Open Access

ARTICLE

MicroRNA-374a Promotes Hepatocellular Carcinoma Cell Proliferation by Targeting Mitogen-Inducible Gene 6 (MIG-6)

Hui Li^*1, Huicheng Chen^†1, Haibin Wang^‡, Yilong Dong^†, Min Yin^†, Liang Zhang^§, Jia Wei^*

* Department of Liver and Infectious Diseases, Liver Disease Research Center, The Second People’s Hospital of Yunnan Province, Kunming, P.R. China
† School of Medicine, Yunnan University, Kunming, P.R. China
‡ The Second Department of Liver Diseases, The Third People’s Hospital of Kunming City, Kunming, P.R. China
§ Liver Disease Research Center, The Second People’s Hospital of Yunnan Province, Kunming, P.R. China

Oncology Research 2018, 26(4), 557-563. https://doi.org/10.3727/096504017X15000784459799

Abstract

Hepatocellular carcinoma (HCC) is a disease with poor prognosis rates and ineffective therapeutic options. Previous studies have reported the involvement of mitogen-inducible gene 6 (MIG-6) as a negative regulator in tumor formation. MicroRNAs (miRNAs) play crucial roles in the development of different types of cancer. However, the underlying mechanisms of miRNAs in HCC are poorly understood. This study was aimed to investigate the role of miR-374a in HCC and its role in the regulation of expression of MIG-6. The results showed that MIG-6 overexpression significantly inhibited cell viability of HepG2 cells after 4 days posttransfection. Moreover, MIG-6 was a direct target of miR-374a, and the expression of MIG-6 was remarkably downregulated by the overexpression of miR-374a in HepG2 cells. Furthermore, we found that overexpression of miR-374a promoted cell viability; however, the protective effect was abolished by MIG-6 overexpression. In addition, overexpression of miR-374a activated the EGFR and AKT/ERK signaling pathways by regulation of MIG-6. Our findings suggest that miR-374a could promote cell viability by targeting MIG-6 and activating the EGFR and AKT/ERK signaling pathways. These data provide a promising therapeutic strategy for HCC treatment.

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