MicroRNA‐761 is upregulated in hepatocellular carcinoma and regulates tumorigenesis by targeting Mitofusin‐2

• DOI: 10.1111/cas.12904
• Publication Date: 2016-02-04T16:43:09Z
• Authors: Xiaohu Zhou; Linshi Zhang; Bichun Zheng; Yingcai Yan; Yuan Zhang; Haiyang Xie; Lin Zhou; Shusen Zheng; Weilin Wang
• Keywords: 0303 health sciences; Carcinoma, Hepatocellular; Carcinogenesis; Liver Neoplasms; Apoptosis; Original Articles; Hep G2 Cells; GTP Phosphohydrolases; Mitochondria; 3. Good health; Gene Expression Regulation, Neoplastic; Mitochondrial Proteins; MicroRNAs; 03 medical and health sciences; Humans; Cell Proliferation

Hepatocellular carcinoma (HCC) is the sixth most prevalent cancer and the third leading cause of cancer‐related deaths worldwide. The fate of a cell is determined by the balance between the processes of fission and fusion that constantly occur in the mitochondria of cells. We previously showed that overexpression of Mitofusin‐2 can induce apoptosis in HCC cells by triggering an influx of Ca2+ into the mitochondria from the ER. The function of Mitofusin‐2 has been studied extensively, but the mechanism underlying the post‐transcriptional regulation of Mitofusin‐2 has not been elucidated. In the present study, we aimed to identify the mechanism of Mitofusin‐2 regulation in HCC. We demonstrated that Mitofusin‐2 is a direct target of miR‐761, which was found to be upregulated in HCC tissues. Furthermore, a miR‐761 inhibitor impaired mitochondrial function by upregulating Mitofusin‐2 and effectively repressed tumor growth and metastasis both in vivo and in vitro. Our findings provide new insight into the mechanism underlying Mitofusin‐2 regulation and the potential role of miR‐761 in HCC, making it a potential candidate for use in HCC therapy in the future.