886	NA	NR_038942	qPCR, RNAi etc.	differential expression	In silico analysis identified additional regions for PARTICLE triplexes at >1600 genomic locations. Multiple PARTICLE triplexes are clustered predominantly within the human and mouse tumor suppressor WW Domain Containing Oxidoreductase (WWOX) gene. Surface plasmon resonance diffraction and electrophoretic mobility shift assays were consistent with PARTICLE triplex formation within human WWOX with high resolution imaging demonstrating its enrichment at this locus on chromosome 16. PARTICLE knockdown and over-expression resulted in inverse changes in WWOX transcripts levels with siRNA interference eliminating PARTICLEs elevated transcription to irradiation. The evidence for a second functional site of PARTICLE triplex formation at WWOX suggests that PARTICLE may form triplex-mediated interactions at multiple positions in the human genome including remote loci.	28769061	2017	PARTICLE triplexes cluster in the tumor suppressor WWOX and may extend throughout the human genome.	0	1	1
NA	NA	NA	PAX8-AS1-N	NA	NA	NA	NA	qPCR, Western blot etc.	down-regulated	we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p, and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4. In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients.	29693272	2018	Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N.	baicalein	0	1
NA	NA	NA	PCAN-1	NA	NA	NA	NA	qPCR, RNAi etc.	up-regulated	The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines.	27322459	2016	Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis.	0	0	1
NA	NA	NA	PCAN-4	NA	NA	NA	NA	qPCR, RNAi etc.	down-regulated	The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines.	27322459	2016	Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis.	0	0	1
NA	NA	NA	PCAN-6	NA	NA	NA	NA	qPCR, RNAi etc.	up-regulated	The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines.	27322459	2016	Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis.	0	0	1
chr8	126556323	127419050	PCAT-1	100750225	HGNC:43022	ENSG00000253438	NR_045262	qPCR etc.	up-regulated	over-expression of PCAT-1 in 12/47 (25.5%) of tumoral tissues compared with their corresponding ANCTs. PCAT-1 is possibly involved in the pathogenesis of fraction of breast cancers. Future studies are needed to evaluate its precise function in breast cancer.In other words, PCAT-1 has a protective effect on cMyc by disruption of MYC regulation by miR-34a. 	28989584	2017	Expression Analysis of Long Non-Coding PCAT-1 in Breast Cancer.	0	0	0
NA	NA	NA	PICART1	NA	NA	NA	NA	qPCR, Cell transfection, Western blot, Cell proliferation assay etc.	down-regulated	In breast and colorectal cancer cells and tissues, PICART1 expression was found to be decreased. Ectopic expression of PICART1 suppressed the growth, proliferation, migration, and invasion of MCF7, MDA-MB-231 and HCT116 cells whereas silencing of PICART1 stimulated cell growth and migration. In these cells, the expression of PICART1 suppressed levels of p-AKT (Thr308 and Ser473) and p-GSK3B (Ser9), and accordingly, B-catenin, cyclin D1 and c-Myc expression were decreased, while p21Waf/cip1 expression was increased.	28339031	2017	p53-inducible long non-coding RNA PICART1 mediates cancer cell proliferation and migration.	0	0	0
chr21	36131767	36175815	PlncRNA-1	100506428	HGNC:43664	ENSG00000236830	NR_038892	qPCR, Western blot etc.	down-regulated	Expression levels of PlncRNA-1 were significantly lower in tumor tissues than those in adjacent healthy tissues. Significantly lower expression levels of  PlncRNA-1 were also found in breast cancer patients than those in healthy controls in both breast tissue and serum. Upregulation of PlncRNA-1 promoted the  expression of TGF-B1, 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-B inhibitor reduced those effects of PlncRNA-1 overexpression.	29626321	2018	LncRNA PlncRNA-1 overexpression inhibits the growth of breast cancer by upregulating TGF-B1 and downregulating PHGDH. 	0	1	0
chr9	33673504	33677499	PTENP1	11191	HGNC:9589	ENSG00000237984	NA	qPCR, Western blot etc.	down-regulated	LncRNA PTENP1 can inhibit the proliferation and migration of breast cancer cells via the AKT and MAPK signaling pathways.Studies show that lncRNA PTENP1 can also regulate the expression of PTEN through the method in ceRNA hypothesis, thus affecting the progression of tumor cells. 	29085464	2017	Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways	tamoxifen	0	0
chr9	33673504	33677499	PTENP1	11191	HGNC:9589	ENSG00000237984	NA	qPCR	down-regulated	The expression of PTENP1 was significantly downregulated in both BC tissues and cell lines.Overexpressed PTENP1 could significantly increase the abilities of cell survival,colony forming, migration and invasion but decrease apoptosis in BC cell lines.PTENP1 performed a negative role in the development of BC via downregulating miR-19 through PTEN-PI3K/Akt pathway.	29212574	2017	Over-expression of long non-coding RNA PTENP1 inhibits cell proliferation and migration via suppression of miR-19b in breast cancer cells.	0	0	1
chr3	62260865	62369330	PTPRG-AS1	100506994	HGNC:44638	ENSG00000241472	NR_038281	qPCR etc.	up-regulated	In this study, we analyzed expression of four long noncoding RNAs (lncRNAs) namely SOX2OT, PTPRG-AS1, ANRASSF1, and ANRIL in 38 breast cancer tissues and their adjacent noncancerous tissues (ANCTs). ANRASSF1 expression was not detected in any noncancerous tissue. All lncRNAs showed significant overexpression in tumor tissues compared with ANCTs.	26409453	2016	Expression analysis of four long noncoding RNAs in breast cancer.	0	0	0
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR	down-regulated	significant inverse correlations were found between CCAT2 expression and stage, as well as lymph node involvement. Besides, a significant inverse correlation was found between the relative MYC expression in tumor tissues compared with their corresponding ANCTs and disease stage.CCAT2 expression level was suggested as a predictor of metastasis and poor survival for a particular subgroup of breast cancer patients. 	28480695	2017	Expression Study and Clinical Correlations of MYC and CCAT2 in Breast Cancer Patients	0	0	1
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR, Western blot, RIP etc.	up-regulated	Here we report that the lncRNA PVT1 promotes KLF5/beta-catenin signaling to drive TNBC tumorigenesis. PVT1 is upregulated in clinical TNBC tumors. Using genetic approaches targeting PVT1 in TNBC cells, we found that PVT1 depletion inhibited cell proliferation, colony formation, and orthotopic xenograft tumor growth. Mechanistically, PVT1 binds with KLF5 and increases its stability via BAP1, which upregulates beta-catenin signaling, resulting in enhanced TNBC tumorigenesis. PVT1, KLF5, and beta-catenin were also revealed to be co-expressed in clinical TNBC samples. Our findings uncover a new singaling pathway to mediate TNBC, and provide PVT1 as a new target for improving treatment of TNBC. 	29760406	2018	LncRNA PVT1 regulates triple-negative breast cancer through KLF5/beta-catenin signaling.	0	0	1
