The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma
Oncogene, ISSN: 1476-5594, Vol: 36, Issue: 8, Page: 1112-1122
2017
- 160Citations
- 35Captures
- 3Mentions
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- Citations160
- Citation Indexes160
- 160
- CrossRef115
- Captures35
- Readers35
- 35
- Mentions3
- References2
- Wikipedia2
- News Mentions1
- News1
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The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma
DOI Not Found 10.1038/onc.2016.278 This DOI cannot be found in the DOI System. Possible reasons are: The DOI is incorrect in your source. Search for
Article Description
The expression of long non-coding RNAs (lncRNAs) is dysregulated in hepatocellular carcinoma (HCC). However, the functions and contributions of lncRNAs remain largely unknown. Here, we identified a critical role of SNHG6-003 in HCC. We found that five SNHG6 transcripts were differentially expressed in HCC tissues while only the SNHG6-003 had an oncogenic function. Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis. Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge The expression of long non-coding RNAs (lncRNAs) is dysregulated in hepatocellular carcinoma (HCC). However, the functions and for miR-26a/b and thereby modulating the expression of transforming growth factor-β-activated kinase 1 (TAK1). Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern. In HCC patients, high expression of SNHG6-003 closely correlated with tumor progression and shorter survival. Thus, targeting the ceRNA network involving SNHG6-003 may be used as a treatment strategy against HCC.
Bibliographic Details
Springer Science and Business Media LLC
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