@Article{096504016X14821952695683,
AUTHOR = {Tinghui Jiang, Mengfan Li, Qiuyin Li, Zhiqiang Guo, Xianjun Sun, Xufeng Zhang, Yan Liu, Wenyi Yao, Ping Xiao},
TITLE = {MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis  in Hepatocellular Carcinoma via Targeting IGF2BP1},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {7},
PAGES = {1117--1127},
URL = {http://www.techscience.com/or/v25n7/56894},
ISSN = {1555-3906},
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 G<sub>1</sub>
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.},
DOI = {10.3727/096504016X14821952695683}
}