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	RNA-seq, qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	We show that the PVT1 promoter has a tumor-suppressor function that is independent of PVT1 lncRNA. CRISPR interference of PVT1 promoter enhances breast cancer cell competition and  growth in vivo. The promoters of the PVT1 and the MYC oncogenes, located 55 kb apart on chromosome 8q24, compete for engagement with four intragenic enhancers in the PVT1 locus, thereby allowing the PVT1 promoter to regulate pause release of MYC transcription. PVT1 undergoes developmentally regulated monoallelic expression, and the PVT1 promoter inhibits MYC expression only from the same chromosome via promoter competition. Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth.	29731168	2018	Promoter of lncRNA Gene PVT1 Is a Tumor-Suppressor DNA Boundary Element.	0	0	0
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR, Western blotting etc.	up-regulated	PVT1 expression is upregulated in human breast cancer tissues and cell lines.And the elevation of PVT1 was correlated with poor prognosis in breast cancer patients. We also identified an interaction between SOX2 and PVT1, which promotes breast cancer growth and invasion through epithelial to mesenchymal transition. To further reveal the function of SOX2/ PVT1 in breast cancer, the MTT and invasion assay were performed through silencing of PVT1 or SOX2. We found that either knockdown PVT1 or blocking SOX2 can suppress breast cancer cell growth and invasion through inhibition of EMT.	28882595	2017	Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion	0	0	1
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR etc.	up-regulated	These results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities. They also suggest that PVT1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms.	17908964	2007	Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer.	0	0	1
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR, Western blot etc.	down-regulated	To achieve cognition into the biological functions of PVT1 on breast cancer, PVT1 expression was downregulated by transfecting PVT1 siRNA into the MCF-7 and MDA-MB-231 cells, employing the scramble siRNA as a negative control.PVT1 DNA in serum and found that circulating PVT1 DNA significantly increased in the serum of breast cancer patients. circulating PVT1 DNA fragments may be a convenient means to predict the prognosis of breast cancer patients.The results demonstrated that breast cancer patients with high PVT1 expression showed significant shorter 5-year overall survival (OS) compared with patients with low PVT1 expression.	28534994	2017	Amplification and the clinical significance of circulating cell-free DNA of PVT1 in breast cancer.	0	1	1
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	0
chr8	127794533	128101253	PVT1	5820	HGNC:9709	ENSG00000249859	NR_003367	qPCR etc.	up-regulated	In the 43 breast cancer tissues, PVT1 expression was significantly higher in those with the GG genotype than that in the GA or AA genotype. Compared to normal tissues with any of the genotypes, PVT1 expression was also higher in the tumors with the GG genotype. These findings suggest that the GG genotype of SNP rs13281615 influences breast cancer development likely by modulating PVT1 expression.	24780616	2014	Frequent mutation of rs13281615 and its association with PVT1 expression and cell proliferation in breast cancer.	0	0	0
chr20	44694892	44746021	RP11-445H22.4	106144538	HGNC:49901	ENSG00000244558	NR_132377	qPCR etc.	up-regulated	In breast cancer patients, the expression level of lncRNA RP11-445H22.4 is significantly increased. Its expression levels were correlated with estrogen receptor (ER), progesterone receptor (PR), and menopausal status of the breast cancer patients.	25929808	2015	Clinical significance of high expression of circulating serum lncRNA RP11-445H22.4 in breast cancer patients: a Chinese population-based study.	0	1	0
chr20	63744689	63745958	RP4-583P15.10	NA	NA	NA	NA	microarray, qPCR etc.	up-regulated	RP4-583P15.10, an up-regulated lncRNA, was found to be located downstream of the natural antisense of the ZBTB46 gene, which may regulated breast cancer through influence immune system.	25661361	2015	Microarray expression profile analysis of long non-coding RNAs in human breast cancer: a study of Chinese women.	0	0	0
chr14	20343048	20343685	RPPH1	85495	HGNC:19273	ENSG00000277209	NR_002312	qPCR etc.	up-regulated	RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer.	29200969	2017	Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression.	0	0	0
GRCh19	47918429	47918550	snaR	NA	NA	NA	NA	qPCR, RNAi, MTT assay etc.	up-regulated	LncRNA snaR was found to be up-regulated in breast cancer cells, and the cancer progression of MDA-MB-231 cells was significantly suppressed by down-regulation of snaR. Therefore, snaR knockdown has potential as a treatment modality for triple-negative breast cancer.	27919948	2016	Long Noncoding RNA snaR Regulates Proliferation, Migration and Invasion of Triple-negative Breast Cancer Cells.	0	0	0
chr1	28578538	28582983	SNHG12	85028	HGNC:30062	ENSG00000197989	NR_024127	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc.	up-regulated	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	2017	C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer.	0	0	1
chr15	24978583	25419462	SNHG14	104472715	HGNC:37462	ENSG00000224078	NR_146177	qRT-PCR ect.	up-regulated	lncRNA?SNHG14 may promote the effect of trastuzumab by targeting the apoptosis regulator Bcl?2 (Bcl?2)/apoptosis regulator BAX (Bax) signaling pathway. Furthermore, the expression level of serum exosomal lncRNA?SNHG14 was upregulated in patients who exhibited resistance to trastuzumab, compared with patients exhibiting a response.	30015837	2018	Exosome-mediated transfer of lncRNA?SNHG14 promotes trastuzumab chemoresistance in breast cancer.	trastuzumab	0	0
chr7	44983023	44986961	SNHG15	285958	HGNC:27797	ENSG00000232956	NR_003697	RT-PC, Western blot, Luciferase reporter assay, in vitro knockdown	up-regulated	SNHG15 downregulation  suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited  epithelial-mesenchymal transition (EMT).In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p,which was downregulated in  breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients.	29217194	2017	Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p.	0	0	1
chr7	44983023	44986961	SNHG15	285958	HGNC:27797	ENSG00000232956	NR_003697	qPCR, Western blot, Luciferase reporter assay, RIP, etc.	down-regulated	Conclusion: 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	2018	LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.	0	0	0
