| Literature DB >> 28231734 |
Yichao Mo1, Yaoyong Lu2, Peng Wang3, Simin Huang4, Longguang He1, Dasheng Li1, Fuliang Li1, Junwei Huang1, Xiaoxia Lin1, Xueru Li5, Siyao Che1, Qinshou Chen1.
Abstract
Abnormal expression of long non-coding RNA often contributes to unrestricted growth of cancer cells. Long non-coding RNA XIST expression is upregulated in several cancers; however, its modulatory mechanisms have not been reported in hepatocellular carcinoma. In this study, we found that XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p. We proposed that XIST was responsible for hepatocellular carcinoma cell proliferation, and XIST exerted its function through the miR-139-5p/PDK1 axis.Entities:
Keywords: PDK1; XIST; hepatocellular carcinoma; miR-139-5p
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Year: 2017 PMID: 28231734 DOI: 10.1177/1010428317690999
Source DB: PubMed Journal: Tumour Biol ISSN: 1010-4283