Epigenetically silenced long noncoding-SRHC promotes proliferation of hepatocellular carcinoma

Zheng, Hao; Yang, Siwei; Yuan, Yuan; Yuan, Shengxian; Wu, Fengyuan; Wang, Lili; Yan, Hongli; Sun, Shuhan; Zhou, Weiping

doi:10.1007/s00432-014-1871-4

Cited by 33 publications

(28 citation statements)

References 32 publications

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“…Aberrant hypermethylation of specific CpG islands can lead to the silencing of tumor suppressor genes involved in key cellular pathways [17]. Promoter hypermethylation may be partly responsible for the downregulation of some lncRNAs including MEG3, H19, SRHC and CAHM in carcinoma [18][19][20][21]. To gain insight into the expression profile of lncRNA in GCA, we investigated the microarray expression profile of lncRNA transcriptome in 5 GCA tissues and 5 paired corresponding normal tissues.…”

Section: Introductionmentioning

confidence: 99%

Methylation-mediated downregulation of long noncoding RNA LOC100130476 in gastric cardia adenocarcinoma

Guo

Zhao

Ya-bin

et al. 2016

Clin Exp Metastasis

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Accumulating evidences indicate that long non-coding RNAs (lncRNAs) play important roles in several biological processes and dysregulated lncRNAs are involved in different kinds of cancer and are associated with carcinogenesis, metastasis, and prognosis of cancer. The role of a new lncRNA LOC100130476 in gastric cardia adenocarcinoma (GCA) has remained unknown. The present study investigated the role and methylation status of LOC100130476 in the pathogenesis of GCA, and further evaluated the potential prognostic role of LOC100130476 in GCA. Significant downregulation of LOC100130476 was detected in SGC-7901 and BGC-823 cell lines and primary GCA tissues. Methylation frequency of LOC100130476 was gradually increased from exon 1 to exon 2 both in tumor tissues and corresponding normal tissues; however, methylation status of region 1 closing to the transcription start site was more tumor-specific among the three regions examined. The findings of the association between LOC100130476 expression, methylation and TNM stage, pathological differentiation, and GCA patients' survival further identified the role of LOC100130476 as a tumor suppressor gene. Furthermore, the hypermethylation of LOC100130476 was also detected in peripheral white blood cells of GCA cases. Thus, LOC100130476 may be act as a tumor suppressor gene in GCA carcinogenesis and aberrant methylation at the CpG sites near the transcription start site within exon 1 may be critical for gene silencing. In addition, aberrant methylation of LOC100130476 in peripheral white blood cells and GCA tissues may be used as a potential valuable biomarker in GCA diagnosis and prognosis.

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Section: Introductionmentioning

confidence: 99%

Methylation-mediated downregulation of long noncoding RNA LOC100130476 in gastric cardia adenocarcinoma

Guo

Zhao

Ya-bin

et al. 2016

Clin Exp Metastasis

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“…Zheng et al found that inhibition of lncRNA SRHC could promote the proliferation of HCC cells and was significantly correlated with a high serum a-fetoprotein level and a low degree of differentiated tumors. Mechanistic analysis of the SRHC downregulation indicated that the promoter region of SRHC contains a CpG-rich island and SRHC is down-regulated in tumors by DNA methylation, suggesting lncRNA might be crucial in methylation-modified phenotype of HCC [63]. LncRNA-MEG3 (maternally expressed gene 3) was down-regulated in HCC and acted as a tumor suppressor for both anchorage-dependent and -independent cell growth.…”

Section: Long Noncoding Rna and Dna Methylationmentioning

confidence: 99%

Long noncoding RNA, the methylation of genomic elements and their emerging crosstalk in hepatocellular carcinoma

Yuan

Zhang

et al. 2016

Cancer Letters

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“…It is known that lncRNAs can promote or suppress cell death pathways through diverse molecular mechanisms including epigenetically silencing (Zheng et al, 2014), acting as sponge or precurors for miRNAs , activating or inhibiting signal molecules and interacting with protiens or nucleic acids in various cell types. For example, recently one lncRNA named PANDAR (promoter of CDKN1A antisence DNA damage-activated RNA) is reported to interacts with the transcription factor NF-YA to limit the expression of pro-apoptotic genes in lung cancer cell lines.…”

Section: Lncrnas and Cell Deathmentioning

confidence: 99%

Long Non-coding RNAs and Drug Resistance

Pan

Xie²,

Xu³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Background: Long non-coding RNAs (lncRNAs) are emerging as key players in gene expression that govern cell developmental processes, and thus contributing to diseases, especially cancers. Many studies have suggested that aberrant expression of lncRNAs is responsible for drug resistance, a substantial obstacle for cancer therapy. Drug resistance not only results from individual variations in patients, but also from genetic and epigenetic differences in tumors. It is reported that drug resistance is tightly modulated by lncRNAs which change the stability and translation of mRNAs encoding factors involved in cell survival, proliferation, and drug metabolism. In this review, we summarize recent advances in research on lncRNAs associated with drug resistance and underlying molecular or cellular mechanisms, which may contribute helpful approaches for the development of new therapeutic strategies to overcome treatment failure.

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Epigenetically silenced long noncoding-SRHC promotes proliferation of hepatocellular carcinoma

Abstract: Here, we identified a new long noncoding RNA designated as SRHC that is capable of inhibiting cancer proliferation and is down-regulated in tumors at least partly by DNA methylation.

Cited by 33 publications

References 32 publications

Methylation-mediated downregulation of long noncoding RNA LOC100130476 in gastric cardia adenocarcinoma

Methylation-mediated downregulation of long noncoding RNA LOC100130476 in gastric cardia adenocarcinoma

Long noncoding RNA, the methylation of genomic elements and their emerging crosstalk in hepatocellular carcinoma

Long Non-coding RNAs and Drug Resistance

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