chr17	76557766	76565348	SNHG16	100507246	HGNC:44352	ENSG00000163597	NR_038108	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	up-regulated	Expression levels of SNHG16 were found to be frequently higher in breast cancer tissues than in the paired noncancerous tissues.Gain- and loss-of-function studies proved that SNHG16 significantly promoted breast cancer cell migration. In addition, we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues. Furthermore,we demonstrated that forced expression of miR-98 could partially abrogate SNHG16-mediated increase of breast cancer cells migration,suggesting that SNHG16 promoted cell migration in a miR-98 dependent manner.	28232182	2017	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.	0	0	0
chr3	181711924	181714436	SOX2	NA	NA	ENSG00000181449	NA	qPCR, Western blotting etc.	up-regulated	An interaction between SOX2 and PVT1, which promotes breast cancer growth and invasion through epithelial to mesenchymal transition. To further reveal the function of SOX2/ PVT1 in breast cancer, the MTT and invasion assay were performed through silencing of PVT1 or SOX2. We found that either knockdown PVT1 or blocking SOX2 can suppress breast cancer cell growth and invasion through inhibition of EMT.	28882595	2017	Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion	0	0	1
chr3	180989762	181836880	SOX2OT	347689	HGNC:20209	ENSG00000242808	NR_004053	qPCR etc.	up-regulated	SOX2OT were overexpressed in BC tissues. SOX2OT SNP rs9839776 was strongly associated with the higher expression of SOX2OT and an increased risk of BC in Chinese women.	28240100	2017	Correlations between lncRNA-SOX2OT polymorphism and susceptibility to breast cancer in a Chinese population.	0	1	0
chr3	180989762	181836880	SOX2OT	347689	HGNC:20209	ENSG00000242808	NR_004053	qPCR etc.	up-regulated	We screened the expression level of two novel transcripts, SOX2OT-7 and SOX2OT-8 in five selected human cancer cell lines (HeLa, MCF7, HepG2, U-87 MG and NT2) by Real time RT-PCR. To facilitate the comparison of cell lines, HeLa cell line (which showed the least expression values) was considered as calibrator. Unexpectedly, all tested cancer cell lines, especially NT2 showed high levels of SOX2OT-7 and SOX2OT-8 expressions; except Mcf-7 which expresses the minimum level of SOX2OT-8.	26703382	2016	Identification of new SOX2OT transcript variants highly expressed in human cancer cell lines and down regulated in stem cell differentiation.	0	0	0
chr3	180989762	181836880	SOX2OT	347689	HGNC:20209	ENSG00000242808	NR_004053	qPCR, Western blot etc.	up-regulated	The expression of SOX2 and SOX2OT is concordant in breast cancer, differentially expressed in estrogen receptor positive and negative breast cancer samples and that both are up-regulated in suspension culture conditions that favor growth of stem cell phenotypes. Importantly, ectopic expression of SOX2OT led to an almost 20-fold increase in SOX2 expression, together with a reduced proliferation and increased breast cancer cell anchorage-independent growth.	25006803	2014	Emerging role of long non-coding RNA SOX2OT in SOX2 regulation in breast cancer.	0	0	0
chr3	180989762	181836880	SOX2OT	347689	HGNC:20209	ENSG00000242808	NR_004053	qPCR etc.	up-regulated	In this study, we analyzed expression of four long noncoding RNAs (lncRNAs) namely SOX2OT, PTPRG-AS1, ANRASSF1, and ANRIL in 38 breast cancer tissues and their adjacent noncancerous tissues (ANCTs). ANRASSF1 expression was not detected in any noncancerous tissue. All lncRNAs showed significant overexpression in tumor tissues compared with ANCTs.	26409453	2016	Expression analysis of four long noncoding RNAs in breast cancer.	0	0	0
NA	NA	NA	SPRY4-IT1	100642175	HGNC:42394	ENSG00000281881	NR_131221	microarray, qPCR, RNAi, Western blot etc.	up-regulated	SPRY4-IT1 expression was significantly upregulated in 48 breast cancer tumor tissues comparedwith normal tissues. Additionally, increased SPRY4-IT1 expression was found to be associated with a larger tumor size and an advanced pathological stage in breast cancer patients. SPRY4-IT1 is a novel prognostic biomarker and a potential therapeutic candidate for breast cancer.	25742952	2015	The long noncoding RNA SPRY4-IT1 increases the proliferation of human breast cancer cells by upregulating ZNF703 expression.	0	0	0
chr5	140537340	140558252	SRA1	NA	NA	ENSG00000213523	NA	qPCR etc.	differential expression	Subgroup analysis showed that SRA expression was similar in ER+/PR+ (median = 65.5, n = 8) and in ER-/PR- (median = 94.6, n = 5) tumors. Interestingly, SRA expression in these two subgroups was significantly lower than that observed in ER+/PR- (median = 156.4, n = 6) and ER-/PR+ (median = 144.8, n = 8) tumors. A variant form of SRA, presenting a deletion of 203 bp within the SRA core sequence, was also observed in breast tumor tissues. The relative expression of this new SRA isoform correlated with tumor grade.	10485452	1999	Expression of the steroid receptor RNA activator in human breast tumors.	0	0	0
chr5	140537340	140558252	SRA1	NA	NA	ENSG00000213523	NA	qPCR, Western blot etc.	differential expression	Disturbance of the balance between SRAP1-coding and non-coding SRA1 RNAs in breast tumor tissues might be involved in breast tumorigenesis.	20079837	2010	Chlamydial protease CT441 interacts with SRAP1 co-activator of estrogen receptor alpha and partially alleviates its co-activation activity.	0	0	0
chr5	140537340	140558252	SRA1	NA	NA	ENSG00000213523	NA	qPCR etc.	differential expression	We recently reported a decreased estrogen receptor activity in breast cancer cells overexpressing SRAP, suggesting antagonist roles played by SRA1 RNA and SRAP. The primary genomic sequence in and around intron-1 is sufficient to lead to a differential splicing of this intron. We propose that alternative splicing of intron-1 is one mechanism used by breast cancer cells to regulate the balance between coding and functional noncoding SRA1 RNAs.	16848684	2006	Alternative splicing of the first intron of the steroid receptor RNA activator (SRA) participates in the generation of coding and noncoding RNA isoforms in breast cancer cell lines.	0	0	0
chr5	140537340	140558252	SRA1	NA	NA	ENSG00000213523	NA	qPCR, Western blot etc.	up-regulated	We report a significant higher SRA-intron-1 relative expression in breast tumors with higher progesterone receptor contents. Using an antisense oligoribonucleotide, we have successfully reprogrammed endogenous SRA splicing and increased SRA RNA-intron-1 relative level in T5 breast cancer cells. Our results suggest that the balance coding/non-coding SRA transcripts not only characterizes particular tumor phenotypes but might also, through regulating the expression of specific genes, be involved in breast tumorigenesis and tumor progression.	19483093	2009	Increasing the relative expression of endogenous non-coding Steroid Receptor RNA Activator (SRA) in human breast cancer cells using modified oligonucleotides.	0	0	0
chr1	160317403	160317706	SUMO1P3	NA	NA	ENSG00000235082	NA	qPCR, Luciferase reporter assay	up-regulated	high levels of SUMO1P3 expression associated significantly with tumor progression and poor survival of breast cancer patients.knockdown of SUMO1P3 suppressed proliferation, migration, and invasion of breast cancer cells. SUMO1P3 binds to miR-320a,which has been identified as a tumor suppressor in various cancers, including breast cancer. the tumor-promoting effects of SUMO1P3 in breast cancer are partly mediated by negative regulation of miR-320a. 	29312511	2017	The long non-coding RNA SUMO1P3 facilitates breast cancer progression by negatively regulating miR-320a.	imatinib	0	1
