LncRNA name	Synonyms	geneid	ensg_name	refseq_id	position	cancer type	ICD-0-3	ICD-0-3	methods	sample	regulated	function description	pubmed id	year	title
7SL	RN7SL1, 7L1a, 7SL, RN7SL, RNSRP1	6029	ENSG00000276168	NR_002715	GRCh38_14:49586580-49586878	breast cancer	C50	NA	qPCR, Western blot, ChIP, Luciferase reporter assay etc.	cell lines (MCF-10A, MCF-7, HeLa, and HCT-116)	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.
AC090952.4.1	RHBDF1P1	NA	ENSG00000234123	NA	GRCh38_3:14572852-14574792	non small cell lung cancer	C34	M8046/3	microarray, qPCR, RNAi, Western blot etc.	cell lines (A549, CDDP etc.)	down-regulated	For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	2013	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.
AK123263	LOC100506974	NA	NA	NA	GRCh38_17:13776832-13777349	non small cell lung cancer	C34	M8046/3	microarray, qPCR, RNAi, Western blot etc.	cell lines (A549, CDDP etc.)	down-regulated	For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	2013	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.
AK126698	NA	NA	NA	NA	NA	non small cell lung cancer	C34	M8046/3	microarray, qPCR, RNAi, Western blot etc.	cell lines (A549, CDDP etc.)	down-regulated	For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	2013	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.
BA318C17.1	MACROD2-AS1, BA318C17.1, NCRNA00186	100379174	ENSG00000235914	NR_037841	GRCh38_20:14884253-14929515	colorectal cancer	C19.9	NA	qPCR, STS-PCR, ISH etc.	primary CRC tissues, cell lines (Co1o205, Co1o320 HSR, Co1o678, Co1o741, HCA7, HCA46, HRA19, LS1034 etc.)	down-regulated	Two noncoding RNA genes located in the region, BA318C17.1 and DJ974N19.1, were investigated by mutation analysis and real-time PCR in colorectal cancer cell lines. Sequence changes in BA318C17.1 and reduced expression of both genes was detected, suggesting that the abrogation of these genes may play a role in colorectal tumorigenesis.	16110499	2005	Deletion at chromosome band 20p12.1 in colorectal cancer revealed by high resolution array comparative genomic hybridization.
BAIAP2-AS1	BAIAP2-AS1	NA	ENSG00000226137	NA	GRCh38_17:81029130-81034881	hepatocellular carcinoma	C22.0	M8170/3	microarray, qPCR, RNAi etc.	HCC tissues	up-regulated	To validate expression of the 6 HH-lncRNAs, qRT-PCR was performed in a cohort of 20 HCC patients, including 10 primary HCC and 10 HBV-related HCC. Expression of 6 HH-lncRNAs validated by qRT-PCR was consistent with microarray results. 	27285756	2016	Comprehensive analysis of long non-coding RNA expression profiles in hepatitis B virus-related hepatocellular carcinoma.
BANCR	BANCR, LINC00586	100885775	ENSG00000278910	NR_047671	GRCh38_9:69296682-69311111	papillary thyroid cancer	NA	M8260/3	qPCR, Cell transfection, Western blot, Flow cytometry assay, Cell proliferation assay etc.	PTC tissues, cell lines (TPC-1, K1, BCPAP and CGTH-W3)	down-regulated	BANCR levels are lower in PTC tumor tissues than control tissues. Decreased BANCR levels correlate with tumor size, the presence of multifocal lesions and advanced PTC stage. BANCR overexpression reduced PTC cell proliferation and promoted apoptosis, which inhibited metastasis. It also inactivated ERK1/2 and p38, and this effect was enhanced by treatment with the MEK inhibitor U0126. Finally, BANCR overexpression dramatically inhibited tumor growth from PTC cells in xenograft mouse models.	27462868	2016	BRAF-activated LncRNA functions as a tumor suppressor in papillary thyroid cancer.
BANCR	BANCR, LINC00586	100885775	ENSG00000278910	NR_047671	GRCh38_9:69296682-69311111	papillary thyroid cancer	NA	M8260/3	qPCR, RNAi, RIP, Flow cytometry assay etc.	PTC tissues, cell line (IHH-4)	up-regulated	The expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown in a PTC-derived cell line (IHH-4) resulted in significant suppression of thyroid stimulating hormone receptor (TSHR). BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR.	26323637	2015	BRAF-activated Long Non-coding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor.
CASC2	CASC2, C10orf5	255082	ENSG00000177640	NR_026939	GRCh38_10:118046279-118210153	astrocytoma	NA	M9400/3 	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay, ISH etc.	astrocytoma tissues, cell lines (U251 and U87)	up-regulated	High CASC2c was positively correlated with astrocytoma progression, and an unfavorable prognosis factor for patients. Knockdown CASC2c inhibited proliferation and tumorgenesis. Overexpression of CASC2c promotes the malignant characteristic of astrocytoma cells.CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1.	28252647	2017	CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis.
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	colorectal cancer	C19.9	NA	qPCR, RIP etc.	CRC tissues, cell lines (COLO320DM, HCT116, RKO, HEK293 etc.)	up-regulated	Here, we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability. Our results support a new mechanism of MYC and WNT regulation by the novel lncRNA CCAT2 in colorectal cancer pathogenesis, and provide an alternative explanation on the SNP-conferred cancer risk.	23796952	2013	CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer.
CNALPTC1	NA	NA	NA	NA	NA	papillary thyroid cancer	NA	M8260/3	Microarray, qRT-PCR, Western blot, Luciferase reporter assay, RIP	PTC tissues, PTC cell lines (TPC-1 and IHH-4)	up-regulated	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC.CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	29416932	2018	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.
DLEU2	DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6	10301	ENSG00000176124	NR_002605	GRCh38_13:50082171-50723236	chronic lymphocytic leukemia	NA	M9823/3	microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc.	blood	up-regulated	In contrast, the lncRNA genes DLEU1 and variant DLEU2/Alt1 that display DNA-hypomethylation at their 5' ends are significantly upregulated in CLL cells. We found a significant inverse correlation of gene expression of the lncRNA genes DLEU1 and the DLEU2 variant Alt1 with DNA-methylation levels in regions D6 and E6 that are localized at their transcriptional start sites.	23593011	2013	Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the In Cis downregulation of a gene cluster that targets NF-kB.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	retinoblastoma	C69.2	M9510/3	Western blot, qPCR, in vitro knockdown RIP etc.	cell lines (WERI-Rb-1, SO-RB50, and Y7, ARPE-19), retinoblastoma tissues	down-regulated	H19 is downregulated in retinoblastoma tissues and cell lines. Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	29143996	2017	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	endometrial cancer	NA	M8380/3	qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	Human EC cell lines (HEC-1-A and Ishikawa)	up-regulated	MiR-646 expression was significantly decreased both in human EC tissues and cell lines compared with the control.Moreover, miR-646 expression was negatively related to HOTAIR in human EC tissues.miR-646 overexpression considerably attenuated the E2-promoted viability, migration and invasion of Ishikawa and HEC-1-A cells in vitro.In addition, HOTAIR was confirmed to regulate the viability, migration and invasion of EC cells through negative regulating miR-646.More importantly, we also demonstrated that NPM1 was the target of miR-646,and HOTAIR promoted NPM1 expression through interacting with miR-646 in EC cells.HOTAIR was well documented in recruiting PRC2 components and subsequent chromosomal gene silencing via coordinated histone H3K27 methylation and H3K4 demethylation.	29466670	2018	Long non-coding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via miR-646/NPM1 axis.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	breast cancer	C50	NA	qPCR, Luciferase reporter assay etc.	Tumor tissues, blood, cell lines (MDA-MB-231 and BT549)	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
Linc00518	C6orf218	221718	ENSG00000183674	NR_027793	GRCh38_6:10429255-10434874	breast cancer	C76.0	NA	qRT-PCR, Western blot assays, Luciferase reporter assays, RIP	Human mammary epithelial cell line (MCF-10A) and human breast cancer cell line (MCF-7), The ADR-resistant variant (MCF-7/ADR) cell line, breast cancer tissue specimens and the adjacent normal tissues	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	glioblastoma	NA	M9440/3	qPCR etc.	cell line (A172)	up-regulated	As the RT-PCR and qPCR analyses revealed, expression levels of LINC00663 were found to be differentially expressed in various cancer cell lines. LINC00663 showed highest expression in A172 glioblastoma cell line.	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	lung cancer	C34	NA	qPCR etc.	cell line (A549)	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	thyroid cancer	C73.9	NA	qPCR etc.	cell line (BCPAP)	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	pancreatic cancer	C25	NA	qPCR etc.	cell line (CRL-1469)	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	gastric cancer	C16	NA	qPCR etc.	cell line (HGC-27)	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	breast cancer	C50	NA	qPCR etc.	cell line (MCF7)	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.
LINC00663	NA	284440	ENSG00000266904	NR_026956	GRCh38_19:19757366-19776423	prostate cancer	C61.9	NA	qPCR etc.	cell lines (DU-145 and PC3)	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.
LINC00673	LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1	100499467	NA	NR_036488	GRCh38_17:72403322-72592804	pancreatic cancer	C25	NA	qPCR, Flow cytometry assay etc.	pancreatic cancer tissues, cell lines (BXPC-3 and CFPAC-1)	up-regulated	Flow cytometry analysis indicated that LINC00673 overexpression resulted in a substantial accumulation of PDAC cells in G0/G1 phase, accompanied by a substantial decrease in the number of cells in S phase. LINC00673 is able to reinforce the interaction of PTPN11 with PRPF19, an E3 ubiquitin ligase, and promote PTPN11 degradation through ubiquitination, which causes diminished SRC-ERK oncogenic signaling and enhanced activation of the STAT1-dependent antitumor response. A G>A change at rs11655237 in exon 4 of LINC00673 creates a target site for miR-1231 binding, which diminishes the effect of LINC00673 in an allele-specific manner and thus confers susceptibility to tumorigenesis.	27213290	2016	Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation.
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	endometrial cancer	NA	M8380/3	qPCR, RNAi, Flow cytometry assay, FISH etc.	endometrial carcinoma tissues	up-regulated	We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 	24589415	2014	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	esophageal squamous cell cancer	NA	NA	qPCR, Western blot, Cell proliferation assay etc.	ESCC tissues	up-regulated	The quantitative real-time RT-PCR results revealed a significant up-regulation of linc-ROR and its variants 2 and 4 in tumor samples of ESCC, compared to their matched non-tumor tissues obtained from the margin of same tumors. Our data also demonstrated a significant up-regulation of variant 4 in high-grade tumor samples, in comparison to the low-grade ones.	27872710	2016	Linc-ROR and its spliced variants 2 and 4 are significantly up-regulated in esophageal squamous cell carcinoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	papillary thyroid cancer	NA	M8260/3	qPCR, ISH etc.	thyroid tumor tissues, cell line (TPC1)	up-regulated	MALAT1 is highly expressed in normal thyroid (NT) tissues and thyroid tumors, with increased expression during progression from NT to papillary thyroid carcinomas (PTCs) but is downregulated in poorly differentiated thyroid cancers (PDCs) and anaplastic thyroid carcinomas (ATCs) compared to NT. Induction of epithelial to mesenchymal transition (EMT) by transforming growth factor (TGF)-beta in a PTC cell line (TPC1) led to increased MALAT1 expression, supporting a role for MALAT1 in EMT in thyroid tumors.	27696303	2017	MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	thyroid cancer	C73.9	NA	qPCR, ISH etc.	thyroid tumor tissues, cell line (TPC1)	down-regulated	MALAT1 is highly expressed in normal thyroid (NT) tissues and thyroid tumors, with increased expression during progression from NT to papillary thyroid carcinomas (PTCs) but is downregulated in poorly differentiated thyroid cancers (PDCs) and anaplastic thyroid carcinomas (ATCs) compared to NT. Induction of epithelial to mesenchymal transition (EMT) by transforming growth factor (TGF)-beta in a PTC cell line (TPC1) led to increased MALAT1 expression, supporting a role for MALAT1 in EMT in thyroid tumors.	27696303	2017	MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR.
MIA-RAB4B	MIA-RAB4B	NA	ENSG00000268975	NA	GRCh38_19:40771648-40796943	colorectal cancer	C19.9	NA	qPCR, Microsatellite instability assay etc.	Peripheral lymphocyte and tissues	down-regulated	Although the expressions of MIA and MIA-RAB4B were consistently down-regulated in the polyps of 421 compared to the matched mucosa, the expressions of these genes were one to five fold up-regulated in the polyps of 344.	28306719	2017	Chromosome 19q13 disruption alters expressions of CYP2A7, MIA and MIA-RAB4B lncRNA and contributes to FAP-like phenotype in APC mutation-negative familial colorectal cancer patients.
MIAT	MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT	440823	ENSG00000225783	NR_003491	GRCh38_22:26646428-26676475	non small cell lung cancer	C34	M8046/3	qPCR	non small cell lung cancer tissues, cell lines (A549 and H1975)	differential expression	C-containing genotypes of MIAT rs1061451 were protective factor of NSCLC, and MIAT, which may act as ceRNA via miR-133a-5p, modulated MYO1B, SGK1 and WNT9A expression level.	29795987	2018	The lncRNA myocardial infarction associated transcript-centric competing endogenous RNA network in non-small-cell lung cancer
NAMA	NAMA	100996569	ENSG00000271086	NR_102270	GRCh38_9:99355337-99377240	papillary thyroid cancer	NA	M8260/3	qPCR, RNAi, RIP, Flow cytometry assay etc.	PTC tissues, cell line (IHH-4)	down-regulated	The expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. 	26323637	2015	BRAF-activated Long Non-coding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor.
