MicroRNA-98-5p inhibits cell proliferation and induces cell apoptosis in hepatocellular carcinoma via targeting IGF2BP1.

Jiang T, Li M, Li Q et al.

Key Laboratory of Nanobiological Technology, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Oncology research. Dec 2016.

Some microRNAs (miRs) have been demonstrated to play promoting or tumor suppressive roles in the development and progression of hepatocellular carcinoma (HCC). However, the regulatory mechanism of miR-98-5p in HCC still remains largely unclear. In the present study, our data showed that miR-98-5p was significantly downregulated in 84 cases of HCC tissues compared to the matched adjacent non-tumor tissues. Besides, downregulation of miR-98-5p was associated with tumor size, portal vein tumor embolus, node metastasis, and clinical stage in HCC. HCC patients with low expression of miR-98-5p showed shorter survival time compared with those with high miR-98-5p levels. Moreover, the expression of miR-98-5p was also reduced in HCC cell lines (HepG2, Hep3B, LM3 and SMCC7721) compared to normal liver cell line THLE-3. Overexpression of miR-98-5p significantly decreased LM3 cell growth through inducing cell cycle arrest at G1 stage and cell apoptosis. Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was then identified as a novel target gene of miR-98-5p, and its protein expression was negatively regulated by miR-98-5p in LM3 cells. Overexpression of IGF2BP1 eliminated the effects of miR-98-5p overexpression on the proliferation, cell cycle, and apoptosis of LM3 cells. Finally, we found that IGF2BP1 was upregulated in HCC, and its expression was negatively correlated to the miR-98-5p levels. In summary, we demonstrate that miR-98-5p could inhibit HCC cell proliferation while induce cell apoptosis, partly at least, via inhibition of its target gene IGF2BP1, and suggest that miR-98-5p may become a promising therapeutic candidate for HCC treatment.


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