chr19	5558167	5578349	TINCR	NA	NA	ENSG00000223573	NA	qPCR, Luciferase reporter assay, in vitro knockdown etc.	up-regulated	TINCR was aberrantly up-regulated by SP1,which in turn stimulated cell proliferation,anchorage-independent growth and suppressed cell apoptosis in breast cancer.TINCR silencing significantly suppressed migration and invasion in vitro and xenograft tumor growth in vivo.Mechanistically, TINCR modulated KLF4 expression via competing with miR-7, which consequently contributed to its oncogenic potential.MiR-7 inhibition severely compromised TINCR silencing-elicited tumor repressive effects	29614984	2018	Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer. 	0	1	1
chr1	3735601	3747336	TP73-AS1	57212	HGNC:29052	ENSG00000227372	NR_033708	qPCR, Luciferase reporter assay, Western blot	up-regulated	TP73-AS1 was specifically upregulated in BC tissues and BC cell lines and was correlated to a poorer prognosis in patients with BC. TP73-AS1 could regulate miR-200a through direct targeting. Moreover, TP73-AS1 might compete with TFAM for miR-200a binding thus to promote TFAM expression.TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a. High TP73-AS1 expression in BC was related with poorer clinicopathological parameters and shorter overall survival.	28639399	2017	TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition.	TZM	0	1
chr1	3735601	3747336	TP73-AS1	57212	HGNC:29052	ENSG00000227372	NR_033708	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	down-regulated	Taken together, we demonstrated a TP73-AS1/miR-200a/ZEB1 regulating loop in breast cancer cells, which promote cancer cell invasion and migration through regulating E-cadherin and Twist expression. 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	2017	A TP73-AS1/miR-200a/ZEB1 regulating loop promotes breast cancer cell invasion and migration.	0	0	0
chr20	50040716	50041504	TRERNA1	100887755	HGNC:44307	ENSG00000231265	NR_051976	qPCR, Lentiviral infection, Luciferase reporter assay, RNA pull-down assay, Cell proliferation assay etc.	up-regulated	We found that treRNA is upregulated in paired clinical breast cancer primary and lymph-node metastasis samples, and that its expression stimulates tumour invasion in vitro and metastasis in vivo. Interestingly, we found that treRNA downregulates the expression of the epithelial marker E-cadherin by suppressing the translation of its mRNA. We identified a novel ribonucleoprotein (RNP) complex, consisting of RNA-binding proteins (hnRNP K, FXR1, and FXR2), PUF60 and SF3B3, that is required for this treRNA functions. Translational suppression by treRNA is dependent on the 3'UTR of the E-cadherin mRNA. Taken together, our study indicates a novel mechanism of gene regulation by lncRNAs in cancer progression.	23974796	2013	Identification of a long non-coding RNA-associated RNP complex regulating metastasis at the translational step.	0	0	0
chr22	30969245	30979395	TUG1	55000	HGNC:26066	ENSG00000253352	NR_002323	qPCR, Western blotting etc.	down-regulated	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 cyclinD1 and CDK4. Further functional assays indicated that TUG1 overexpression significantly promoted cell migration and invasion while TUG1 knockdown had the opposite effects. Our findings indicate that the lncRNA TUG1 is a tumor suppressor in breast cancer, and may serve as a novel prognostic biomarker and potential therapeutic target for patients with breast cancer.	28950664	2017	Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer	0	0	1
chr22	30969245	30979395	TUG1	55000	HGNC:26066	ENSG00000253352	NR_002323	qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay, MTT assay etc.	up-regulated	Higher expression of TUG1 was observed in breast cancer tissues and cell lines than in the corresponding controls. TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of 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. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells.	28053623	2016	LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells.	0	0	0
chr22	30969245	30979395	TUG1	55000	HGNC:26066	ENSG00000253352	NR_002323	qPCR, RNAi, Cell proliferation assay etc.	up-regulated	The expression of TUG1 was enhanced in breast cancerous tissues and in highly invasive breast cancer cell lines and was associated with clinical variables, including tumor size, distant metastasis and TNM staging. Knockdown of TUG1 significantly slowed down cell proliferation, cell migration, and invasion in breast cancer cell lines MDA-MB-231 and MDA-MB-436. In addition, cell apoptotic rate was shown to increase upon siTUG1 treatment as evidenced by increases of the activities of caspase-3 and caspase-9.	27848085	2016	Long non-coding RNA TUG1 promotes cell proliferation and metastasis in human breast cancer.	0	0	0
chr14	95876392	95925571	TUNAR	100507043	HGNC:44088	ENSG00000250366	NR_038861	qPCR, Western blot, RIP, ChIP, Luciferase reporter assay, RNA pull-down assay etc.	up-regulated	We found the human ortholog of TUNA, linc00617, was upregulated in breast cancer samples. Linc00617 promoted motility and invasion of breast cancer cells and induced epithelial-mesenchymal-transition (EMT), which was accompanied by generation of stem cell properties. Moreover, knockdown of linc00617 repressed lung metastasis in vivo. We demonstrated that linc00617 upregulated 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	26207516	2015	Long noncoding RNA linc00617 exhibits oncogenic activity in breast cancer	0	0	0
chr3	116709235	116723581	TUSC7	285194	HGNC:27701	ENSG00000243197	NR_015391	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay, ISH etc.	differential expression	To evaluate the biological consequence of p53 induction of loc285194 and the role of loc285194 in tumorigenesis, we ectopically expressed loc285194 in HCT-116 WT and MCF-7 cells for cell proliferation assays. As expected, loc285194 significantly inhibited tumor cell growth.	23558749	2013	LncRNA loc285194 is a p53-regulated tumor suppressor.	0	0	0
NA	NA	NA	uc.38	NA	NA	NA	NA	qPCR, Western blot, RIP	down-regulated	The expression of uc.38, a T-UCR, was down-regulated in both breast cancer tissues and breast cancer cell lines. uc.38 was expressed at significantly lower levels in larger tumours and tumours of more advanced stages.up-regulation of uc.38 expression inhibited cell proliferation and induced cell apoptosis.uc.38 suppressed breast cancer. 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.The level of expression and type of TUCR have been shown to be closely related to the survival rates of patients with cancer. 	29312798	2017	uc.38 induces breast cancer cell apoptosis via PBX1.	0	0	1