ncNRFR	NA	NA	NA	NA	NA	colorectal cancer	C19.9	NA	qPCR, RNAi, Northern blot, in vitro knockdown etc.	colonic epithelial cell tumor tissues	up-regulated	Stable overexpression of ncNRFR in non-transformed, conditionally immortalized mouse colonocytes results in malignant transformation, as determined by growth in soft agar and formation of highly invasive tumors in nude mice. Moreover, ncNRFR appears to inhibit the function of the tumor suppressor let-7. These results suggest precise regulation of ncNRFR is necessary for proper cell growth in the colonic crypt, and its misregulation results in neoplastic transformation.	24045012	2013	Malignant transformation of colonic epithelial cells by a colon-derived long noncoding RNA.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	pancreatic cancer	C25	NA	qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc.	primary PC tissues, cell lines (AsPC-1, BxPC-3, SW1990 and PANC-1)	up-regulated	Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. Besides, our findings indicate that high NEAT1 expression level is closely correlated with tumor progression and poor survival in PC patients. Furthermore, we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers.	27888106	2016	Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	clear cell renal cell carcinoma	C64.9	M8005/0	qPCR, Luciferase assays etc.	clear cell renal cell carcinoma tissues, cell lines (293T, ACHN and HK-2)	up-regulated	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	29156724	2017	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	colorectal cancer	C19.9	NA	microarray, qPCR etc.	cell lines (HT-29, HCT-116 etc.)	up-regulated	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	26990997	2016	Role of cancer stem cells in racial disparity in colorectal cancer.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot, RIP	cell lines (HepG2, Hep3B, Huh-7, HCCLM9, SK-Hep1, and SMMC-7721)	up-regulated	It was determined that plasmacytoma variant translocation 1 was significantly higher, while miR-186-5p was statistically lower in the hepatocellular carcinoma tissues than that in the adjacent normal tissues.	28656879	2017	Long non-coding RNA PVT1 serves as a competing endogenous RNA for miR-186-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	cervical cancer	C53	NA	qPCR, RNAi, Luciferase reporter assay, Cell proliferation assay etc.	cervical cancer tissues, cell lines (HeLa, SiHa, Ect1/E6E7)	up-regulated	PVT1 was up-regulated in cervical cancer tissue and cell lines. After transfecting PVT1 siRNA, the proliferation, migration and invasion of cervical cancer cells were markedly decreased. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay. Finally, miR-424 lower-expression could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines.	28276314	2017	Long Non-Coding RNA PVT1 Facilitates Cervical Cancer Progression Via Negative Regulating of miR-424.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	pancreatic ductal adenocarcinoma	NA	M9380/3	qRT-PCR, Western blot assay, Luciferase reporter assay, RNA pull-down assay, RIP	PDA cell lines (HPAF-II, PANC-1, SW1990, BxPC-3, MIA PaCa-2, Capan-2 and AsPC-1)The immortalized pancreatic ductal epithelial cell line H6C7, The cell line (HEK 293 T), PDA specimens and adjacent non-tumor tissues	up-regulated	PVT1 levels paralleled those of ULK1 protein in PDA cancer tissues. PVT1 promoted cyto-protective autophagy and cell growth by targeting ULK1 both in vitro and in vivo. Moreover, high PVT1 expression was associated with poor prognosis. Furthermore, we found that PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression and the development of pancreatic ductal adenocarcinoma.	30001707	2018	LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	ovarian cancer	C56.9	NA	qPCR, Cell proliferation assay, Flow cytometric assay, Luciferase reporter assay, etc.	Three human OC cell lines (HEY, SKOV-3, OVCAR-3), normal human ovary cell line (IOSE80). OC tissues. 	up-regulated	Taken together, our finding shows that PVT1 may be a novel biomarker for prognosis and a promising therapeutic target for OC.Patients were divided into high PVT1 expression group and low PVT1 expression group on the basis of the median of PVT1 expression levels in OC tissues. Kaplan-Meier survival analysis and log-rank test were used to evaluate the correlation between PVT1 expression levels and overall survival rate of OC patients. *P < 0.05, **P < 0.01.Mechanistically, miR-133a was identified to serve as a direct downstream target of PVT1 in OC. Knockdown of PVT1 inhibited cell proliferation, migration and invasion through negative regulating miR-133a in OC cells.The long non-coding RNA, plasmacytoma variant translocation 1 (PVT1), was reportedly to be highly expressed in a variety of tumors including ovarian cancer (OC). 	29957467	2018	Long non-coding RNA PVT1 promotes cell proliferation and invasion through regulating miR-133a in ovarian cancer.
SIRT1-AS	SIRT1-AS	106633813	NA	NA	NA	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, Northern blot etc.	cell line (HCC-9903)	up-regulated	SIRT1-AS overexpression promoted the proliferation of the human HCC cell lines by upregulating the SIRT1 protein level. The mechanism was that SIRT1-AS bound to SIRT1 mRNA at 3'UTR, masked the miR-29c binding site and stabilized SIRT1 mRNA.	26324025	2015	A novel mutation in SIRT1-AS leading to a decreased risk of HCC
SNHG7	SNHG7, NCRNA00061	84973	ENSG00000233016	NR_003672	GRCh38_9:136721366-136728184	glioblastoma	NA	M9440/3	Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown	Glioblastoma tissue, human GBM cell lines (A172, U87, T98G and SHG44)	up-regulated	the expression of SNHG7 was significantly upregulated in GBM tissues and cell lines compared with non-cancerous brain tissues. Furthermore,SNHG7 knockdown remarkably suppressed the proliferation, migration and invasion of A172 and U87-cells while inducing their apoptosis. Subsequently, SNHG7 knockdown significantly inhibited tumor growth and metastasis in-vivo by using xenograft experiments in nude mice.SNHG7 directly inhibited miR-5095,which targeted the 3'UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/B-catenin signaling pathway in GBM. Using rescue experiments, we demonstrated that SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095 and concomitant activation of Wnt/B-catenin signaling pathway.	29360452	2018	Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095.
TDRG1	TDRG1, LINC00532	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	qPCR, Cell proliferation assay etc.	ESCC tissues, cell lines (TE1, TE13, T.Tn, Yes-2, and Eca109)	up-regulated	The expression level of lincRNA-NR_024015 in ESCC tumor tissues was significantly higher than that in corresponding normal tissues and rs8506 genotype has a genotype-specific effect on lincRNA-NR_024015 expression. Furthermore, rs8506 G to A variant might influence lincRNA-NR_024015 expression and function by disrupting the binding of hsa-miR-526b to the site. High expression level of lincRNA-NR_024015 and rs8506 A allele were associated with poor ESCC patients' survival.	27583835	2016	A genetic polymorphism at miR-526b binding-site in the lincRNA-NR_024015 exon confers risk of esophageal squamous cell carcinoma in a population of North China.
ADARB2-AS1	NA	642394	ENSG00000205696	NR_033387	GRCh38_10:1526637-1556984	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification. PVT1 has been shown to be upregulated in PDAC tissues, to be correlated with clinical stage and poor survival, to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR,etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	neurofibromatosis type 1	NA	M9540/1	microarray, qPCR etc.	blood	up-regulated	Single-nucleotide polymorphism rs2151280 (located in ANRIL) was statistically significantly associated with the number of PNFs in NF1 patients. In addition, allele T of rs2151280 was statistically significantly associated with reduced ANRIL transcript levels, suggesting that modulation of ANRIL expression mediates PNF susceptibility. Identification of ANRIL as a modifier gene in NF1 may offer clues to the molecular pathogenesis of PNFs, particularly neurofibroma formation, and emphasizes the unanticipated role of large noncoding RNA in activation of critical regulators of tumor development.	22034633	2011	Role of noncoding RNA ANRIL in genesis of plexiform neurofibromas in neurofibromatosis type 1.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	acute lymphoblastic leukemia	NA	M9835/3	MassARRAY assay etc.	acute lymphoblastic leukemia tissues	differential expression	Rs564398 (A>G), mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype, with a risk pattern that was compatible with an overdominant model of disease susceptibility. We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.	21414664	2011	A polymorphism in the chromosome 9p21 ANRIL locus is associated to Philadelphia positive acute lymphoblastic leukemia.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	glioma	NA	M9380/3	qPCR etc.	glioma tissues	differential expression	Risk SNPs (rs3217992, A>G; rs1063192, C>T) for coronary disease, stroke, diabetes, melanoma, and glioma were all associated with allelic expression of ANRIL. Our data show that multiple independent sites in the chromosome 9p21 region influence CDKN2A, CDKN2B and ANRIL expression. SNPs associated with disease in GWA studies are all associated with ANRIL expression, indicating that modulation of ANRIL expression mediates susceptibility to a variety of conditions.	20386740	2010	Chromosome 9p21 SNPs Associated with Multiple Disease Phenotypes Correlate with ANRIL Expression.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	melanoma	NA	M8720/3	qPCR etc.	melanoma tissues	differential expression	Risk SNPs (rs3217992, A>G; rs1063192, C>T) for coronary disease, stroke, diabetes, melanoma, and glioma were all associated with allelic expression of ANRIL. Our data show that multiple independent sites in the chromosome 9p21 region influence CDKN2A, CDKN2B and ANRIL expression. SNPs associated with disease in GWA studies are all associated with ANRIL expression, indicating that modulation of ANRIL expression mediates susceptibility to a variety of conditions.	20386740	2010	Chromosome 9p21 SNPs Associated with Multiple Disease Phenotypes Correlate with ANRIL Expression.
AOC4P	AOC4P, AOC4, UPAT	90586	ENSG00000260105	NA	GRCh38_17:42865922-42874369	non small cell lung cancer	C18	NA	qRT-PCR, Western blot assay, luciferase reporter assay	The human lung epithelial cell line (BEAS-2B) and NSCLC cell lines(H1299, H1650, H358 and A549), tumor tissues and matched normal tissues	up-regulated	lncRNA UPAT expression was upregulated in NSCLC tissues and significantly associated with tumor size and Tumor-Node-Metastasis stage. Furthermore, UPAT promoted NSCLC cell proliferation, partly via increasing UHRF1 expression and consequently epigenetically silencing RASSF1 and CDH13 transcription. In addition, the knockdown of UHRF1 partially decreased the promotion of cell growth and G1-S phase transition caused by UPAT overexpression.	30008828	2018	Long noncoding RNA UPAT promoted cell proliferation via increasing UHRF1 expression in non-small cell lung cancer.
BC200	BCYRN1, BC200, BC200a, LINC00004, NCRNA00004	618	ENSG00000236824	NR_001568	GRCh38_2:47335315-47335514	breast cancer	C50	NA	qPCR, ChIP etc.	cell lines (MCF-7, T47D, MDA-MB-231)	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.
CAI2	NA	NA	NA	NA	NA	neuroblastoma	NA	M9500/3	qPCR etc.	neuroblastoma tissues, cell line (NMB7)	up-regulated	Concordant expression of CAI2 with p16 and ARF in normal tissue along with the ability of CAI2 to induce p16 expression suggested that CAI2 may regulate p16 and/or ARF. In neuroblastoma cells transformed by serial passage in vitro, leading to more rapid proliferation, CAI2, p16, and ARF expression all increased dramatically. Consistent with its association with high-risk disease, CAI2 expression was also significantly associated with poor clinical outcomes, although this effect was reduced when adjusted for MYCN amplification.	25028366	2014	High expression of CAI2, a 9p21-embedded long noncoding RNA, contributes to advanced-stage neuroblastoma.
CCAT1	CCAT1, CARLo-5, onco-lncRNA-40	100507056	ENSG00000247844	NR_108049	GRCh38_8:127207382-127219268	endometrial cancer	NA	M8380/3	qPCR etc.	EC tissues	up-regulated	CARLo-5 expression was significantly higher in EC tissues than in NETs and significantly associated with FIGO stage and lymph node metastasis. Patients with high CARLo-5 expression had significantly shorter overall survival than those with low CARLo-5 expression. The rs6983267 genotype was significantly correlated with CARLo-5 expression.	27432114	2016	The rs6983267 SNP and long non-coding RNA CARLo-5 are associated with endometrial carcinoma.
CCAT1	CCAT1, CARLo-5, onco-lncRNA-40	100507056	ENSG00000247844	NR_108049	GRCh38_8:127207382-127219268	colorectal cancer	C19.9	NA	qPCR, RNAi etc.	primary prostate cancer tissues	up-regulated	CARLo-5 is highly expressed in CRC-derived cell lines compared with normal colon-derived fibroblasts and CRC primary tissues compared with their matched normal adjacent tissues (NATs). In addition, CARLo-5 is highly expressed in prostate cancer (PC) tissues compared with their NATs. CARLo-5 is significantly correlated with the rs6983267 allele associated with increased cancer susceptibility. We also found the MYC enhancer region physically interacts with the active regulatory region of the CARLo-5 promoter, suggesting long-range interaction of MYC enhancer with the CARLo-5 promoter regulates CARLo-5 expression.	24594601	2014	Long-range interaction and correlation between MYC enhancer and oncogenic long noncoding RNA CARLo-5.
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	colon cancer	C18	NA	qPCR etc.	colon tumor tissues	down-regulated	Here, we show that the long ncRNA CCAT2, located at the 8q24 amplicon on cancer risk-associated rs6983267 SNP, regulates cancer metabolism in vitro and in vivo in an allele-specific manner by binding the Cleavage Factor I (CFIm) complex with distinct affinities for the two subunits (CFIm25 and CFIm68).Moreover, when we assessed the proliferation of HCT116 control and CCAT2-overexpressing cells treated with the GLS inhibitor 968, we found that cells overexpressing CCAT2 were more sensitive to GLS (GAC in this case) inhibition, implying that cells with high CCAT2 expression are dependent on GAC for survival.	28934601	2016	Allele-Specific Reprogramming of Cancer Metabolism by the Long Non-coding RNA CCAT2
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	gastric cancer	C16	NA	qPCR, Western blot etc.	cell lines (BGC-823)	up-regulated	CCAT2 was able to positively regulate the expression of POU5F1B gene. Furthermore, silencing of CCAT2 gene inhibited the proliferation of BGC-823 cells, as well as induced apoptosis and autophagy in BGC-823 cells, by suppression of the PI3K/mTOR signaling pathways.Recent studies confirmed that the lncRNA CCAT2, located at the 8q24 amplicon of the cancer risk-associated rs6983267 SNP, regulated the cancer metabolism in vitro and in vivo by directly interacting in an allele-specific manner with a protein complex. The chromosomal region 8q24 emerged as an important region for genetic susceptibility in various cancer types, thus DNA methylation or SNPs at this locus may contribute to cancer risk. RT-qPCR results revealed that CCAT2 gene expression was effectively suppressed by the transfection, while POU domain class 5 transcription factor 1B (POU5F1B) gene expression was significantly decreased. 	29435046	2017	Effect of silencing colon cancer-associated transcript 2 on the proliferation,apoptosis and autophagy of gastric cancer BGC-823 cells.
CRNDE	CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5	NA	ENSG00000245694	NA	GRCh38_16:54845189-54929189	ovarian cancer	C56.9	NA	microarray, qPCR etc.	ovarian cancer tissues	up-regulated	We have shown that the elevated level of CRNDE transcripts significantly increases the risk of death and recurrence in ovarian cancer patients. Elevated levels of two different CRNDE transcripts were a negative prognostic factor; they increased the risk of death and recurrence in the group of patients treated with TP, but not PC (DNA-damaging agents only).	26556866	2015	The putative oncogene, CRNDE, is a negative prognostic factor in ovarian cancer patients.
CRNDE	CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5	NA	ENSG00000245694	NA	GRCh38_16:54845189-54929189	colorectal cancer	C19.9	NA	qPCR etc.	CRC tissues	up-regulated	We have presented expression microarray data showing that an increase in CRNDE expression is an early event in colorectal neoplasia, its transcription being elevated in >90% of colorectal adenomas and adenocarcinomas.	22393467	2011	Colorectal Neoplasia Differentially Expressed (CRNDE), a Novel Gene with Elevated Expression in Colorectal Adenomas and Adenocarcinomas.
CRNDE	CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5	NA	ENSG00000245694	NA	GRCh38_16:54845189-54929189	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Luciferase reporter assay etc.	hepatocellular carcinoma tissues, cell line(QSG-7701)	up-regulated	CRNDE is more commonly up-regulated in HCC malignant tissues and associated with poor clinical outcomes. Furthermore, both loss- and gain-functions assays revealed that CRNDE promotes HCC cell proliferation and growth in vitro and in vivo. In addition, we found that CRNDE regulates PI3K/Akt/GSK3B-Wnt/B-catenin axis to exert its oncogenic role in HCC cell proliferation and growth. The full length T1 and another variant T3, especially T1, were significantly elevated in HCC malignant tissues as compared with variant T2 and T4. 	29864897	2018	Long non-coding RNA CRNDE promotes heptaocellular carcinoma cell proliferation by regulating PI3K/Akt /β-catenin signaling.
