Open AccessMicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1
Author(s) -
Tinghui Jiang,
Mengfan Li,
Qiuyin Li,
Zhiqiang Guo,
Xianjun Sun,
Xufeng Zhang,
Yan Liu,
Wenyi Yao,
Ping Xiao
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504016x14821952695683
Subject(s) - microrna , apoptosis , cell growth , downregulation and upregulation , cell cycle , cancer research , hepatocellular carcinoma , cell , cell culture , metastasis , biology , medicine , cancer , gene , biochemistry , genetics
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.