chr10	1526637	1556984	uc.57	642394	HGNC:23299	ENSG00000205696	NR_033387	qPCR, Western blot, RIP etc.	down-regulated	uc.57 binds to BCL11A. Uc.57 overexpression downregulated BCL11A and reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo. 	29179465	2017	Shikonin reduces tamoxifen resistance through long non-coding RNA uc.57	Shikonin, tamoxifen	0	0
chr5	10627260	10628225	uc.63	100874247	HGNC:41298	ENSG00000250106	NA	qPCR, RNAi, Western blot etc.	up-regulated	We found that overexpression of one specific T-UCRs named uc.63 is associated with bad outcome in luminal A subtype of breast cancer patients.	27447964	2016	Ultraconserved long non-coding RNA uc.63 in breast cancer.	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown	up-regulated	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. Meanwhile,reciprocal repression of UCA1 and miR-18a were found to be Argonaute 2-dependent. Knockdown of YAP1 recapitulated the effect of UCA1 silencing by reducing the viability of trastuzumab-treated breast cancer cells, whereas inhibition of miR-18a abrogated UCA1 knockdown-induced improvement of trastuzumab sensitivity in breast cancer cells.	29408336	2018	Long non-coding RNA UCA1 desensitizes breast cancer cells to trastuzumab by impeding miR-18a repression of Yes-associated protein 1.	Trastuzumab	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot etc.	up-regulated	In breast cancer cells,IMP1 interacts with UCA1 via the ACACCC motifs within UCA1 and destabilizes UCA1 through the recruitment of CCR4-NOT1 deadenylase complex.Meanwhile,binding of IMP1 prevents the association of miR-122-5p with UCA1,thereby shifting the availability of miR-122-5p from UCA1 to the target mRNAs and reducing the UCA1-mediated cell invasion.Accordingly, either IMP1 silencing or UCA1 overexpression resulted in reduced levels of free miR-122-5p within the cytoplasm, affecting miR-122-5p in regulating its target mRNAs.Our study provides initial evidence that interaction between IMP1 and UCA1 enhances UCA1 decay and competes for miR-122-5p binding,leading to the liberation of miR-122-5p activity and the reduction of cell invasiveness. 	29669595	2018	IMP1 regulates UCA1-mediated cell invasion through facilitating UCA1 decay and decreasing the sponge effect of UCA1 for miR-122-5p.	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot, Dual-luciferase reporter assay, Flow cytometry assay etc.	up-regulated	Our findings reveal that tamoxifen induces UCA1 upregulation in ER-positive breast cancer cells in a HIF1a-dependent manner. UCA1 upregulation results in significantly enhanced tamoxifen resistance. The upregulated UCA1 sponges miR-18a, which is a negative regulator of HIF1a. Therefore, UCA1 upregulation is further enhanced through a miR-18a-HIF1a feedback loop.	27629141	2016	Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1a feedback regulatory loop.	1	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	microarray, qPCR etc.	up-regulated	Expression level of these 3 lncRNAs was determined in plasma samples of 60 patients with BC and 40 healthy individuals by performing real-time PCR. As expected, the relative expression of ANRIL, HIF1A-AS2, and UCA1 was significantly higher in patients with TNBC than in patients with NTNBC, which was consistent with the results of microarray analysis.	28248879	2017	A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers.	0	1	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot, Flow cytometry assay etc.	up-regulated	UCA1 is significantly increased not only in LCC2 cells, but also in exosomes released from LCC2 cells. The increase in exosomes is more evident than in cells. MCF-7 cells pretreated with exos/LCC2 had a significantly increased cell viability, a decreased expression of cleaved caspase-3 and a lower ratio of apoptosis after tamoxifen treatment. The exos/LCC2 with impaired UCA1 loading had significantly suppressed capability to promote tamoxifen resistance in MCF-7 cells.	27831634	2016	Exosomes mediated transfer of lncRNA UCA1 results in increased tamoxifen resistance in breast cancer cells.	1	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, RNAi, Western blot, Cell proliferation assay etc.	differential expression	Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. Furthermore, simultaneous depletion of SATB1 and UCA1 potentiated suppression of tumor growth and cell survival. Thus, SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells.	27697109	2016	Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer.	0	0	1
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	Western blot, Cell invasion assay etc.	differential expression	Knockdown of endogenous UCA1 significantly reduced the number of invading cells. MDA-MB-231 cells with UCA1 knockdown had significantly increased expression of E-cadherin but decreased expression of N-cadherin, Vimentin and Snail. UCA1 inhibition substantially increased the expression of p-GSK-3B and GSK-3B and suppressed the protein expression of B-catenin and transcription of the downstream genes, including cyclin D1 and MMP-7.	27424981	2016	LncRNA UCA1 promotes epithelial-mesenchymal transition (EMT) of breast cancer cells via enhancing Wnt/beta-catenin signaling pathway.	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot, Flow cytometry assay etc.	up-regulated	LncRNA UCA1 was significantly upregulated in tamoxifen resistant breast cancer cells compared to tamoxifen sensitive cells. LCC2 and LCC9 cells transfected with UCA1 siRNA had significantly higher ratio of apoptosis after tamoxifen treatment. UCA1 siRNA significantly decreased the protein levels of p-AKT and p-mTOR in LCC2 and LCC9 cells. Enforced UCA1 expression substantially reduced tamoxifen induced apoptosis in MCF-7 cells, while rapamycin treatment abrogated the protective effect of UCA1.	27765938	2016	Long Non-Coding RNA (lncRNA) Urothelial Carcinoma-Associated 1 (UCA1) Enhances Tamoxifen Resistance in Breast Cancer Cells via Inhibiting mTOR Signaling Pathway.	1	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR etc.	up-regulated	We found that treatment with macrophage CM induced the expression of numerous lncRNAs, including urothelial cancer associated 1 (UCA1). Knockdown of UCA1 using shRNA inhibited AKT phosphorylation and abolished invasiveness of tumor cells induced by macrophage CM. Consistent with these results; we further showed that UCA1 level was significantly enhanced in human primary breast tumors and correlated with advanced clinical stage, supporting its role in promoting carcinogenesis and progression of breast cancer	26464647	2015	Macrophage infiltration promotes invasiveness of breast cancer cells via activating long non-coding RNA UCA1	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	microarray, qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	up-regulated	We found that UCA1 was upregulated in breast tumors compared with the normal breast tissue. In contrast, p27 was downregulated in breast tumors, which was derived from the same core. This negative correlation between UCA1 and p27 was further supported by the data from breast cancer TMA.	24457952	2014	Long non-coding RNA UCA1 promotes breast tumor growth by suppression of p27 (Kip1).	