CTBP1-AS	CTBP1-AS, PCAT10	285463	ENSG00000280927	NR_104331	GRCh38_4:1210120-1218591	prostate cancer	C61.9	NA	qPCR, Western blot, Northern blot, RIP etc.	prostate cancer tissues, cell lines (VCaP, LNCaP, DU145, RWPE etc.)	up-regulated	CTBP1-AS is predominantly localized in the nucleus and its expression is generally upregulated in prostate cancer. CTBP1-AS promotes both hormone-dependent and castration-resistant tumour growth. Mechanistically, CTBP1-AS directly represses CTBP1 expression by recruiting the RNA-binding transcriptional repressor PSF together with histone deacetylases. CTBP1-AS also exhibits global androgen-dependent functions by inhibiting tumour-suppressor genes via the PSF-dependent mechanism thus promoting cell cycle progression.	23644382	2013	Androgen-responsive long noncoding RNA CTBP1-AS promotes prostate cancer.
DJ974N19.1	NA	NA	NA	NA	NA	colorectal cancer	C19.9	NA	qPCR, STS-PCR, ISH etc.	primary CRC tissues, cell lines (Co1o205, Co1o320 HSR, Co1o678, Co1o741, HCA7, HCA46, HRA19, LS1034 etc.)	down-regulated	Two noncoding RNA genes located in the region, BA318C17.1 and DJ974N19.1, were investigated by mutation analysis and real-time PCR in colorectal cancer cell lines. Sequence changes in BA318C17.1 and reduced expression of both genes was detected, suggesting that the abrogation of these genes may play a role in colorectal tumorigenesis.	16110499	2005	Deletion at chromosome band 20p12.1 in colorectal cancer revealed by high resolution array comparative genomic hybridization.
DLEU2	DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6	8847	ENSG00000231607	NR_002612	GRCh38_13:49982552-50125720	chronic lymphocytic leukemia	NA	M9823/3	microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc.	blood	up-regulated	In contrast, the lncRNA genes DLEU1 and variant DLEU2/Alt1 that display DNA-hypomethylation at their 5' ends are significantly upregulated in CLL cells. We found a significant inverse correlation of gene expression of the lncRNA genes DLEU1 and the DLEU2 variant Alt1 with DNA-methylation levels in regions D6 and E6 that are localized at their transcriptional start sites.	23593011	2013	Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the In Cis downregulation of a gene cluster that targets NF-kB.
DRAIC	DRAIC	145837	ENSG00000245750	NR_026979	GRCh38_15:69463026-69843120	prostate cancer	C61.9	NA	qPCR, Western blot etc.	cell lines (VCap, PC3M-luc, LNCaP etc.)	down-regulated	This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAIC and PCAT29, that are prognostic for a wide variety of cancer types.This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAICand PCAT29, that are prognostic for a wide variety of cancer types. 	25700553	2015	The lncRNA DRAIC/PCAT29 locus constitutes a tumor suppressive nexus.
EGFR-AS1	NA	100507500	ENSG00000224057	NR_047551	GRCh38_7:55179750-55188934	squamous cell carcinoma	NA	M8070/3	qPCR etc.	cell lines (NCC-NH1, NCC-NH43, NCC-NH73, NCC-NH26, NCC-NH64, NCC-NH119)	up-regulated	Remarkably, single-copy G>A nucleotide editing in isogenic models conferred a 70-fold increase in sensitivity due to decreased stability of the EGFR-AS1 long noncoding RNA (lncRNA). In the appropriate context, sensitivity could be recapitulated through EGFR-AS1 knockdown in vitro and in vivo, whereas overexpression was sufficient to induce resistance to TKIs. Reduced EGFR-AS1 levels shifted splicing toward EGFR isoform D, leading to ligand-mediated pathway activation. In co-clinical trials involving patients and patient-derived xenograft (PDX) models, tumor shrinkage was most pronounced in the context of the A/A genotype for EGFR-Q787Q, low expression of EGFR-AS1 and high expression of EGFR isoform D. Our study reveals how a ‘silent’ mutation influences the levels of a lncRNA, resulting in noncanonical EGFR addiction, and delineates a new predictive biomarker suite for response to EGFR TKIs.	28920960	2017	Long noncoding RNA EGFR-AS1 mediates epidermal growth factor receptor addiction and modulates treatment response in squamous cell carcinoma
ENST00000457390	RP11-14N7.2, LOC100996732	NA	NA	NA	GRCh38_1:144245027-144245821	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000476909	LINC00856	NA	NA	NA	GRCh38_10:78267410-78280213	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000502076	NA	NA	NA	NA	NA	colorectal cancer	C19.9	NA	microarray, qPCR etc.	CRC tissues	up-regulated	To verify the microarray results, we randomly selected 4 upregulated lncRNAs and 3 downregulated lncRNAs from the differentially expressed lncRNAs in the microarray. qRT-PCR method was used to confirm the expression levels of the selected lncRNAs in the CRC tissues and paired adjacent normal tissues used in the microarray test. Despite the fact that the fold change of each selected lncRNA in the qRT-PCR test was not in full accord with the microarray data, the variation tendency of each lncRNA was consistent with the result of the micro-array.	26847923	2016	Expression profile of long non-coding RNAs in colorectal cancer: A microarray analysis.
ENST00000552364	KRT73-AS1	NA	ENSG00000257495	NA	GRCh38_12:52609851-52615305	colorectal cancer	C19.9	NA	microarray, qPCR etc.	CRC tissues	down-regulated	To verify the microarray results, we randomly selected 4 upregulated lncRNAs and 3 downregulated lncRNAs from the differentially expressed lncRNAs in the microarray. qRT-PCR method was used to confirm the expression levels of the selected lncRNAs in the CRC tissues and paired adjacent normal tissues used in the microarray test. Despite the fact that the fold change of each selected lncRNA in the qRT-PCR test was not in full accord with the microarray data, the variation tendency of each lncRNA was consistent with the result of the micro-array.	26847923	2016	Expression profile of long non-coding RNAs in colorectal cancer: A microarray analysis.
ENST00000553559	SNHG10, C14orf62, LINC00063, NCRNA00063	283596	ENSG00000247092	NR_001459	GRCh38_14:95532914-95534872	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000565617	KB-1460A1.5	NA	NA	NA	GRCh38_8:101166805-101169629	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000568031	RP11-863P13.3	NA	NA	NA	GRCh38_16:88177298-88178610	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000576810	RP11-462G12.1, LOC102724927	NA	NA	NA	GRCh38_16:3947609-3950444	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
EZR-AS1	NA	101409257	ENSG00000233893	NR_102425	GRCh38_6:158818011-158820593	esophageal squamous cell cancer	NA	NA	RNA-seq, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	esophageal squamous cell carcinoma (ESCC) tissues and cell lines (KYSE150 and KYSE510)	up-regulated	Both in vivo and in vitro studies revealed that EZR-AS1 promoted cell migration through up-regulation of EZR expression. Mechanistically, antisense lncRNA EZR-AS1 formed a complex with RNA polymerase II to activate the transcription of EZR. Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Finally, the interaction of EZR-AS1 with SMYD3 further enhanced EZR transcription and expression. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.EZR-AS1 regulates EZR transcriptional activity in ESCC cells by interacting with RNA polymerase II, but not by affecting the binding of SP1 and AP-1 transcription factors. the overexpression of EZR-AS1 accompanied the enhanced expression of EZR (variant 1), both at the mRNA and protein levels, in KYSE150 cells (Figure 1H and I). 	29253179	2018	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.
FAM83H-AS1	FAM83H-AS1, onco-lncRNA-3	100128338	NA	NR_033849	NA	pancreatic ductal adenocarcinoma	C25.3	M8500/3	RNA-seq, qrT-PCR, Western blot	cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1)	up-regulated	We identified lncRNAs in genomic regions with SCNA and single nucleotide polymorphisms associated with lifetime risk of PDA and associated with clinical outcome using genomic and clinical data in PDA. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4). We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA	29440233	2018	Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma.
FAM99A	FAM99A	387742	ENSG00000205866	NR_026643	GRCh38_11:1665597-1667856	hepatocellular carcinoma	C22.0	M8170/3	RNA-seq, qPCR etc.	HCC tissues	down-regulated	We found that LINC01093, FAM99A and CRNDE were differentially expressed in HCC compared with cirrhotic tissues, confirming the data we obtained in the RNA-Seq experiment. Moreover, we found that LINC01093 and FAM99A were already significantly downregulated in cirrhotic tissues compared with normal livers.	26887054	2016	Identification of novel long non-coding RNAs deregulated in hepatocellular carcinoma using RNA-sequencing.
FGFR3-AS1	NA	NA	NA	NA	NA	bladder cancer	C67	NA	RT-qPCR, Western blot, in vitro knockdown	bladder cancer tissues, cell lines (T24, 5637, UM-UC-3, SW-780 and SV-HUC-1)	up-regulated	Both FGFR3-AS1 and FGFR3 were overexpressed in bladder cancer tissues compared to matched normal tissues. They were also positively expressed in bladder cancer. FGFR3-AS1 expression levels were higher in high grade tumors than those in low grade tumors. FGFR3-AS1 expression levels were higher in invasive tumors than those in non-invasive tumors. Cell proliferation inhibition, increased apoptosis, and decreased motility were observed in FGFR3-AS1 siRNA-transfected T24 and 5637 cell lines.Genomic alterations of FGFR3, such as translocations and activating mutations, have been found in advanced and metastatic urothelialcarcinoma.	29226855	2018	Knockdown of long noncoding RNA FGFR3- AS1 induces cell proliferation inhibition, apoptosis and motility reduction in bladder cancer.
FOXC2-AS1	FOXC2-AS1, ODRUL	103752587	ENSG00000260944	NR_125795	GRCh38_16:86565145-86567761	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
FR0257520	NA	NA	NA	NA	NA	prostate cancer	C61.9	NA	RNA-seq, qPCR etc.	prostate cancer tissues	down-regulated	Consistent with the RNA-seq results, PCA3, FR0348383 and MALAT1 overexpression was found in 80% (32/40), 72.5% (29/40), and 82.5% (33/40) of the prostate cancers respectively, whereas decreased FR0257520 expression was found in 82.5% (33/40) of the prostate cancers.	22349460	2012	RNA-seq analysis of prostate cancer in the Chinese population identifies recurrent gene fusions, cancer-associated long noncoding RNAs and aberrant alternative splicings.
FR0348383	NA	NA	NA	NA	NA	prostate cancer	C61.9	NA	RNA-seq, qPCR etc.	prostate cancer tissues	up-regulated	Consistent with the RNA-seq results, PCA3, FR0348383 and MALAT1 overexpression was found in 80% (32/40), 72.5% (29/40), and 82.5% (33/40) of the prostate cancers respectively, whereas decreased FR0257520 expression was found in 82.5% (33/40) of the prostate cancers.	22349460	2012	RNA-seq analysis of prostate cancer in the Chinese population identifies recurrent gene fusions, cancer-associated long noncoding RNAs and aberrant alternative splicings.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	neuroblastoma	NA	M9500/3	RNA-seq, qPCR, RNAi, Western blot, RNA-FISH, Cell proliferation assay etc.	cell lines (LA-N-6, SK-N-Be(1), SK-N-FI, SMS-KAN etc.)	up-regulated	GAS5 in neuroblastoma has revealed robust expression in both MYCN-amplified and non-amplified cell lines. Knockdown of GAS5 In vitro resulted in defects in cell proliferation, apoptosis, and induced cell cycle arrest. Further analysis of GAS5 clones revealed multiple novel splice variants, two of which inversely modulated with MYCN status. Complementation studies of the variants post-knockdown of GAS5 indicated alternate phenotypes, with one variant (FL) considerably enhancing cell proliferation by rescuing cell cycle arrest and the other (C2) driving apoptosis, suggesting a unique role for each in neuroblastoma cancer physiology.	28035057	2017	The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	myeloid leukemia	NA	M9860/3	qPCR, luciferase reporter assay etc.	cell line (PBMCs)	up-regulated	Meanwhile, GAS5 is downregulated in breast cancer cells.Survival analysis indicated that GAS5 rs55829688 (T > C) was significantly associated with prognosis of AML (p=0.018).Patients with rs55829688 CC genotype showed higher GAS5 expression in peripheral blood mononuclear cells (PBMCs) (p=0.025) and harbored a longer platelets recovery (p=0.040) than carriers of rs55829688T allele. In conclusion, rs55829688 polymorphism could increase GAS5 expression by interacting with TP63, which might aggravate the myelosuppression and in turn lead to poor prognosis in AML. GAS5 is observed to be a key mediator of glucocorticoids (GCs) resistance rather than a growth arrest-specific transcript in PBMCs.	27951730	2017	Long non-coding RNA GAS5 polymorphism predicts a poor prognosis of acute myeloid leukemia in Chinese patients via affecting hematopoietic reconstitution.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	nasopharyngeal cancer	C11	NA	DNA Extraction and genotyping, SNPs selections etc.	NPC tissues	differential expression	the potential role of lncRNA GAS5 polymorphisms rs2067079 and rs6790 as predictive biomarkers for chemoradiotherapy induced toxic reactions in NPC patients.This decrement was significantly correlated with poor survival in HCC patients.	28977945	2017	Genetic polymorphisms of long non-coding RNA GAS5 predict platinum-based concurrent chemoradiotherapy response in nasopharyngeal carcinoma patients.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	lung cancer	C34	NA	qPCR etc.	lung cancer tissues 	differential expression	In current study, we investigated the possible association between susceptibility of lung cancer and GAS5 rs145204276, which showed contradictory roles in carcinogenesis of colorectal cancer and hepatocellular carcinoma. Taken together, our findings provided strong evidence for the hypothesis that GAS5 rs145204276 were significantly associated with the susceptibility of lung cancer, and GAS5 functions as a tumor suppressor in carcinogenesis of lung cancer. In summary, we demonstrated that SNP rs145204276 of GAS5 was associated with decreased risk of lung cancer in the Chinese populations. These findings should be verified by larger, well-designed epidemiologic and functional studies.	29207621	2017	Genetic variation of lncRNA GAS5 contributes to the development of lung cancer.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	malignant pleural mesothelioma	NA	M9050/3	qPCR, RNAi etc.	MPM tissues, cell lines (SPC111, SPC212, ZL34, ZL55)	down-regulated	GAS5 expression was lower in MPM cell lines compared to normal mesothelial cells. GAS5 was upregulated upon growth arrest induced by inhibition of Hedgehog and PI3K/mTOR signalling in in vitro MPM models. The increase in GAS5 lncRNA was accompanied by increased promoter activity. Silencing of GAS5 increased the expression of glucocorticoid responsive genes glucocorticoid inducible leucine-zipper and serum/glucocorticoid-regulated kinase-1 and shortened the length of the cell cycle. Drug induced growth arrest was associated with GAS5 accumulation in the nuclei. GAS5 was abundant in tumoral quiescent cells and it was correlated to podoplanin expression.	24885398	2014	GAS5 long non-coding RNA in malignant pleural mesothelioma.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	gastric cancer	C16	NA	qPCR etc.	GC tissues	differential expression	Genotype del/del was significantly associated with a higher survival rate. Patients with late tumor stage were found to have a significantly lower  rate of genotype del/del than those with an early tumor stage . Patients with UICC III and IV were found to have a significantly lower rate of genotype del/del than those with UICC I and II. The variant rs145204276 of GAS5 is associated with the development and prognosis of GC.The allele del of rs145204276 is associated with a remarkably lower incidence of cancer progression and metastasis. Methylation percentage of the 7th CpG site significantly correlated with GAS5 expression in the tumor tissues  	29557411	2018	The Variant rs145204276 of GAS5 is Associated with the Development and Prognosis  of Gastric Cancer.  
