Mo Yichao, Lu Yaoyong, Wang Peng, Huang Simin, He Longguang, Li Dasheng, Li Fuliang, Huang Junwei, Lin Xiaoxia, Li Xueru, Che Siyao, Chen Qinshou
1 Department of Hepatobiliary Surgery, Gaozhou People's Hospital, Gaozhou, China.
2 Department of Radiation Oncology, Gaozhou People's Hospital, Gaozhou, China.
Tumour Biol. 2017 Feb;39(2):1010428317690999. doi: 10.1177/1010428317690999.
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.
长链非编码RNA的异常表达常常促使癌细胞无节制地生长。长链非编码RNA XIST的表达在几种癌症中上调；然而，其调控机制在肝细胞癌中尚未见报道。在本研究中，我们发现XIST在肝细胞癌组织和细胞系中表达显著增加。XIST促进细胞周期从G1期进展到S期，并保护细胞免于凋亡，这有助于肝细胞癌细胞生长。此外，我们揭示XIST与miR-139-5p之间存在相互抑制。PDK1被鉴定为miR-139-5p的直接靶标。我们提出XIST负责肝细胞癌细胞增殖，且XIST通过miR-139-5p/PDK1轴发挥其功能。
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