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot, Northern blot, Flow cytometry assay etc.	up-regulated	Results from Northern blot analysis indicated that CUDR was detectable only in human placenta but not in other normal tissues. For expression in human cancer cells, CUDR was detected in most cells of different tissue origins. CUDR mRNA was detected in human hepatocellular carcinoma HepG2 and Hep3B cells, human breast carcinoma MCF-7 and MDA-468 cells, human squamous carcinoma HeLa cells, human colon carcinoma HT-29 and CaCO-2 cells, as well as human lung carcinoma Calu-6 cells. However, CUDR was barely detectable in human prostate carcinoma PC3 cells. The differential expression of CUDR between human normal and cancer tissues is further demonstrated in tissues from cancer patients. 	17416635	2007	Induction of drug resistance and transformation in human cancer cells by the noncoding RNA CUDR.	1	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	microarray, qPCR, RNAi, ISH etc.	up-regulated	UC1 was significantly upregulated, while miR-143 was significantly downregulated in the tumor tissues than in the adjacent normal tissues. 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	2015	Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, Western blot, Cell proliferation assay etc.	up-regulated	We found that the expression of UCA1 positively correlated with the pathological grade and mortality of breast cancer patients, moreover, expressions of UCA1 was increased significantly in the tamoxifen-resistant cell lines compared with the wild type parental cells. Ectopic expression of UCA1 promoted cell survival and resistance to tamoxifen treatment, whereas inhibition of UCA1 enhanced tamoxifen sensitivity of BC cells and induced more apoptotic cells. In line with these data, UCA1 depletion attenuated the activity of Wnt/B-catenin pathway activation and the tumorigenicity of the tamoxifen-resistant BC cells.	27977766	2016	Knockdown of Long Non-Coding RNA UCA1 Increases the Tamoxifen Sensitivity of Breast Cancer Cells through Inhibition of Wnt/B-Catenin Pathway.	1	0	1
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	qPCR, RNAi, Western blot, Cell proliferation assay etc.	up-regulated	Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly.	26550436	2015	Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5.	0	0	0
chr19	15828206	15836326	UCA1	652995	HGNC:37126	ENSG00000214049	NR_015379	Microarray, qPCR, RIP, Luciferase reporter assay etc.	up-regulated	We observed that TGF-B induced genome-wide changes in lncRNA levels in breast cancer cells, among which AC026904.1 and UCA1 were highly expressed in metastatic breast cancer and closely associated with poor prognosis. UCA1 exerts a competitive endogenous RNA (ceRNA) activity in the cytoplasm.	29774079	2018	Long non-coding RNAs AC026904.1 and UCA1: a ¡°one-two punch¡± for TGF-B-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer	0	0	1
NA	NA	NA	X15675	NA	NA	NA	NA	microarray, qPCR, RNAi, Western blot etc.	up-regulated	From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results.	28003470	2016	Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.	oestrogen	0	0
chrX	73820651	73852753	XIST	7503	HGNC:12810	ENSG00000229807	NR_001564	qPCR, RNAi, IHC, ISH etc.	down-regulated	Here, we show that Xist expression is significantly reduced in breast tumor samples and cancer cell lines. Xist knockdown or overexpression resulted in increased or decreased levels, respectively, of AKT phosphorylation and cell viability. Further studies revealed an inverse correlation between Xist and phospho-AKT levels in breast cancer samples. Additionally, Xist knockdown-elicited increase of cell viability was attenuated by AKT inhibitor. These results suggest that Xist negatively regulates cell viability via inhibition of AKT activation.	27248326	2016	Xist reduction in breast cancer upregulates AKT phosphorylation via HDAC3-mediated repression of PHLPP1 expression.	0	0	0
chrX	73820651	73852753	XIST	7503	HGNC:12810	ENSG00000229807	NR_001564	qPCR, Cell cycle assay etc.	down-regulated	Using gene expression profiling, we identified the long noncoding RNA Xist (X-inactive specific transcript) as a biomarker predicting BCL response to HDACi. We validated that low Xist expression predicts drug response in PDXs associated with a significant reduction of the breast CSC population.	24141629	2013	The histone deacetylase inhibitor abexinostat induces cancer stem cells differentiation in breast cancer with low Xist expression.	1	0	0
chrX	73820651	73852753	XIST	7503	HGNC:12810	ENSG00000229807	NR_001564	microarray, FISH etc.	differential expression	The intratumoral and intertumoral variability in XIST RNA domain number in BRCA1 tumors correlates with chromosomal genetic abnormalities, including gains, losses, reduplications, and rearrangements of the X-chromosome. Finally, we also show the necessity for combined global and single-cell approaches in the assessment of tumors with such a high degree of heterogeneity.	17545591	2007	X inactive-specific transcript RNA coating and genetic instability of the X chromosome in BRCA1 breast tumors.	0	0	0
chrX	73820651	73852753	XIST	7503	HGNC:12810	ENSG00000229807	NR_001564	qPCR, Western blot, Luciferase reporter assay etc.	up-regulated	XIST was significantly down-regulated in breast cancer tissues and cell lines. Further functional analysis indicated that overexpression of XIST remarkably inhibited breast cancer cell growth, migration, and invasion.The results of luciferase reporter assays verified that miR-155 was a direct target of XIST in breast cancer. Moreover, caudal-type homeobox 1 (CDX1) was identified as a direct target of miR-155 and miR-155/CDX1 rescued the effects of XIST in breast cancer cells. Taken together,XIST is down-regulated in breast cancer and suppresses breast cancer cell growth, migration, and invasion via the miR-155/CDX1 axis. 	29550489	2018	Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis.	0	0	0
chrX	73820651	73852753	XIST	7503	HGNC:12810	ENSG00000229807	NR_001564	qPCR, RNAi, RNA-FISH, DNA-FISH, Methylation assay etc.	up-regulated	XIST RNA levels comparable to those of non-BLC and significantly higher than those detected in sporadic BLC. In this tumor cell line XIST shows a misbehaviour, because it is expressed by an active X chromosome and does not stably coat the XIST expressing X chromosome.	19440381	2009	Misbehaviour of XIST RNA in breast cancer cells.	0	0	0
chr1	213924749	213926654	Yiya	100861504	HGNC:43655	ENSG00000281664	NR_046189	qPCR, etc.	up-regulated	Our results define a functional role for lncRNA in metabolic reprogramming in cancer, with potential clinical implications for its therapeutic targeting. In clinical specimens of breast cancer, YIYA was expressed in ~40% of cases where it correlated with CDK6 expression and unfavorable survival outcomes. 	29967256	2018	Expression of long non-coding RNA YIYA promotes glycolysis in breast cancer.	0	0	1