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	colorectal cancer	C19.9	NA	qPCR etc.	HCC tissues	down-regulated	Among all the pairs of CRC patients, the expression levels of lncRNA GAS5 in CRC tissues were significantly lower than those in the corresponding normal tissues. We found the allele del of rs145204276 was significantly associated with 21% decreased risk of CRC. Compared with the genotype ins/ins, both the genotype ins/del and del/del showed decreased susceptibility.	27863421	2016	LncRNA GAS5 contributes to lymphatic metastasis in colorectal cancer.
GLIS3-AS1	NA	84850	ENSG00000237009	NR_026663	GRCh38_9:3898642-3901248	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
GNG12-AS1	GNG12-AS1	100289178	ENSG00000232284	NR_040077	GRCh38_1:67832303-68202987	breast cancer	C50	NA	qPCR, RNAi, ChIP etc.	cell lines (HB2, SUM159, MCF7, K562, Hs27, CAL51, MCF10A 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.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	bladder cancer	C67	NA	qPCR etc.	blood	differential expression	A significantly decreased risk of bladder cancer was found for the rs2839698 TC genotype, but not for CC homozygotes. The rs2839698 TC genotype was especially associated with a reduced risk of developing non-muscle-invasive disease. Borderline significantly decreased risks of bladder cancer were found for the rs2107425 CT genotype, but not for TT homozygotes or for T allele carriers of rs217727. Haplotype analysis did not result in stronger associations with bladder cancer compared with the single-locus analyses. An SNP polymorphism in the nonprotein-encoding H19 gene is associated with a decreased risk of developing nonmuscleinvasive bladder cancer. This association was found for only heterozygotes, not for homozygotes.	18262338	2008	Polymorphisms in the H19 gene and the risk of bladder cancer.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	gastric adenocarcinoma	C16	M8140/3	other	gastric adenocarcinoma tissues	up-regulated	The rs2839698 SNP of H19 may have potential as a novel prognostic factor for survival in T3 gastric adenocarcinoma after surgery alone; these finding have special relevance to patients who are not suitable for postoperative chemotherapy.	29479897	2018	The rs2839698 Single Nucleotide Polymorphism of lncRNA H19 is Associated with Post-Operative Prognosis in T3 Gastric Adenocarcinoma.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	acute myeloid leukemia	NA	M9861/3	qPCR etc.	acute myeloid leukemia tissues, cell lines (HL60 and K562)	up-regulated	H19 expression was significantly increased in AML patients but not associated with embedded miR-675 expression. Moreover, H19 overexpression was not dependent on the methylation pattern in H19 differentially methylated region/imprinting control region. Strong association was observed between H19 overexpression and patients' characteristics including sex, higher white blood cells, older age, and intermediate karyotype, FLT3-ITD, and DNMT3A mutations. In addition, H19 overexpression correlated with lower complete remission (CR) rate and shorter overall survival, and further confirmed by multivariate analyses. Importantly, the prognostic effect of H19 expression was validated by TCGA and GEO data. In the follow-up of patients, H19 expression in CR phase was lower than diagnosis time and returned at relapse time. 	29643943	2018	H19 overexpression promotes leukemogenesis and predicts unfavorable prognosis in  acute myeloid leukemia.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	glioma	NA	M9380/3	qPCR, RNAi, Western blot etc.	glioma tissues, cell lines (U87, U251)	up-regulated	Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas. Importantly, expression of H19 variant 1 was significantly higher in TMZ-resistant tumor tissues than in TMZ-sensitive tumor tissues.	27366087	2016	Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	breast cancer	C50	NA	qPCR etc.	breast cancer tissues	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.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	breast cancer	C50	NA	qPCR etc.	BC patients tissues	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 1.01–1.71), 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.
HAR1A	NA	NA	ENSG00000225978	NA	NA	diffuse glioma	NA	M8145/3	qPCR	breast and ovarian cancer cell lines, glioma tissue	down-regulated	These results implied that these four lncRNAs might play important role in diffuse gliomas progression, particularly, PVT1 and HAR1A could be explored as promising biomarkers for diagnosis, prognosis and target therapy of diffuse gliomas.Kaplan-Meier survival curve and Cox regression analyses showed that glioma patients with high PVT1 expression or low HAR1A expression had poor survival outcome, aberrantly expressed PVT1 and HAR1A could be the independent prognosis biomarkers for glioma patients. LncRNA CYTOR was up-regulated in HCC tissues, circulating CYTOR were also highly expressed in plasma samples of HCC patients, and could serve as potential biomarker for diagnosis of HHC. 	29108264	2017	lncRNAs PVT1 and HAR1A are prognosis biomarkers and indicate therapy outcome for diffuse glioma patients.
HNF1A-AS1	HNF1A-AS1, C12orf27, NCRNA00262	283460	ENSG00000241388	NR_024345	GRCh38_12:120941728-120980965	hepatocellular carcinoma	C22.0	M8170/3	Microarray, RT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	human HCC cell lines (Huh-7, MHCC-97 L, MHCC-97H, MHCC-LM3, SMMC-7721 and YY-8103 ), 	down-regulated	HNF1a activated the transcription of HNF1A-AS1 by directly binding to its promoter region. HNF1A-AS1 inhibited the growth and the metastasis of HCC cells in vitro and in vivo. Moreover, knockdown of HNF1A-AS1 reversed the suppressive effects of HNF1a on the migration and invasion of HCC cells. Importantly, HNF1A-AS1 directly bound to the C-terminal of SHP-1 with a high binding affinity (KD=59.57±14.29nM) and increased the phosphatase activity of SHP-1. Inhibition of SHP-1 enzymatic activity substantially reversed the HNF1a- or HNF1A-AS1-induced reduction on the metastatic property of HCC cells.	29466992	2018	The HNF1a-regulated lncRNA HNF1A-AS1 reverses the malignancy of hepatocellular carcinoma by enhancing the phosphatase activity of SHP-1.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	osteosarcoma	NA	M9180/3	qPCR etc.	blood	up-regulated	The expression level of HOTAIR in OS tissues was significantly higher than that in corresponding normal tissues. Subjects with the rs7958904 CC genotype had significantly lower HOTAIR RNA levels than those with the GG genotypes in normal and OS tissues.	26967389	2016	Genetic variants of lncRNA HOTAIR contribute to the risk of osteosarcoma.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	epithelial ovarian cancer	C56.9	NA	qPCR, Genotyping etc.	blood	differential expression	we hypothesized that abnormal expression of HOTAIR and common variants of HOTAIR are associated with risk of Epithelial ovarian cancer (EOC). We first evaluated the HOTAIR levels in 100 paired tissues of EOC patients and corresponding normal tissues. Results showed that the expression level of HOTAIR in EOC tissues was significantly higher than that in corresponding normal tissues. Then the genotyping analyses of HOTAIR gene was conducted in a Chinese population. The results indicated that rs4759314 and rs7958904 were significantly associated with EOC susceptibility. For rs4759314, the difference between the G allele (as the reference) and the A allele was statistically significant. For rs7958904, C allele was associated a significantly decreased EOC risk when compared with G allele. 	27166268	2016	Genetic variants of lncRNA HOTAIR and risk of epithelial ovarian cancer among Chinese women
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	gastric cardia adenocarcinoma	C16.0	M8140/3	qPCR, RFLP-PCR etc.	blood	up-regulated	Among three htSNPs of the HOTAIR gene (rs12826786 C>T, rs4759314 A>G, and rs10783618 C>T), only the T allele of rs12826786 was found to increase the risk of developing GCA and was associated with smoking habit and tumor-node-metastasis (TNM) stage. In addition, higher expression levels of HOTAIR were found in tumor tissues and rs12826786 SNP has a genotype-specific effetc on HOTAIR expression. A high HOTAIR expression level was associated with poor GCA patients' survival.	25476857	2014	Associations between polymorphisms of HOTAIR and risk of gastric cardia adenocarcinoma in a population of north China.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	colon cancer	C18	NA	qPCR, Western blot, Luciferase reporter assay etc.	cell lines (CCL228, HeLa, MCF7, SH-SY5Y) 	up-regulated	Along with HIF1a, histone methylases MLL1 and histone acetylase p300 are enriched at the HOTAIR promoter under hypoxia. The levels of H3K4-trimethylation and histone acetylation are also enriched at the HOTAIR promoter. Furthermore, knockdown of MLL1 downregulated the hypoxia-induced HOTAIR expression, indicating key roles of MLL1 in hypoxia-induced HOTAIR expression. HIFs are transcription factors and regulate the expression of a variety of target genes under hypoxia and that contribute to the tumor growth and metastasis.Misregulation and mutations in lncRNAs are widely associated with a variety of human diseases.	28756022	2017	Histone methylase MLL1 coordinates with HIF and regulate lncRNA HOTAIR expression under hypoxia.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	papillary thyroid cancer	NA	M8260/3	qPCR, RNAi, Cell proliferation assay etc.	PTC tissues, cell line (HEK293)	up-regulated	By detecting HOTAIR RNA expression in sixty paired PTC and normal tissues, we found higher expression of HOTAIR in PTC tissues compared to normal tissues. In BCPAP or HEK293 cells, ectopic expression of lncRNA HOTAIR significantly promoted cell proliferation. On the contrary, depletion of endogenous HOTAIR expression significantly suppresses PTC cell proliferation.	27549736	2016	Onco-lncRNA HOTAIR and its functional genetic variants in papillary thyroid carcinoma.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	glioma	NA	M9380/3	qPCR etc.	glioma tissues	up-regulated	In contrast, glioma subjects with the rs12826786 CT genotype had significantly higher tumor HOTAIR RNA levels than those with the TT genotype	28083786	2017	Effects of the functional HOTAIR rs920778 and rs12826786 genetic variants in glioma susceptibility and patient prognosis.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	colorectal cancer	C19.9	NA	qPCR, RNAi etc.	CRC tissues	up-regulated	Our study showed that genetic variants in HOTAIR were associated with risk of colorectal cancer and rs7958904 may act as a potential biomarker for predicting the risk of colorectal cancer.	25432874	2014	Genetic variants in lncRNA HOTAIR are associated with risk of colorectal cancer.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	hepatocellular carcinoma	C22.0	M8170/3	qPCR	hepatocellular carcinoma tissues	differential expression	Significant associations were observed between the HOTAIR rs920778 C>T polymorphism and HCC risk (TT versus CC: OR = 1.634, 95% CI =1.028-2.598, P = 0.046) and the allelic model (allele T versus allele C: OR =1.293, 95% CI = 1.060-1.577, P = 0.011).	29141248	2017	Association of Functional Genetic Variants of HOTAIR with Hepatocellular Carcinoma (HCC) Susceptibility in a Chinese Population
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	gastric cancer	C16	NA	qPCR, Dual-luciferase reporter assay etc.	gastric cancer tissues	up-regulated	MGC803 cells with the rs920778TT genotype show significantly higher endogenous HOTAIR expression compared to AGS cells with the TC genotype. During inspecting functional relevance of the rs920778 SNP, we observed an allelic regulation of rs920778 on HOTAIR expression in both gastric cancer cell lines and tissue samples, with higher HOTAIR expression among T allele carriers.	25640751	2016	A functional lncRNA HOTAIR genetic variant contributes to gastric cancer susceptibility.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	cervical cancer	C53	NA	qPCR etc.	cervical cancer tissues	differential expression	Compared with the CC genotype, TT genotype was significantly correlated with the elevated expression of HOTAIR; however, the CT genotype did not associate with the HOTAIR upregulation. In addition, we also found that the TT genotype of rs920778 was correlated with advanced tumor stage, highly histological grade, lympho node metastasis and positive infection of high risk HPV. Among the patients who underwent concurrent chemo-radiotherapy, TT genotype carriers present notably resistance to the combination of EBRT + ICBT + cisplatin.	27229487	2016	Analysis of the association of HOTAIR single nucleotide polymorphism (rs920778) and risk of cervical cancer.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	breast cancer	C50	NA	qPCR etc.	cell line (MCF7)	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.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	cervical cancer	C53	NA	qPCR, Luciferase reporter assay etc.	cervical cancer tissues, cell lines (SiHa, HeLa)	up-regulated	Real-time PCR assay in the 38 normal cervical tissues revealed that HOTAIR mRNA expression level increased with the presence of the risk allele T at rs920778 than those with the CC genotypes. Moreover, the cervical cancer patients with homozygous TT genotype were significantly associated with tumor-node-metastasis (TNM) stage. Furthermore, HOTAIR expression was higher in cervical cancer tissues than that in corresponding normal tissues, and the high expression was associated with the risk-associated allele T.	27467165	2016	Association of Long Non-Coding RNA HOTAIR Polymorphisms with Cervical Cancer Risk in a Chinese Population.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	cervical cancer	C53	NA	qPCR, Luciferase reporter assay etc.	osteosarcoma tissues, cell lines (MNNG and U3OS)	down-regulated	We found that rs2366152C was over-represented in low HOTAIR expressing HPV positive cervical cancer cases compared to HPV negative controls. We assessed the HOTAIR expression levels among samples genotyped for rs2366152C and found that the expression was significantly reduced in the C allele positive samples compared to the C allele negative samples, exclusively among the LH CaCx cases.	27683269	2016	Identification of genetic variation in the lncRNA HOTAIR associated with HPV16-related cervical cancer pathogenesis.
HOTTIP	HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213	100316868	ENSG00000243766	NR_037843	GRCh38_7:27198575-27207259	pancreatic cancer	C25	NA	qPCR, Luciferase reporter assay	PC cell line, PC tissues.	down-regulated	The current findings provided evidence that the functional rs1859168 A > C polymorphism may decrease the PC risk by down-regulating the HOTTIP expression.In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31]. In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31].	28818070	2017	rs1859168 A>C polymorphism regulates HOTTIP expression and reduces risk of pancreatic cancer in a Chinese population.
HOTTIP	HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213	100316868	ENSG00000243766	NR_037843	GRCh38_7:27198575-27207259	pancreatic cancer	C25	NA	microarray, qPCR etc.	pancreatic cancer tissues, cell lines (PANC-1, BxPC-3, Capan2, MIAPaCa-2, SW1990, and AsPC-1)	up-regulated	Compared with the HPDE6 cells, all PC cell lines had higher HOTTIP-005, XLOC_006390, and RP11-567G11.1 expression. The most increased lncRNAs in PC tissues were HOTTIP-005, XLOC_006390, and RP11-567G11.1. Increased HOTTIP-005 and RP11-567G11.1 expression were poor prognostic factors for patients with PC.	26447755	2015	Expression profile of long non-coding RNAs in pancreatic cancer and their clinical significance as biomarkers.
