Open Access

ARTICLE

MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1

Tinghui Jiang^*, Mengfan Li^†, Qiuyin Li^‡, Zhiqiang Guo^§, Xianjun Sun^‡, Xufeng Zhang^§, Yan Liu^‡, Wenyi Yao^‡, Ping Xiao^*

* Key Laboratory of Nanobiological Technology, Xiangya Hospital of Central South University, Changsha, Hunan, P.R. China
† Department of Vascular Surgery, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China
‡ Department of Interventional Radiology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China
§ Department of Thoracic Surgery, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China

Oncology Research 2017, 25(7), 1117-1127. https://doi.org/10.3727/096504016X14821952695683

Abstract

Some microRNAs (miRs) have been demonstrated to play promoting or tumor-suppressing 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 nontumor tissues. In addition, 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 a 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 the normal liver cell line THLE-3. Overexpression of miR-98-5p significantly decreased LM3 cell growth by inducing cell cycle arrest at the 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 miR-98-5p levels. In summary, we demonstrate that miR-98-5p could inhibit HCC cell proliferation while inducing cell apoptosis, partly at least, via inhibition of its target gene IGF2BP1, and we suggest that miR-98-5p may become a promising therapeutic candidate for HCC treatment.

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