chr3	98497912	98523066	Z38	56650	HGNC:1322	ENSG00000080822	NA	microarray, qPCR etc.	up-regulated	Z38 was upregulated in breast cancer tissues. Furthermore, of 110 breast cancer patients, high Z38 expression was significantly associated with tumor-node-metastasis stage and lymph node metastasis.	28247935	2017	Prognostic significance of long noncoding RNA Z38 as a candidate biomarker in breast cancer.	0	0	1
chr3	98497912	98523066	Z38	56650	HGNC:1322	ENSG00000080822	NA	qPCR, Western blot etc.	up-regulated	In the current study, a newly found lncRNA Z38, which was identified through combining experiments of suppression subtractive hybridization (SSH) and reverse dot-blotting, was found to have high expression in breast cancer. More importantly, inhibiting Z38 expression by gene silencing greatly suppressed breast cancer cell proliferation and tumorigenesis, and treatment with Z38 siRNAs significantly induced cell apoptosis and inhibited tumor growth.	27053956	2016	High Expression of the Newly Found Long Noncoding RNA Z38 Promotes Cell Proliferation and Oncogenic Activity in Breast Cancer	0	0	0
chr20	49278178	49295738	ZFAS1	441951	HGNC:33101	ENSG00000177410	NR_003604	qPCR, Western blot etc.	down-regulated	The results revealed that ZFAS1 expression was significantly downregulated in breast cancer cell lines when compared with the levels in controls. In vitro experiments also demonstrated that ZFAS1 overexpression significantly suppressed cell proliferation by causing cell  cycle arrest and inducing apoptosis in breast cancer cells. Further functional assays indicated that ZFAS1 overexpression inhibited cell migration and invasion  by regulating epithelial mesenchymal transition. These findings indicated that the lncRNA ZFAS1 may be a tumor suppressor in breast cancer, and thus, may serve  as a potential therapeutic target for patients with breast cancer. ZFAS1 overexpression  in MCF-7 and MDA-MB-231 cells resulted in significantly  decreased clonogenic survival.	29532866	2018	Downregulation of the long non-coding RNA ZFAS1 is associated with cell proliferation, migration and invasion in breast cancer.	0	0	1
chr20	49278178	49295738	ZFAS1	441951	HGNC:33101	ENSG00000177410	NR_003604	qPCR etc.	down-regulated	Using human breast cancer cell lines, ZFAS1 was found to be expressed in all cell lines tested, albeit at different levels of abundance. Following subcellular fractionation, human ZFAS1 was found in both nucleus and cytoplasm (as is the mouse orthologue) in an isoform-independent manner. Sucrose gradients based on velocity sedimentation were utilised to separate the different components of total cell lysate, and surprisingly ZFAS1 was primarily co-localised with light polysomes. Further investigation into ribosome association through subunit dissociation studies showed that ZFAS1 was predominantly associated with the 40S small ribosomal subunit. The expression levels of ZFAS1 and of mRNAs encoding several ribosomal proteins that have roles in ribosome assembly, production and maturation were tightly correlated. ZFAS1 knockdown significantly reduced RPS6 phosphorylation.	27871336	2016	ZFAS1: a long noncoding RNA associated with ribosomes in breast cancer cells.	0	0	0
chr20	49278178	49295738	ZFAS1	441951	HGNC:33101	ENSG00000177410	NR_003604	microarray, Northern blot, ISH etc.	down-regulated	The result shows ZFAS1 expression is decreased in ductal carcinoma relative to normal epithelial cells. We propose a functional role for Zfas1/ ZFAS1 in the regulation of alveolar development and epithelial cell differentiation in the mammary gland, which, together with its dysregulation in human breast cancer, suggests ZFAS1 as a putative tumor suppressor gene.	21460236	2011	SNORD-host RNA Zfas1 is a regulator of mammary development and a potential marker for breast cancer.	0	0	0
chr6	1605531	1606079	FOXCUT	101927703	HGNC:50650	ENSG00000280916	NR_125804	qPCR, RNAi etc.	up-regulated	The results showed that the expression of FOXCUT and FOXC1 were positively correlated. When the expression of FOXCUT was downregulated by small interfering RNA, the expression of FOXC1 was similarly reduced. Furthermore, in MDA-MB-231 and MDA-MB-468 breast cancer cells, knockdown of FOXCUT markedly inhibited cell proliferation and migration in vitro. In conclusion, FOXCUT lncRNA may be functionally involved in the tumor progression of BLBCs through the regulation of its paired mRNA, FOXC1, demonstrating that FOXCUT may serve as a novel biomarker and therapeutic target in BLBCs.	25516208	2014	Forkhead box C1 promoter upstream transcript, a novel long non-coding RNA, regulates proliferation and migration in basal-like breast cancer.	0	0	0
chr9	21994778	22121097	ANRIL	100048912	HGNC:34341	ENSG00000240498	NR_003529	qPCR, Luciferase reporter assay, RIP.	up-regulated	Expression level of ANRIL was up-regulated in TNBC tumor tissue and cell lines compared to noncancerous tissue and non-TNBC cells.the up-regulated ANRIL expression was closely correlated to poor prognosis.ANRIL knockdown interfered by interference oligonucleotide could markedly suppress TNBC cells proliferation and enhance apoptosis. ANRIL overexpression modulated TNBC tumorigenesis through acting as molecular 'sponge' for miR-199a.	28961506	2017	Long non-coding RNA ANRIL promotes carcinogenesis via sponging miR-199a in triple-negative breast cancer.	0	0	1
NA	NA	NA	ARNILA	NA	NA	NA	NA	Microarray, qPCR, Luciferase reporter assay, Western blot, ChIP etc.	up-regulated	We performed experiments with or without DHT treatment in three TNBC cell lines, and we identified an AR negatively induced lncRNA (ARNILA), which correlated with poor progression-free survival (PFS) in TNBC patients and promoted epithelial-mesenchymal transition (EMT), invasion and metastasis in vitro and in vivo. Subsequently, we demonstrated that ARNILA functioned as a competing endogenous RNA (ceRNA) for miR-204 to facilitate expression of its target gene Sox4, which is known to induce EMT and contribute to breast cancer progression, thereby promoting EMT, invasion and metastasis of TNBC. High ARNILA expression was correlated with poor PFS(HR, 2.72; 95%CI, 1.26?5.70; P = 0.012) in TNBC.	29844570	2018	An androgen receptor negatively induced long non-coding RNA ARNILA binding to miR-204 promotes the invasion and metastasis of triple-negative breast cancer.	0	0	1
chr17	16438822	16478678	ASHGA5P018902	125144	HGNC:28619	ENSG00000175061	NA	microarray, qPCR etc.	up-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
NA	NA	NA	BC016831	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated. However, there are some differences between the lncRNA expression patterns of tissues and cell lines. Briefly, compared with the non-TNBC cell group, only 4 lncRNAs (BC016831, IGKV, LINC00052, and RP11-434D9.1) were down-regulated congruously in all 4 TNBC cells.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr5	181261212	181272307	CTC-338M12.3	100507602	HGNC:49006	ENSG00000248275	NR_102759	microarray, qPCR etc.	up-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr4	52712404	52720351	DANCR	57291	HGNC:28964	ENSG00000226950	NR_024031	qPCR, Western blot,RNAi, etc.	up-regulated	In the present study, our results showed that DANCR expression was increased in TNBC tissues compared with the adjacent normal tissues using quantitative real-time PCR (qRT-PCR) in 63TNBC specimens. The correlation between lncRNA DANCR expression and the overall survival of TNBC patients. Kaplan-Meier analysis of overall survival was analyzed according to lncRNA DANCR expression levels. 	28760736	2017	Targeting long non-coding RNA DANCR inhibits triple negative breast cancer progression.	0	0	1