HOXA11-AS	HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076	221883	ENSG00000240990	NR_002795	GRCh38_7:27184518-27189293	ovarian cancer	C56.9	NA	qPCR, Western blot etc.	ovarian cancer tissues	down-regulated	Functional studies of ectopic expression of HOXA11-AS minor allele T in EOC cells showed decreased survival, proliferation, migration, and invasion compared to common allele A expression. Additionally, stable expression of HOXA11-AS minor allele T reduced primary tumor growth in mouse xenograft models to a greater extent than common allele A. Furthermore, HOXA11-AS expression levels were significantly lower in human EOC tumors than normal ovarian tissues, suggesting that HOXA11-AS has a tumor suppressor function in EOC which may be enhanced by the T allele	26430965	2015	A functional variant in HOXA11-AS, a novel long non-coding RNA, inhibits the oncogenic phenotype of epithelial ovarian cancer
HSP90AA1-IT1	NA	NA	NA	NA	NA	glioma	NA	M9380/3	qPCR, Western blot, Luciferase reporter assay, Luciferase reporter assay	brain tissue	down-regulated	Taken together, it is concluded that HSP90AA1-IT1, performs its function via regulating the development of gliomas through miR-885-5p-CDK2 signaling axis, and this has added new perspective to its role in tumorigenesis, thus providing potential therapeutic targets for glioma treatment.Curve graph indicated survival time of the xenograft mice. A dual-luciferase reporter vector was used to generate the luciferase constructs. The putative binding sites and its homologous mutation sites in the 3’-UTR region of CDK2 mRNA and HSP90AA1-IT1 were amplified and cloned into pmiRGLO luciferase reporter plasmid.	29088865	2017	LncRNA HSP90AA1-IT1 promotes gliomas by targeting miR-885-5p-CDK2 pathway.
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	hepatocellular carcinoma	C22.0	M8170/3	TaqMan allelic discrimination assay	blood	differential expression	The variant genotypes of rs7763881 were significantly associated with decreased HCC risk in a dominant genetic model.The variant genotypes of rs7763881 in HULC may contribute to decreased susceptibility to HCC in HBV persistent carriers.	22493738	2012	A genetic variant in long non-coding RNA HULC contributes to risk of HBV-related hepatocellular carcinoma in a Chinese population
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	hepatocellular carcinoma	C22.0	M8170/3	qPCR etc.	hepatocellular carcinoma tissues	differential expression	We found a promoter SNP, rs1041279, was associated with a 1.41-fold increased HCC risk (P = 0.032).	29803923	2018	The association of lncRNA-HULC polymorphisms with hepatocellular cancer risk and prognosis
IGFBP4-1	NA	NA	NA	NA	NA	lung cancer	C34	NA	qPCR, RNAi, etc.	Liver Cancer cell lines (PC9, A549, GLiver Cancer -82, L78)	down-regulated	Here, we conducted bioinformatics analysis and found insulin-like growth factor binding protein 4–1 (IGFBP4–1) as a new candidate lncRNA located in the upstream region of IGFBP4 gene.In cancer, abnormal expression and mutations of lncRNAs as important regulators can contribute to tumor development and progression through pathophysiological activities such as cell growth, apoptosis, invasion, and metastasis [4, 5, 6, 7, 8].	28946875	2017	Overexpression of lncRNA IGFBP4-1 reprograms energy metabolism to promote lung cancer progression.
LCAL1	LCAL1, onco-lncRNA-27	80078	NA	NR_130915	NA	lung cancer	C34	NA	RNA-seq, qPCR, RNAi etc.	lung cancer tissues	up-regulated	Stable overexpression of LCAL1, using two different clones, in the control cell line BEAS-2B showed a significant increase in cellular proliferation starting on day 2 and continuing until the end of the experiment at day 6 with a 38% and 43% growth increase, respetcively. Overexpression of LCAL1 in normal BEAS-2B cells is proof of principle that this lncRNA is sufficient to affetc cellular growth independently of other common cancer mutations, thus highlighting the importance of LCAL1 in lung cancer biology.	25116943	2014	Transcriptome sequencing reveals altered long intergenic non-coding RNAs in lung cancer.
LINC00152	CYTOR, C2orf59, LINC00152, NCRNA00152	112597	ENSG00000222041	NR_024204	GRCh38_2:87454781-87636740	cervical cancer	C53	NA	western blot, in vitro konckdown	cell line	up-regulated	This transcript was ubiquitously expressed in many human cell lines and its RNA levels were significantly upregulated in lung, liver and breast cancer tissues. A comprehensive sequence analysis of LINC00152 revealed a highly similar paralog annotated as MIR4435-2HG and several splice variants of both transcripts.	28536419	2017	The long non-coding RNA LINC00152 is essential for cell cycle progression through mitosis in HeLa cells
LINC00472	LINC00472, C6orf155	79940	ENSG00000233237	NR_121612	GRCh38_6:71344344-71420769	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
LINC00673	LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1	100499467	NA	NR_036488	GRCh38_17:72403322-72592804	pancreatic ductal adenocarcinoma	C25.3	M8500/3	RNA-seq, qPCR, Western blot	cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1,)	up-regulated	We generated a catalogue of PDA-associated lncRNAs. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4).We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA	29440233	2018	Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma.
lincRNA-p21	TP53COR1, TRP53COR1, linc-p21, lincRNA-p21	102800311	NA	NA	NA	glioma	NA	M9380/3	qPCR, Western blot etc.	cell lines (SMMC7721, U251MG)	down-regulated	In this work, we found that X-ray irradiation or hypoxia treatment elevated lincRNA-p21 expression in SMMC7721 hepatoma and U251MG glioma  cells.High lincRNA-p21 levels were associated with poor cancer-specific survival in patients. F.. However, tumor cells can express a wide range of transcription factors, such as hypoxia-inducible factor-1a (HIF-1a).found that LincRNA-p21 was downregulated in non-small-cell lung cancer tissue, but no association was observed with TP53 mutational status. 	28689810	2017	LincRNA-p21 knockdown enhances radiosensitivity of hypoxic tumor cells by reducing autophagy through HIF-1/Akt/mTOR/P70S6K pathway.
lincRNA-p21	TP53COR1, TRP53COR1, linc-p21, lincRNA-p21	102800311	NA	NA	NA	lung cancer	C34	NA	qPCR etc.	cell lines (wt MEFs, NIH/3T3 MEFs etc.)	down-regulated	Indeed, lincRNA-p21 overexpression in a lung cancer cell line harboring a KRAS mutation (referred to as LKR) and in NIH/3T3 MEFs caused a significant decrease in cell viability. This decrease in viability was due to increased apoptosis in response to DNA damage and not to an effect in cell cycle regulation. 	20673990	2010	A large intergenic noncoding RNA induced by p53 mediates global gene repression in the p53 response.
lincRNA-p21	TP53COR1, TRP53COR1, linc-p21, lincRNA-p21	102800311	NA	NA	NA	colorectal cancer	C19.9	NA	qPCR, Western blot, RIP	cancer tissues, human colorectal cancer cell lines (SW480, SW620)	down-regulated	In our study, we determined the anti-metastatic effect of EGb 761 on colorectal cancer cells and further explored the potential underlying regulatory mechanism.Plants have provided a rich source of therapeutic agents and bases for synthetic drugs. Previous studies indicated that LincRNA-p21 functioned as an tumor suppressor gene through participation in epigenetic regulation, such as histone methylation and/or CpG methylation at pluripotency gene promoters. Long intergenic non-coding RNA-p21 (LincRNA-p21) (3100 nt) is located on chromosome 6, approximately 15 kb upstream from the Cdkn1a (p21) gene.	29207671	2017	Ginkgo biloba extract EGb 761-induced upregulation of LincRNA-p21 inhibits colorectal cancer metastasis by associating with EZH2.
LINK-A	LINC01139, LINK-A, LINKA	339535	ENSG00000215808	NR_015407	GRCh38_1:238480384-238486023	breast cancer	C50	NA	Cell transfection, Fluorescence quenching assay, Lipid-RNA pulldown assay etc.	TNBC tissues, cell lines (MDA-MB-231, MDA-MB-468, MCF-10A)	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.
lncRNA-SVUGP2	NA	NA	NA	NA	NA	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot etc.	hepatocellular carcinoma tissues, cell lines (HepG2, Hep3B)	down-regulated	We found lncRNA-SVUGP2, which is a splice variant of the UGP2 gene, was down-regulated in HCC samples and correlates with a better prognosis in patients with HCC. 	29228655	2017	LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma
LOC100292680	LINC00942	100292680	ENSG00000249628	NR_028415	GRCh38_12:1500525-1507318	lung cancer	C34	NA	qPCR	cell line (A549, H838)	differential expression	Three repressed lncRNAs were further evaluated with RT-qPCR: LINC00942, RP11-284F21.7 and RP11-345L23.1. In all cases, this confirmed responsiveness to NFE2L2 siRNA silencing in A549, as well as one additional lung cancer cell line, H838, which similarly harbours a loss-of-function mutation in KEAP1	28959951	2016	Pan-cancer transcriptomic analysis associates long non-coding RNAs with key mutational driver events
LOC100507661	LINC02082	NA	ENSG00000242268	NA	GRCh38_3:168903366-168921996	thyroid cancer	C73.9	NA	qPCR etc.	cell lines (HEK293T, HEK293FT, FTC133, TPC1 etc.)	up-regulated	LOC100507661, was strongly upregulated in thyroid cancer tissues relative to paired contralateral normal tissue. LOC100507661 was easily detectable in papillary and anaplastic thyroid cancer cell lines such as TPC1, BCPAP, C643, and 8505C, but not in the follicular thyroid cancer cell line FTC133. Stable overexpression of LOC100507661 promoted cell proliferation, migration, and invasion of thyroid cancer cells. Lymph node metastasis and BRAF V600E mutations were more frequent in papillary thyroid cancers with high LOC100507661 expression.	27151833	2016	Upregulation of long noncoding RNA LOC100507661 promotes tumor aggressiveness in thyroid cancer
MAGI2-AS3	NA	100505881	ENSG00000234456	NR_038343	GRCh38_7:79452877-79471208	non small cell lung cancer	C34	M8046/3	qPCR, etc.	blood	down-regulated	MAGI2-AS3 level significantly correlated with tumor-node-metastasis (TNM) stage (p=0.001 in TEPs, p=0.003 in plasma), lymph-node metastasis (p=0.016 in TEPs, p=0.023 in plasma), and distant metastasis (p=0.045 in TEPs, p=0.045 in plasma).  Our data suggested that EGFRvIII can also be detected in blood platelets and there was no difference with detection in plasma.  EGFRvIII RNA existed in both TEPs and plasma, but EGFR intracellular mutations cannot be detected in DNA of TEPs isolated from NSCLC.	29922089	2018	LncRNAs and EGFRvIII sequestered in TEPs enable blood-based NSCLC diagnosis.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	hepatoblastoma	C22.0	M8970/3	microarray, PCR etc.	HCC tissues	up-regulated	HCC and HPBL have clearly different patterns of gene expression, with genes IGF2, Fibronectin, DLK1, TGFb1, MALAT1 and MIG6 being over-expressed in HPBL versus HCC. In addition, specific areas of the genome appear unstable in HCC, with the same regions undergoing either deletion or increased gene dosage in all HCC.	17006932	2006	Transcriptomic and genomic analysis of human hepatocellular carcinomas and hepatoblastomas.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	colorectal cancer	C19.9	NA	qPCR etc.	CRC tissues	up-regulated	The subsequently stratified analyses showed that the protective effect of rs1194338 was more pronounced in several subgroups. Furthermore, gene expression profiling analysis revealed overexpression of MALAT1 mRNA in colorectal cancer tissue compared with normal controls. Confirmation studies with large sample size and further mechanistic investigations into the function of MALAT1 and its genetic variants are warranted to advance our understanding of their roles in colorectal carcinogenesis, and to aid in the development of novel and targeted therapeutic strategies.	29190941	2017	Associations between novel genetic variants in the promoter region of MALAT1 and risk of colorectal cancer
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	hepatocellular carcinoma	C22.0	M8170/3	microarray, PCR etc.	HCC tissues	up-regulated	HCC and HPBL have clearly different patterns of gene expression, with genes IGF2, Fibronectin, DLK1, TGFb1, MALAT1 and MIG6 being over-expressed in HPBL versus HCC. In addition, specific areas of the genome appear unstable in HCC, with the same regions undergoing either deletion or increased gene dosage in all HCC.	17006932	2006	Transcriptomic and genomic analysis of human hepatocellular carcinomas and hepatoblastomas.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	colorectal cancer	C19.9	NA	qPCR etc.	CRC tissues, cell lines (SW620, SW480 etc.)	differential expression	We were successful in detecting the following mutations: fragment 5434 nt-6951 nt of the MALAT-1 was mutated in SW620 cells, while fragments 5434 nt-6951 nt and 6918 nt-8441 nt of MALAT-1 were mutated in SW480 cancer cells and primary CRC tissues. Our data illustrated that one of the 5 fragments (6918 nt-8441 nt) located at the 3' end of MALAT-1 plays a pivotal role in the biological processes of cell proliferation, migration and invasion. Based on these observations, we can infer that the 3' end of MALAT-1 is an important biological motif in the invasion and metastasis of CRC cells.	21503572	2011	MALAT-1: a long non-coding RNA and its important 3' end functional motif in colorectal cancer metastasis.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	breast cancer	C50	NA	qRT-PCR	BC tissues and para-carcinoma tissues	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±0.490), GG (0.511±0.149) and AG+GG genotypes (0.743±0.447) of rs619586 was significantly lower than that with genotype AA (1.511±0.737).	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.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	breast cancer	C50	NA	qPCR, Western blot, RIP, ChIP etc.	cell lines (SKBR3, MDA-MB-468, MDA-MB-231, MCF7 ,H1299, HEK T293, OVCAR-3)	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–Meier 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.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	osteosarcoma	NA	M9180/3	qPCR, Western blot, Luciferase reporter assay etc.	cancer tissues, osteosarcoma cell lines (MG-63, SAOS-2, U2OS, SW1353)	up-regulated	In conclusion, we revealed that enhanced MALAT1 expression predicted unfavourable outcome in osteosarcoma and promoted cell proliferation through suppressing miR-205 and activating SMAD4 function. Thus, lncRNA MALAT1 may serve as a promising prognostic and therapeutic target for osteosarcoma patients. Kaplan-Meier analysis indicated that patients with high expression of MALAT1 was associated with poor overall survival compared with the low expressing patients. Illustration of the putative predicted miR-205 binding site in the SMAD4 mRNA 3’UTR region, and the mutation within the binding site was generated. 	29290978	2017	Long noncoding RNA MALAT1 promotes cell proliferation through suppressing miR-205 and promoting SMAD4 expression in osteosarcoma.
MDC1-AS	MDC1-AS1, MDC1-AS	106478956	ENSG00000224328	NR_133647	GRCh38_6:30703067-30713184	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	down-regulated	The expression levels of MDC1-AS and MDC1 was down-regulated in bladder cancer. After over-expression of MDC1-AS, increased levels of MDC1 were observed in bladder cancer cells. We also found a remarkably inhibitory role of antisense lncRNA MDC1-AS on malignant cell behaviors in bladder cancer cells EJ and T24. 	25514464	2014	A novel antisense long noncoding RNA regulates the expression of MDC1 in bladder cancer.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	colorectal cancer	C19.9	NA	Genotyping etc.	blood	differential expression	We found that MEG3 rs7158663 AA genotype, but not GA genotype, had significant increased colorectal cancer risk, compared with GG genotype. Further stratified analysis indicated that the increased risk was significantly correlated with individuals with age less than 60 and family history of cancer. However, there was no significant association between rs7158663 and colorectal tumor site and stage.	26934323	2016	Associations between polymorphisms of long non-coding RNA MEG3 and risk of colorectal cancer in Chinese
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	nasopharyngeal cancer	C11	NA	qPCR, MSP-PCR, Western blot, FISH etc.	cell lines (C666-1, HK-1, NP69, NP361 and NP460)	down-regulated	In the present study, two MEG3 variants, AF119863 (MEG3-AF) and BX247998 (MEG3-BX), were found abundantly expressed in a normal nasopharyngeal epithelial cell line, NP69. Significant downregulation of MEG3-AF was further verified in a panel of NPC samples including xenografts and primary biopsies. Besides, ectopic expression of MEG3 in NPC cell lines resulted in considerable repression of in vitro anchorage-independent growth and in vivo tumorigenicity, in addition to significant inhibition in cell proliferation, colony formation, and induction of cell cycle arrest.	27597634	2017	Downregulation of long non-coding RNA MEG3 in nasopharyngeal carcinoma.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	pancreatic neuroendocrine tumor	C25	M8246/3	microarray, qPCR, Luciferase reporter assay etc.	pancreatic neuroendocrine tumors tissues, cell lines (MIN6 and MIN6-4N)	down-regulated	We found that Meg3 has tumor-suppressor activity in PNET cells because the overexpression of Meg3 in MIN6 cells (insulin-secreting mouse PNET cell line) blocked cell proliferation and delayed cell cycle progression. Gene expression microarray analysis showed that Meg3 overexpression in MIN6 mouse insulinoma cells down-regulated the expression of the protooncogene c-Met (hepatocyte growth factor receptor), and these cells showed significantly reduced cell migration/invasion. Compared with normal islets, mouse or human MEN1-associated PNETs expressed less MEG3 and more c-MET	25565142	2015	Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	down-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	acute myeloid leukemia	NA	M9861/3	qPCR, Luciferase reporter assay, Western blot	AML tissues, cell lines (TF-1, U937, NB4, KG-1, Kasumi-1, HL-60 and K562) 	down-regulated	MEG3 is significantly downregulated in AML and suppresses leukemogenesis not only in a p53-dependent, but also a p53-independent manner.MEG3 is proven to be transcriptionally activated by Wilms' tumor 1 (WT1), dysregulation of which by epigenetic silencing or mutations is causally involved in AML.Therefore MEG3 is identified as a novel target of the WT1 molecule. Ten-eleven translocation-2 (TET2) mutations frequently occur in AML and significantly promote leukemogenesis of this disorder.TET2, acting as a cofactor of WT1, increases MEG3 expression.  	28400619	2017	Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	hepatocellular carcinoma	C22.0	M8170/3	microarray, qPCR, Western blot, RIP, Flow cytometry assay, RNA pull-down assay etc.	HCC tissues, cell lines (HepG2, SK-Hep-1, HEK293, HCT116)	down-regulated	Our results demonstrate for the first time that MEG3 can interact with p53 DNA binding domain and various p53 target genes are deregulated after overexpression of MEG3 in hepatoma cells. Furthermore, results of qRT-PCR have shown that MEG3 RNA is lost or reduced in the majority of HCC samples compared with adjacent non-tumorous samples. Ectopic expression of MEG3 in hepatoma cells significantly inhibits proliferation and induces apoptosis.	26444285	2015	Long Noncoding RNA MEG3 Interacts with p53 Protein and Regulates Partial p53 Target Genes in Hepatoma Cells.
MIR100HG	MIR100HG, AGD1, linc-NeD125, lncRNA-N2	399959	ENSG00000255248	NR_024430	GRCh38_11:122028327-122556721	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Cell proliferation assay, Cell migration assay etc.	cell lines (HepG2, SMMC-7721 and HCCLM9)	differential expression	Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration	28194035	2017	Recurrently deregulated lncRNAs in hepatocellular carcinoma.
MVIH	AK094613	NA	NA	NA	NA	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot, etc.	Hepatoma cell line HepG2, liver tumor-derived cell lines SKHEP-1, Huh7	up-Regulated	Our data suggests that deficiency or loss of functional mutations of ARID1A in HCC cells might contribute to the increased activity ofcertain cancer-promoting lncRNAs。AIRD1A fragments (A-1, aa 1e310; A-2, aa 311e600; A-3, aa 601e950; A-4, aa 951e1300; A-5, aa 1301e1600; A-6, aa 1601e1900; A-7, aa 1901e2285) were amplified by PCR and subcloned into pGEX-4T-1 vectors (GE Healthcare Life Sciences) to generate recombinant GST-ARID1A fusion proteins. As a subunit of SWI/SNF complex, ARID1A could contribute to its chromatin remodeling activity by recruiting and binding of specific transcription factor and transcriptional coactivator/corepressor complexes.ARID1A, encoding the BAF250a subunit of SWI/SNF complex, has a high mutation frequency in numerous types of cancer. 	28716731	2017	ARID1A represses hepatocellular carcinoma cell proliferation and migration through lncRNA MVIH.
MYCNOS	MYCNOS, MYCN-AS1, N-CYM, NCYM, NYCM	10408	ENSG00000233718	NM_001329968	GRCh38_2:15921037-15942249	neuroblastoma	NA	M9500/3	qPCR, Western blot etc.	neuroblastoma tissues	up-regulated	Both DeltaMYCN and MYCNOS are expressed in all NBs examined. In NBs with MYCN-amplification, these transcripts are significantly higher expressed. Expression of the antisense gene MYCNOS might be relevant to the progression of NB, potentially by directly inhibiting MYCN transcription by transcriptional interference at the DNA level. The MYCNOS:MYCN-ratio in NBs is significantly correlated with both MYCN-amplification and NB-stage. Our data indicate that in NB, MYCN expression levels might be influenced by MYCNOS but not by MYCN.	19615087	2009	Regulation of MYCN expression in human neuroblastoma cells.
NAMA	NAMA	100996569	ENSG00000271086	NR_102270	GRCh38_9:99355337-99377240	papillary thyroid cancer	NA	M8260/3	qPCR, RNAi, Western blot, Northern blot etc.	PTA tissues tissues, cell lines (NPA87, K1, K2 etc.)	down-regulated	The downregulation of NAMA in PTCs with the BRAF*V600E mutation led us to test whether NAMA is regulated by the MAP kinase pathway. We suggest that NAMA is a noncoding RNA associated with growth arrest.	17415708	2007	Identification of a novel noncoding RNA gene, NAMA, that is downregulated in papillary thyroid carcinoma with BRAF mutation and associated with growth arrest.
NR_033878	LINC00944	387895	ENSG00000256128	NR_033878	GRCh38_12:126752164-126761045	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
OVAL	OVAAL, LINC01131, OVAL	148756	ENSG00000236719	NR_125716	GRCh38_1:180558976-180566518	ovarian cancer	C56.9	NA	RNA-seq, qPCR etc.	ovarian cancer tissues	down-regulated	OVAL expression was low or absent in both normal fallopian tube and in the majority of tumors, including most cases with wide 1q amplification. However, focal amplification of the OVAL locus coincided strikingly with OVAL transcriptional activation. 	24265805	2013	Comprehensive analysis of long non-coding RNAs in ovarian cancer reveals global patterns and targeted DNA amplification.
P2RX7-V3	P2RX7, P2X7	NA	NA	NA	NA	uveal melanoma	C69.9	M8720/3	microarray, qPCR, RNAi etc.	cell lines (MUM2B, OM431, and 293T)	up-regulated	Here, we identified a transcriptional variant transcribed from the P2RX7 gene locus, named P2RX7-V3 (P2RX7 variant 3), which was expressed at a high level in UM cells. P2RX7-V3 silencing revealed that this variant acts as a necessary UM oncoRNA. Knockdown of P2RX7-V3 expression significantly suppressed tumor growth in vitro and in vivo.	27468714	2016	P2RX7-V3 is a novel oncogene that promotes tumorigenesis in uveal melanoma.
PANDAR	PANDAR, PANDA	101154753	ENSG00000281450	NR_109836	GRCh38_6:36673621-36675126	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
PANDAR	PANDAR, PANDA	101154753	ENSG00000281450	NR_109836	GRCh38_6:36673621-36675126	gastric cancer	C16	NA	Microarray, qRT-PCR, RIP	GC tissues, normal gastric tissues, Gastric cancer cell lines (SNU-484, SNU-520, SNU-620, SNU-638, SNU-668, AGS, NCI-N87, SNU-1, SNU-5, KATO)	up-regulated	Upregulated PANDAR in GC patients was positively correlated with increased tumour size, advanced TNM classification and a poor survival rate in GC patients. As a target, the CDKN1A gene was successfully downregulated by PANDAR. PANDAR controlled the transcription of the CDKN1A gene by competitively binding with p53 protein. In combination with a p53 activator (nutlin3), the knockout of PANDAR by CRISPR/Cas9 technology synergistically inhibited GC tumour growth in vivo.upregulated HOTAIR inhibits the expression of p53 by enhancing the p53 promoter histone H3 lysine 27 trimethylation (H3K27me3), and the overexpression of PANDAR increases the stability of the p53 protein in response to DNA damage. 	29416011	2018	Long noncoding RNA PANDAR blocks CDKN1A gene transcription by competitive interaction with p53 protein in gastric cancer.
PCA3	PCA3, DD3, NCRNA00019, PCAT3	50652	ENSG00000225937	NR_015342	GRCh38_9:76691980-76863307	prostate cancer	C61.9	NA	PCR etc.	prostate cancer tissues, blood (leukocytes)	up-regulated	PCA3 TAAA STR polymorphisms and 8 genotypes were found in both peripheral blood leukocytes and prostate tissues, the carriers with more TAAA repeats were associated with increased risk for PCa than individuals having less TAAA repeats. Interestingly, 18 (15.0%) of 120 PCa patients had more (TAAA)n repeats in prostate tissues than that in peripheral blood leukocytes, and 3 (2.5%) of 120 had less (TAAA)n repeats in prostate tissues. Short tandem repeat polymorphism of TAAA in the promoter region of PCA3 gene is a risk-increasing factor for prostate cancer in the Chinese population.	25445501	2014	Long noncoding RNA PCA3 gene promoter region is related to the risk of prostate cancer on Chinese males.
PCA3	PCA3, DD3, NCRNA00019, PCAT3	50652	ENSG00000225937	NR_015342	GRCh38_9:76691980-76863307	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PCAT-1	LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1	100750225	ENSG00000253438	NR_045262	GRCh38_8:126556323-127419050	bladder cancer	C67	NA	qPCR etc.	bladder cancer cell lines (5637, T24), bladder cancer tissues	up-regulated	This study indicates that genetic variants in lncRNA PCAT1 were associated with bladder cancer susceptibility and the SNP rs710886 may act as a potential biomarker for bladder cancer risk.Single nucleotide polymorphisms (SNPs) are the most common genetic variants.f genes. Accumulated evidence hasshownthat plenty of functional SNPs are converged upon lncRNAs and responsible for bladder cancer carcinogenesis [17]. 	28627442	2017	The association of rs710886 in lncRNA PCAT1 with bladder cancer risk in a Chinese population.
PCAT-1	LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1	100750225	ENSG00000253438	NR_045262	GRCh38_8:126556323-127419050	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PCAT29	PCAT29	104472713	ENSG00000259641	NR_126437	GRCh38_15:69592200-69695750	prostate cancer	C61.9	NA	qPCR, Western blot etc.	cell lines (VCap, PC3M-luc, LNCaP etc.)	down-regulated	This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAIC and PCAT30, that are prognostic for a wide variety of cancer types.This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAICand PCAT29, that are prognostic for a wide variety of cancer types.	25700553	2015	The lncRNA DRAIC/PCAT29 locus constitutes a tumor suppressive nexus.
PCAT6	PCAT6, KDM5B-AS1, KDM5BAS1, PCAN-R1, ncRNA-a2, onco-lncRNA-96	100506696	ENSG00000228288	NR_046325	GRCh38_1:202810954-202812156	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Both lncRNA showed positive correlation between gene expression and SCNA. The criteria of increasing expression from normal to primary to metastatic prostate cancer aimed to uncover lncRNA that may be important therapeutic targets for both primary and metastatic cancers.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PCAT7	PCAT7, PCAN-R2	101928099	ENSG00000231806	NR_121566	GRCh38_9:94555054-94603990	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Both lncRNA showed positive correlation between gene expression and SCNA. The criteria of increasing expression from normal to primary to metastatic prostate cancer aimed to uncover lncRNA that may be important therapeutic targets for both primary and metastatic cancers.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, MTT assay etc.	cell lines (LNCaP and CWR22Rv1)	up-regulated	We show transcriptional regulation of PCGEM1 in response to androgen deprivation by p54/nrb. While ectopic expression of p54/nrb increases, suppression of p54/nrb by RNAi or knockout (KO) reduces PCGEM1. Moreover, rescue experiments indicate that re-expression of p54/nrb in KO cells restores the ability to induce PCGEM1, leading to upregulation of the androgen receptor splice variant AR3 which has been shown to play a role in castration resistance.	27682980	2016	Regulation of PCGEM1 by p54/nrb in prostate cancer.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	qPCR etc.	prostate cancer tissues	differential expression	We found a significantly decreased risk of PCa for rs6434568 AC and AC/AA genotype, as well as rs16834898 AC and AC/CC genotype, compared with the CC and AA genotypes, respectively. Additional functional analyses are required to detect the detailed mechanism underlying the observed association.	23459097	2013	Association between lncrna PCGEM1 polymorphisms and prostate cancer risk.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PCNA-AS1	PCNA-AS1, PCNA-AS, PCNAAS	100302739	NA	NR_028370	GRCh38_20:5119586-5119969	hepatocellular carcinoma	C22.0	M8170/3	microarray, qPCR etc.	cell lines (Huh7, SMMC7721)	up-regulated	PCNA-AS1 was up-regulated in HCC and its expression status was associated with multiple tumor nodules. The effects of PCNA-AS1 rely on regulation of PCNA via forming RNA hybridization to increase PCNA mRNA stability.	24704293	2014	Antisense long non-coding RNA PCNA-AS1 promotes tumor growth by regulating proliferating cell nuclear antigen in hepatocellular carcinoma.
PCOTH	PCOTH, C1QTNF9B-AS1	NA	ENSG00000205861	NA	GRCh38_13:23888889-23897263	prostate cancer	C61.9	NA	qPCR, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, DU145, PC-3CaP etc.)	up-regulated	We identified a novel gene, prostate collagen triple helix (PCOTH), showing overexpression in prostate cancer cells and its precursor cells, prostatic intraepithelial neoplasia (PIN). Knocking down PCOTH expression by small interfering RNA (siRNA) resulted in drastic attenuation of prostate cancer cell growth, and concordantly, LNCaP derivative cells that were designed to constitutively express exogenous PCOTH showed higher growth rate than LNCaP cells transfected with mock vector, suggesting the growth-promoting effect of PCOTH on prostate cancer cell.	15930275	2005	PCOTH, a novel gene overexpressed in prostate cancers, promotes prostate cancer cell growth through phosphorylation of oncoprotein TAF-Ibeta/SET.