NA	NA	NA	ENST00000460164	NA	NA	NA	NA	microarray, qPCR etc.	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.	0	0	0
chr4	13546075	13546964	ENST00000503938	NA	NA	ENSG00000246095	NA	microarray, qPCR etc.	down-regulated	The results demonstrated that lncRNAs NONHSAT125629 and ENST00000503938 were upregulated and that XR_250621.1 and NONHSAT012762 were down-regulated in the tumor samples compared with NT samples. These qPCR results are consistent with the microarray data.	26078338	2015	Identification of novel long non-coding RNAs in triple-negative breast cancer.	0	0	0
chr12	53962308	53974956	HOTAIR	100124700	HGNC:33510	ENSG00000228630	NR_003716	microarray, qPCR etc.	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.	0	0	0
NA	NA	NA	IGKV	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated. However, there are some differences between the lncRNA expression patterns of tissues and cell lines. Briefly, compared with the non-TNBC cell group, only 4 lncRNAs (BC016831, IGKV, LINC00052, and RP11-434D9.1) were down-regulated congruously in all 4 TNBC cells.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr15	87576929	87579866	LINC00052	145978	HGNC:26455	ENSG00000259527	NR_026869	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated. However, there are some differences between the lncRNA expression patterns of tissues and cell lines. Briefly, compared with the non-TNBC cell group, only 4 lncRNAs (BC016831, IGKV, LINC00052, and RP11-434D9.1) were down-regulated congruously in all 4 TNBC cells.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr2	87454781	87636740	LINC00152	112597	HGNC:28717	ENSG00000222041	NR_024204	qPCR, Western blot	up-regulated	linc00152 was highly expressed in all basal-like cell lines and in the majority of TNBC tissues. Linc00152 suppression by shRNA significantly inhibited invasion and colony growth. Such suppression also triggered apoptosis in vitro and inhibited tumor growth in vivo.linc00152 partially enhanced breast cancer tumorigenesis by inactivation of the BRCA1/PTEN through DNA methyltransferases.linc00152 as a promising biomarker and therapeutic target for human TNBC treatment.	29156515	2017	Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer.	0	0	0
chr18	57054558	57072119	linc-ROR	100885779	HGNC:43773	ENSG00000258609	NR_048536	qPCR etc.	down-regulated	lincRNA-ROR was upregulated in TNBC cell lines and tissue samples.The aberrant expression of lincRNA-ROR was shown to increase invasion and metastasis in MDA-MB-231 and loss of function by siRNA reverse these process.Furthermore, lincRNA-ROR functions as a competing endogenous RNAs (ceRNA) which sponges miR-145 and therefore upregulate the expression of Mucin1 (MUC1).Studies showed that downregulated SPRY4-IT1 could facilitate bladder cancer cell apoptosis via acting as a ceRNA for miR-101-3p.	29673594	2018	LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1.	0	0	0
NA	NA	NA	LOC441242	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr11	65497688	65506516	MALAT1	378938	HGNC:29665	ENSG00000251562	NR_002819	microarray, qPCR etc.	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.	0	0	0
NA	NA	NA	NONHSAT012762	NA	NA	NA	NA	microarray, qPCR etc.	up-regulated	The results demonstrated that lncRNAs NONHSAT125629 and ENST00000503938 were upregulated and that XR_250621.1 and NONHSAT012762 were down-regulated in the tumor samples compared with NT samples. These qPCR results are consistent with the microarray data.	26078338	2015	Identification of novel long non-coding RNAs in triple-negative breast cancer.	0	0	0
NA	NA	NA	NONHSAT125629	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The results demonstrated that lncRNAs NONHSAT125629 and ENST00000503938 were upregulated and that XR_250621.1 and NONHSAT012762 were down-regulated in the tumor samples compared with NT samples. These qPCR results are consistent with the microarray data.	26078338	2015	Identification of novel long non-coding RNAs in triple-negative breast cancer.	0	0	0
chr1	202810962	202811913	PCAT6	100506696	HGNC:43714	ENSG00000228288	NR_046325	microarray, qPCR etc.	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.	0	0	0
chr5	67379378	67805238	RP11-434D9.1	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated. However, there are some differences between the lncRNA expression patterns of tissues and cell lines. Briefly, compared with the non-TNBC cell group, only 4 lncRNAs (BC016831, IGKV, LINC00052, and RP11-434D9.1) were down-regulated congruously in all 4 TNBC cells.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
chr1	234646289	234683176	RP4-781K5.4	NA	NA	NA	NA	microarray, qPCR etc.	down-regulated	The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated.	26910840	2016	LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer.	0	0	0
NA	NA	NA	SKAI1BC	NA	NA	NA	NA	qPCR, Luciferase reporter assay etc.	up-regulated	We have identified and characterized a primarily nuclear non-polyadenylated, antisense (as)-lncRNA, initiating upstream of the KAI1 human metastasis suppressor gene transcription start site; and elongating in the opposite direction to KAI1 mRNA. We show that the KAI1 promoter is bi-directional giving rise to KAI1 mRNA and its as-lncRNA. Moreover, expression of this lncRNA transcript emerges to be inversely related to the KAI1 mRNA expression, and in direct relationship to the invasiveness level of human breast cancer derived cell lines. Importantly, knockdown of the KAI1 as-lncRNA in the triple-negative breast cancer cell line MDA-MB-231 have led to increased KAI1 mRNA and protein expression, manifested in stronger adhesion to fibronectin, retardation of cell migration and reduced cell invasion in vitro. Accordingly we have named this lncRNA, SKAI1BC, standing for Suppressor of KAI1 in Breast Cancer.	28978052	2017	Identification of a novel metastasis inducing lncRNA which suppresses the KAI1/CD82 metastasis suppressor gene and is upregulated in triple-negative breast cancer.	0	0	0
NA	NA	NA	TCONS_l2_00003938	NA	NA	NA	NA	microarray, qPCR etc.	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.	0	0	0
NA	NA	NA	XR_250621.1	NA	NA	NA	NA	microarray, qPCR etc.	up-regulated	The results demonstrated that lncRNAs NONHSAT125629 and ENST00000503938 were upregulated and that XR_250621.1 and NONHSAT012762 were down-regulated in the tumor samples compared with NT samples. These qPCR results are consistent with the microarray data.	26078338	2015	Identification of novel long non-coding RNAs in triple-negative breast cancer.	0	0	0