POLR2E	NA	NA	ENSG00000099817	NA	GRCh38_19:1086579-1095380	papillary thyroid cancer	NA	M8260/3	qPCR etc.	papillary thyroid carcinoma tissues	differential expression	The meta-analysis further revealed that POLR2E rs3787016T allele was associated with an increased cancer risk in Chinese population. Collectively, the POLR2E rs3787016 may be used as a genetic biomarker to predict cancer risk in Chinese population. 	29724531	2018	Long non-coding RNA POLR2E rs3787016 is associated with the risk of papillary thyroid carcinoma in Chinese population.
PRINS	PRINS, NCRNA00074	100169750	NA	NA	NA	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	down-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PRNCR1	PRNCR1, CARLo-3, PCAT8	101867536	ENSG00000282961	NR_109833	GRCh38_8:127079874-127092600	gastric cancer	C16	NA	qPCR etc.	gastric cancer tissues	differential expression	We found that patients with the rs13252298AG genotype displayed a 1.50-fold increased risk of GC. Interestingly, the rs7007694CT and CC and the rs1456315GG genotypes displayed a decreased risk of GC. Our results suggest that SNPs in the lncRNA PRNCR1 may be a biomarker for the etiology of GC	26206497	2015	Association between polymorphisms in long non-coding RNA PRNCR1 in 8q24 and risk of gastric cancer
PRNCR1	PRNCR1, CARLo-3, PCAT8	101867536	ENSG00000282961	NR_109833	GRCh38_8:127079874-127092600	colorectal cancer	C19.9	NA	qPCR etc.	CRC tissues	differential expression	In overall analyses, we found that the rs13252298 and rs1456315 were associated with significantly decreased risks of CRC. In stratification analyses, we found that CRC patients carrying the rs1456315G were likely to have a tumor size of greater than 5 cm (G vs. A: adjusted OR = 1.56, 95% CI: 1.10-2.23). Additionally, patients with the rs7007694C and rs16901946G had decreased risks to develop poorly differentiated CRC, whereas patients with the rs1456315G had an increased risk to develop poorly differentiated CRC.	24330491	2013	Association between polymorphisms in long non-coding RNA PRNCR1 in 8q24 and risk of colorectal cancer.
PRNCR1	PRNCR1, CARLo-3, PCAT8	101867536	ENSG00000282961	NR_109833	GRCh38_8:127079874-127092600	prostate cancer	C61.9	NA	qPCR, Northern blot etc.	cell lines (LNCaP, 22Rv1, PC-3 etc.)	up-regulated	PRNCR1 expression was upregulated in some of the PC cells as well as precursor lesion prostatic intraepithelial neoplasia. Knockdown of PRNCR1 by siRNA attenuated the viability of PC cells and the transactivation activity of androgen receptor, which indicates that PRNCR1 could be involved in prostate carcinogenesis possibly through androgen receptor activity.	20874843	2011	Association of a novel long non-coding RNA in 8q24 with prostate cancer susceptibility.
PTCSC2	NA	101928337	ENSG00000236130	NR_147055	GRCh38_9:97805935-97810008	thyroid cancer	C73.9	NA	RIP, Dual-luciferase reporter assay, RNA pull-down assay etc.	thyroid cancer tissues, cell lines (KTC1, BCPAP, C643, SW1736, TPC1, FTC133)	differential expression	Here we report that PTCSC2 binds myosin-9 (MYH9). In a bidirectional promoter shared by FOXE1 and PTCSC2, MYH9 inhibits the promoter activity in both directions. This inhibition can be reversed by PTCSC2, which acts as a suppressor. RNA knockdown of FOXE1 in primary thyroid cells profoundly interferes with the p53 pathway. We propose that the interaction between the lncRNA, its binding protein MYH9, and the coding gene FOXE1 underlies the predisposition to PTC triggered by rs965513.	28049826	2017	MYH9 binds to lncRNA gene PTCSC2 and regulates FOXE1 in the 9q22 thyroid cancer risk locus.
PTENP1	PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN	11191	ENSG00000237984	NA	GRCh38_9:33673504-33677499	gastric cancer	C16	NA	qPCR	gastric tumor tissue	up-regulated	We also found that relative PTENP1 mRNA expression levels were higher in rs7853346 CG/GG genotype carriers than those with common genotype in both GC and normal tissues. Our results suggested that lncRNA PTENP1 polymorphism rs7853346 may predict GC susceptibility.	28931965	2017	Polymorphisms in lncRNA PTENP1 and the Risk of Gastric Cancer in a Chinese Population
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	B-cell lymphoma	NA	M9591/3	qPCR, FISH, ISH etc.	bone marrow, lymph node, pleural effusion	differential expression	In addition, not only MYC rearrangement but also PVT1 rearrangement may also be implicated in the disease development of HABCLs with 8q24 abnormalities.	23547836	2013	Deletion or methylation of CDKN2A/2B and PVT1 rearrangement occur frequently in highly aggressive B-cell lymphomas harboring 8q24 abnormality.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	bladder urothelial cancer	NA	M8120/3	qPCR, Western blot, Luciferase reporter assay etc.	cell lines (BUC, J82 and T24) 	up-regulated	lncRNA PVT1 is overexpressed in multidrug resistant BUC tissues and cell lines, and PVT1 knockdown reduces BUC cell proliferation, invasiveness, and chemoresistance by modulating Wnt/B-catenin signaling. PVT1 was upregulated in BC, where it promoted tumor cell proliferation and suppressed apoptosis. 	28969069	2017	LncRNA plasmacytoma variant translocation 1 is an oncogene in bladder urothelial carcinoma.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	multiple myeloma	C42.1	M9732/3	qPCR, FISH etc.	cell lines (AMU-MM1, KMS-12-BM, KMS-18, KMS-20 etc.)	differential expression	PVT1 rearrangements were most common and found in 7 of 12 patients (58.3%) and 5 of 8 cell lines (62.5%) with 8q24 abnormalities. A combination of spectral karyotyping (SKY), FISH, and oligonucleotide array identified several partner loci of PVT1 rearrangements, such as 4p16, 4q13, 13q13, 14q32, and 16q23-24. The PVT1-NBEA chimera in which PVT1 exon 1 was fused to NBEA exon 2 and the PVT1-WWOX in which PVT1 exon 1 was fused to WWOX exon 9 were associated with the expression of abnormal NBEA and WWOX lacking their N-terminus, respectively. These findings suggest that PVT1 rearrangements may represent a novel molecular paradigm underlying the pathology of 8q24 rearrangement-positive multiple myeloma.	22869583	2012	Frequent PVT1 rearrangement and novel chimeric genes PVT1-NBEA and PVT1-WWOX occur in multiple myeloma with 8q24 abnormality.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	lung cancer	C34	NA	qPCR, Luciferase reporter assay etc.	cell lines (A549, 95D, HCC827, NCI-H1650)	up-regulated	YY1 could directly bind to the promoter region of (long noncoding RNAplasmacytoma variant translocation 1 [lncRNA-PVT1]) and activated its transcription through the consensus YY1 motif. Knockdown of the expression of YY1 reduced cell proliferation in vivo, consistent with the results obtained from silencing the expression of YY1 in lung cancer cells. Collectively, our study showed a critical role of YY1 in the regulation of tumorigenesis, partly through its downstream target PVT1	28972861	2017	Transcription Factor YY1 Modulates Lung Cancer Progression by Activating lncRNA-PVT1
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	diffuse glioma	NA	M8145/3	qPCR	breast and ovarian cancer cell lines, glioma tumor tissue.	up-regulated	These results implied that these four lncRNAs might play important role in diffuse gliomas progression, particularly, PVT1 and HAR1A could be explored as promising biomarkers for diagnosis, prognosis and target therapy of diffuse gliomas.Kaplan-Meier survival curve and Cox regression analyses showed that glioma patients with high PVT1 expression or low HAR1A expression had poor survival outcome, aberrantly expressed PVT1 and HAR1A could be the independent prognosis biomarkers for glioma patients. LncRNA CYTOR was up-regulated in HCC tissues, circulating CYTOR were also highly expressed in plasma samples of HCC patients, and could serve as potential biomarker for diagnosis of HHC. High expression of PVT1 and CYTOR as well as low HAR1A and MIAT expression were associated with high Ki-67 level and more TP53 mutation. 	29108264	2017	lncRNAs PVT1 and HAR1A are prognosis biomarkers and indicate therapy outcome for diffuse glioma patients
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	ovarian cancer	C56.9	NA	qPCR etc.	cell lines (A2780, DOV13, PA-1 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.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	cervical cancer	C53	NA	qPCR, RNAi, Western blot, Cell proliferation assay etc.	cell lines (SiHa, HeLa, DoTc2 4510)	up-regulated	Our results demonstrate that PVT1 expression is significantly increased in ICC tissue versus normal cervix and that higher expression of PVT1 correlates with poorer overall survival. In cervical cancer cell lines, PVT1 knockdown resulted in significantly decreased cell proliferation, migration and invasion, while apoptosis and cisplatin cytotoxicity were significantly increased in these cells. Finally, we show that PVT1 expression is augmented in response to hypoxia and immune response stimulation and that this lncRNA associates with the multifunctional and stress-responsive protein, Nucleolin.	27232880	2016	The lncRNA PVT1 Contributes to the Cervical Cancer Phenotype and Associates with Poor Patient Prognosis.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	prostate cancer	C61.9	NA	qPCR, ChIP etc.	cell lines (PC3, 1542-CP)	differential expression	The risk allele (G) of rs378854 (A>G) reduces binding of the transcription factor YY1 in vitro. The region surrounding rs378854 interacts with the MYC and PVT1 promoters.Expression of the PVT1 oncogene in normal prostate tissue increased with the presence of the risk allele of rs378854, while expression of MYC was not affetced.	21814516	2011	A functional variant at a prostate cancer predisposition locus at 8q24 is associated with PVT1 expression.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	colorectal cancer	C19.9	NA	qPCR, Western blot etc.	cell lines (HCT116, SW480, HT29, NCM460, SW620, CaCO2)	up-regulated	The present study demonstrated that the expression of PVT1 in CRC cell lines was higher than that in normal colon mucosal cell lines. Using GEO database analysis and the measurement of clinical samples, it was revealed that CRC patients with high PVT1 expression demonstrated poor OS. Multivariate analysis indicated that high PVT1 expression is an independent risk  factor for patients with CRC. In addition, PVT1 knockdown suppressed the proliferation, invasion and metastasis of CRC cells in vitro, which were associated with decreasing vimentin, cyclin D1 and cyclin-dependent kinase 4 expression and enhanced E-cadherin expression. The results of the present study suggest that PVT1 may serve a critical role in CRC progression and metastasis and may serve as a potential prognostic biomarker for CRC.	29512788	2018	Upregulated plasmacytoma variant translocation 1 promotes cell proliferation, invasion and metastasis in colorectal cancer.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	breast cancer	C50	NA	RNA-seq, qPCR, Western blot, Luciferase reporter assay etc.	cell lines (MDA-MB-231 and MCF-7)	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.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	breast cancer	C50	NA	qPCR etc.	cell lines (A2780, DOV13, PA-1 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.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	pancreatic cancer	C25	NA	qPCR, Western blot	pancreatic cancer tissues, cell line (PANC-1)	up-regulated	It showed that plasmacytoma variant translocation 1 (PVT1) expression was significantly upregulated in pancreatic cancer tissues or cell line compared to normal groups. PVT1 promoted epithelial-mesenchymal transition and cell proliferation and migration through downregulating p21 in pancreatic cancer cells.	28355965	2017	Long Noncoding RNA PVT1 Promotes EMT and Cell Proliferation and Migration Through Downregulating p21 in Pancreatic Cancer Cells
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	prostate cancer	C61.9	NA	RNA-seq, microarray, qPCR, RNAi, Northern blot etc.	prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.)	up-regulated	Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer.	23728290	2013	Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	colorectal cancer	C19.9	NA	microarray, qPCR, RNAi, Western blot etc.	CRC tissues, cell lines (RKO, HCT116 etc.)	up-regulated	CRC cells transfected with PVT-1 siRNA exhibited significant loss of their proliferation and invasion capabilities. In these cells, the TGFB1 signalling pathway and apoptotic signals were significantly activated. In addition, univariate and multivariate analysis revealed that PVT-1 expression level was an independent risk factor for overall survival of colorectal cancer patients.	24196785	2014	Amplification of PVT-1 is involved in poor prognosis via apoptosis inhibition in colorectal cancers.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	breast cancer	C50	NA	qPCR etc.	breast cancer tissues, cell lines (BRF71T1, HCC38, HCC1143 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.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	colorectal cancer	C19.9	NA	qPCR, etc.	Cancer tissues, 210 matched adjacent normal tissues. 	up-regulated             	Our results suggest that high PVT1 expression might be a potential biomarker for assessing tumor recurrence and prognosis in colorectal cancer patients. PVT1 plays a role similar to the relevant proto-oncogene to promote the metastasis, proliferation, and invasion of malignant cells, and enhances the resistance of tumor cells to chemotherapeutic drugs. Kaplan–Meier survival curve in CRC patients based on lncRNA PVT1 expression. Plasmacytoma variant translocation 1 (PVT1) transcripts are homologous to murine PVT1 genes and belong to the intergenic lncRNA.	29888675	2018	Long non-coding RNA PVT1 as a novel potential biomarker for predicting the prognosis of colorectal cancer.
ROPNR	NA	NA	NA	NA	NA	acute myeloid leukemia	NA	M9861/3	qPCR, ChIP etc.	bone marrow, cell lines (KG-1, KG-1a, Kasumi-1, K562)	up-regulated	We describe a RUNX1-intragenic long noncoding RNA ROPNR that is transcribed as unspliced transcript from an upstream overlapping promoter. ROPNR was upregulated in AML samples and in response to Ara-C treatment in vitro. ROPNR utilizes its 3'-terminal fragment to directly interact with the RUNX1 promoter and enhancers and participates in the orchestration of an intrachromosomal loop. The 3' region of ROPNR also participates in long-range interchromosomal interactions with chromatin regions that are involved in multiple RUNX1 translocations.	24752773	2014	An intragenic long noncoding RNA interacts epigenetically with the RUNX1 promoter and enhancer chromatin DNA in hematopoietic malignancies.
RP11-284F21.7	NA	NA	NA	NA	GRCh38_1:156646507-156661424	lung cancer	C34	NA	qPCR	cell line (A549, H838)	differential expression	Three repressed lncRNAs were further evaluated with RT-qPCR: LINC00942, RP11-284F21.7 and RP11-345L23.1. In all cases, this confirmed responsiveness to NFE2L2 siRNA silencing in A549, as well as one additional lung cancer cell line, H838, which similarly harbours a loss-of-function mutation in KEAP1	28959951	2016	Pan-cancer transcriptomic analysis associates long non-coding RNAs with key mutational driver events
RP11-345L23.1	NA	NA	NA	NA	GRCh38_6:53628380-53631394	lung cancer	C34	NA	qPCR	cell line (A549, H838)	differential expression	Three repressed lncRNAs were further evaluated with RT-qPCR: LINC00942, RP11-284F21.7 and RP11-345L23.1. In all cases, this confirmed responsiveness to NFE2L2 siRNA silencing in A549, as well as one additional lung cancer cell line, H838, which similarly harbours a loss-of-function mutation in KEAP1	28959951	2016	Pan-cancer transcriptomic analysis associates long non-coding RNAs with key mutational driver events
RP1-153P14.5	RP1-153P14.5	NA	NA	NA	GRCh38_6:37545145-37550860	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Cell proliferation assay, Cell migration assay etc.	cell lines (HepG2, SMMC-7721 and HCCLM9)	differential expression	Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration	28194035	2017	Recurrently deregulated lncRNAs in hepatocellular carcinoma.
SAMMSON	LINC01212	101927152	ENSG00000240405	NR_110000	GRCh38_3: 69999550-70518064	melanoma	NA	M8720/3	qPCR, RIP etc.	cell lines (Mel501, SK-MEL-28), melanoma tissues	up-regulated	Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted antimelanoma therapeutic responses.	27008969	2016	Melanoma addiction to the long non-coding RNA SAMMSON
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	lung squamous cell carcinoma	C34	M8070/3	qPCR etc.	LSCC tissues	up-regulated	In conclusion, eight out of the nine tested genes were recurrently over-expressed, but SOX2 and SOX2OT were the most consistently highly over-expressed and thus are the best candidates to be driver genes of 3q26.3 amplifications.	20126410	2010	SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas.
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	breast cancer	C50	NA	qPCR etc.	breast cancer tissues	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.
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	non small cell lung cancer	C34	M8046/3	qPCR, RNAi, Flow cytometry assay etc.	NSCLC tissues, cell lines (A549, U-87 MG)	up-regulated	Our data revealed that SOX2OT variants 4 and 7 were upregulated around six times in lung tumor tissues, compared to their non-tumor counterparts. The SOX2OT knockdown significantly reduced the colony formation ability of cancer cells; however, no alterations in the rate of apoptosis were detected. On the other hand, SOX2OT-suppressed cells had elevated accumulation in G2/M phase of cell cycle and exhibited limited mobility.	26846097	2016	Overexpression of the non-coding SOX2OT variants 4 and 7 in lung tumors suggests an oncogenic role in lung cancer.
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	esophageal squamous cell cancer	NA	NA	qPCR, RNAi etc.	ESCC tissues, cell lines (NT2, U-87 MG etc.)	up-regulated	The results of qPCR revealed that SOX2OT-S1 and SOX2OT-S2 were overexpressed in tumor samples of ESCC, compared to their marginal non-tumor tissue counterparts. Furthermore, overexpression of SOX2OT-S2 in tumor samples, similar to SOX2 and OCT4, was statistically significant.	24105929	2014	Two novel splice variants of SOX2OT, SOX2OT-S1, and SOX2OT-S2 are coupregulated with SOX2 and OCT4 in esophageal squamous cell carcinoma.
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	esophageal squamous cell cancer	NA	NA	qPCR, RNAi etc.	ESCC tissues, cell lines (NT2, U-87 MG etc.)	up-regulated	The results of qPCR revealed that SOX2OT-S1 and SOX2OT-S2 were overexpressed in tumor samples of ESCC, compared to their marginal non-tumor tissue counterparts. Furthermore, overexpression of SOX2OT-S2 in tumor samples, similar to SOX2 and OCT4, was statistically significant.	24105929	2014	Two novel splice variants of SOX2OT, SOX2OT-S1, and SOX2OT-S2 are coupregulated with SOX2 and OCT4 in esophageal squamous cell carcinoma.
SOX2OTV7	NA	NA	NA	NA	NA	osteosarcoma	NA	M9180/3	qPCR, Western blot, in vitro knockdown	cell lines (U2OS and SaoS2, U-87 MG )	down-regulated	EGCG targeting LncRNA SOX2OT variant 7 produced synergistic effects with Doxorubicin on osteosarcoma cell growth inhibition. On the one hand, EGCG could reduce the Doxorubicin-induced pro-survival autophagy through decreasing SOX2OT variant 7 to improve the growth inhibition of Doxorubicin. On the other hand, EGCG could partially inactivate Notch3/DLL3 signaling cascade targeting SOX2OT variant 7 to reduce the stemness then abated drug-resistance of osteosarcoma cells.	29475441	2018	SOX2OT variant 7 contributes to the synergistic interaction between EGCG and Doxorubicin to kill osteosarcoma via autophagy and stemness inhibition.
SRA1	SRA1, SRA, SRAP, STRAA1, pp7684	NA	ENSG00000213523	NA	GRCh38_5:140537340-140558252	breast cancer	C50	NA	qPCR etc.	breast cancer tissues	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.
TINCR	TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16	NA	ENSG00000223573	NA	GRCh38_19:5558167-5578349	gastric cancer	C16	NA	qPCR etc.	gastric cancer tissues	differential expression	A allele genotypes of rs8113645 and G allele genotypes of rs2288947 (rs8113645 GA and AA; rs2288947 AG and GG) were also significantly associated with decreased GC risk. Stratification analysis displayed that the correlations between GC risk and variant genotypes of both rs8113645 and rs2288947were more evident in younger individuals, men, nonsmokers, and individuals from rural areas. We also demonstrated that rs8113645 GA+AA genotype carriers had lower TINCR mRNA expression levels compared with common genotype in both normal and GC tissues.	27893425	2016	Tag SNPs of long non-coding RNA TINCR affect the genetic susceptibility to gastric cancer in a Chinese population.
TPM1-AS	NA	111064646	ENSG00000259498	NR_147233	GRCh38_15:63046034-63049387	esophageal cancer	C15	NA	RIP, qPCR, Western blot	cell lines (KYSE140, KYSE150, KYSE180, KYSE450 ,KYSE510, SHEEC)	up-regulated	TPM1-AS overexpression or RBM4 knockdown decreased endogenous exon 2a expression of TPM1, resulting in specifically down-regulation of TPM1variant V2 and V7 in human esophageal cancer cells. overexpression of TPM1-AS inhibited migration and filopodium formation, whereas TPM1variant V2 and V7 promoted these behaviors of human esophageal cancer cells.	28754317	2017	Natural antisense transcript TPM1-AS regulates the alternative splicing of tropomyosin I through an interaction with RNA-binding motif protein 4.
TUG1	TUG1, LINC00080, NCRNA00080, TI-227H	55000	ENSG00000253352	NR_002323	GRCh38_22:30969245-30979395	acute myeloid leukemia	NA	M9861/3	qPCR, Western blot etc.	cell lines (KG-1, MOLM-14, HL-60, NB-4 and THP-1)	up-regulated	LncRNA TUG1 expression was higher in AML patients compared to controls and correlated with higher white blood cell counts, monosomal karyotype, FLT3-ITD mutation, poor-risk stratification, and poor prognosis, which independently predicted worse event-free survival and overall survival. In vitro, lncRNA TUG1 expression was higher in AML cell lines (KG-1, MOLM-14, HL-60, NB-4, and THP-1 cells) compared to controls. LncRNA TUG1 mimic promoted cell proliferation and decreased cell apoptosis rate, while lncRNA TUG1 inhibitor repressed cell proliferation and increased cell apoptosis rate. Rescue experiment showed that AURKA attenuated the influence of lncRNA TUG1 on AML cell proliferation and apoptosis. In conclusion,  lncRNA TUG1 associates with advanced disease and worse prognosis in adult AML patients, and it induces AML cell proliferation and represses cell apoptosis via  targeting AURKA. 	29654398	2018	Long non-coding RNA taurine-upregulated gene 1 correlates with poor prognosis, induces cell proliferation, and represses cell apoptosis via targeting aurora kinase A in adult acute myeloid leukemia.
uc003opf.1	LINC00951, lincRNA-uc003opf.1, FLJ41649	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	qPCR, Luciferase reporter assay, Cell cycle assay, Transient transfection etc.	cell lines (TE-1 and EC9706)	differential expression	Significant differences were found between patients and controls in the genotype frequencies for the rs11752942A>G site in the lincRNA-uc003opf.1 exon. Compared with the rs11752942AA genotype, AG and GG genotypes had a significantly reduced risk of ESCC (adjusted odds ratio = 0.73; 95% confidence interval = 0.63-0.84). Biochemical analysis demonstrated that, when compared with the A allele, the rs11752942G allele could markedly attenuate the level of lincRNA-uc003opf.1 both in vivo and in vitro by binding micro-RNA-149*, thereby affecting cell proliferation and tumor growth.	23872665	2013	A genetic polymorphism in lincRNA-uc003opf.1 is associated with susceptibility to esophageal squamous cell carcinoma in Chinese populations.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	Intraductal Papillary Mucinous Neoplasms of the Pancreas	C25	M8453/0	qPCR etc.	blood	differential expression	We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study.  	28874676	2017	Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	acute myeloid leukemia	NA	M9861/3	RNA-seq, qPCR, RIP, in vitro knockdown etc.	cell lines (K562, CEBPA, CEBPA-P30, K562etc.)	up-regulated	In this study, we identified the oncogenic urothelial carcinoma associated 1 (UCA1) lncRNA as a novel target of the C/EBPa-p30. While wild-type C/EBPa represses, C/EBPa-p30 can induce UCA1 transcription. Notably, we also show that UCA1 expression increases in cytogenetically normal AML cases carrying biallelic CEBPA mutations.Thus, we identified, for the first time, an oncogenic lncRNA functioning in concert with the dominant negative isoform of C/EBPa-p30 in AML.	26053097	2015	C/EBPa-p30 protein induces expression of the oncogenic long non-coding RNA UCA1 in acute myeloid leukemia.
XIST	XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66	7503	ENSG00000229807	NR_001564	GRCh38_X:73820651-73852753	renal collecting duct carcinoma	C64.9	M8319/3	microarray, Western blot etc.	cell lines (AP3, AP8-CDC etc.)	up-regulated	In cell lines created from the tissue of both a male patient and a female patient with collecting duct carcinoma of the kidney, the XIST gene, along with several other chromosome X genes, was found to have an increase in copy number. The results suggest that TOP1 might be one of the molecular targets in AP8 CDC cells. Thus, these novel CDC cell lines will be useful for discovering therapeutic targets and developing effective anticancer drugs against CDC.	19154479	2009	Genetic alterations and chemosensitivity profile in newly established human renal collecting duct carcinoma cell lines.
XIST	XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66	7503	ENSG00000229807	NR_001564	GRCh38_X:73820651-73852753	glioma	NA	M9380/3	qPCR, Western blot, Luciferase assay, RIP etc.	glioma tissues, PTBE tissues.Human glioma cell lines (U251, U373, LN229, U118, LN229)	up-regulated	Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT. XIST/miR-29c may be a potential therapeutic target for glioma treatment.Low XIST expression predicts drug response in PDXs associated with a significant reduction in the breast cancer stem cells population. Kaplan–Meier overall survival curves for 69 patients with glioma classified according to relative XIST expression level.Methylation damage can be reversed by MGMT. In addition, SP1 has been reported to regulate one of the key MMR proteins, MSH6. Recent evidence emphasizes the key regulatory roles of non-coding RNAs (lncRNAs and miRNAs) in tumor biology, including the chemoresistance of cancers.Additionally, the effect of miR-29c mimics or inhibitor on luciferase activity was offset by mutations in XIST.	28831025	2017	LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway.
ZEB1-AS1	NR_024284	220930	ENSG00000237036	NR_024284	GRCh38_10:31206278-31320447	prostate cancer	C61.9	NA	Western blot, Luciferase reporter, RIP	cell lines (PC3, DU145, NCI-H1299, A549, T98G, U251, A375, A875, HUVEC, HBE, SK-MES-1, HeLa, 293, LO2).	up-regulated	Collectively, ZEB1-AS1 functions as an oncogene in prostate cancer via epigenetically activating ZEB1 and indirectly regulating downstream molecules of ZEB1. Also, BMI1 promotes cell survival and attenuated chemosensitivity to docetaxelin prostate cancer. Work in mammalian H3K4 methylation has primarily focused on MLL1, the function of which depends on the participation of the helper proteins WDR5, RBBP5 and ASH2L. The discrepancies above might be explained by different cell lines used in different studies or different splicing variants of ZEB1-AS1.A construct with site-directed mutation of the corresponding seed sequence GTCATAT was prepared by overlapping PCR and designated as pGL3-BMI1-MUT. Dual reporter gene assay was performed as described. 	28830551	2017	Long noncoding RNA ZEB1-AS1 epigenetically regulates the expressions of ZEB1 and downstream molecules in prostate cancer.
ZFAS1	ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1	441951	ENSG00000177410	NR_003604	GRCh38_20:49278178-49295738	non small cell lung cancer	C34	M8046/3	qPCR, etc.	blood	down-regulated	while ZFAS1 level was only correlated with TNM stage (p=0.005 in TEPs, p=0.044 in plasma).  Our data suggested that EGFRvIII can also be detected in blood platelets and there was no difference with detection in plasma.  EGFRvIII RNA existed in both TEPs and plasma, but EGFR intracellular mutations cannot be detected in DNA of TEPs isolated from NSCLC.	29922089	2018	LncRNAs and EGFRvIII sequestered in TEPs enable blood-based NSCLC diagnosis.
ZMAT1	ZMAT1	NA	ENSG00000166432	NA	GRCh38_X:101882288-101932031	gastric cancer	C16	NA	qPCR etc.	gastric cancer tissues	down-regulated	We found for the first time that the lncRNA ZMAT1 transcript variant 2 is downregulated in gastric cancer tissues compared with adjacent normal tissues. The expression of ZMAT1 transcript variant 2 was inversely correlated with lymph node metastasis, depth of tumor invasion and tumor node metastasis stage. Univariate and multivariate analyses showed that ZMAT1 transcript variant 2 expression was an independent predictor for overall survival	26191264	2015	Downregulation of long noncoding RNA ZMAT1 transcript variant 2 predicts a poor prognosis in patients with gastric cancer
ZNRD1-AS1	ZNRD1ASP, C6orf12, HCG8, HCGVIII, HCGVIII-1, HTEX4, NCRNA00171, TCTEX4, ZNRD1-AS, ZNRD1-AS1, ZNRD1AS, ZNRD1AS1	NA	NA	NA	NA	lung cancer	C34	NA	qPCR, Genotyping etc.	blood	down-regulated	we first evaluated the expression ZNRD1-AS1 and ZNRD1 among lung cancer tissues and corresponding normal tissues, which showed higher expression of ZNRD1-AS1 and lower expression of ZNRD1. To reveal the underlying mechanisms, we then investigated the associations between ZNRD1 eQTLs SNPs in ZNRD1-AS1 and risk of lung cancer in Han Chinese populations. G allele of SNP rs9261204 was significantly associated with an increased risk of lung cancer when compared with A allele. A weaker, but similar effect was also observed in bladder cancer. SNP rs3757328 was also associated with increased risk of lung cancer.	27166266	2016	Strong evidence for LncRNA ZNRD1-AS1, and its functional Cis-eQTL locus contributing more to the susceptibility of lung cancer