J Cancer 2018; 9(17):3006-3015. doi:10.7150/jca.25956 This issue Cite
Research Paper
1. Ningxia Medical University, Clinical Medicine College, Yinchuan, 750004, China
2. The General Hospital of Ningxia Medical University, Department of Beijing National Biochip Research Center Sub-Center in Ningxia, Yinchuan, 750004, China
3. Qingdao Municipal Hospital, Department of stomatology, Qingdao, 266071, China
4. The Affiliated Hospital of Qingdao University, Medical Animal Lab, Qingdao, 266003, China
5. The General Hospital of Ningxia Medical University, Yinchuan, 750004, China
* These authors have contributed equally to this work
MicroRNAs (miRNAs) being proved to be involved in the carcinogenesis of numerous tumors. MicroRNA-124 (miR-124), identified as a tumor suppressor, has been demonstrated to exert pivotal roles in multiple processes of tumorigenesis. The present study demonstrated that miR-124 was low-expressed in human hepatocellular carcinoma (HCC) tissues and cell lines. In addition, overexpression of miR-124 through infected with miR-124 lentivirus inhibited the proliferation and migration of HCC in vitro and tumorigenesis in vivo, whereas inhibition of miR-124 expression can reverse the process. Moreover, Baculoviral IAP Repeat Containing 3 (BIRC3) was identified as a target gene of miR-124. The BIRC3 mRNA expression was increased in HCC tissues and negatively correlated with miR-124 expression. Knockdown of BIRC3 recovered the miR-124-induced inhibiting effect on HCC progression. Furthermore, we found that up-regulation of miR-124 significantly inhibited p-P65, p-IκBα and c-Myc proteins expression. However, the effect of miR-124 up-regulation on HCC development was partly reversed by BIRC3 restoration. In conclusion, our data proved that miR-124 inhibits the proliferation and migration of HCC at least partly through targeting BIRC3 and regulating NF-κB signaling pathway, and it may be a therapeutic target for HCC prognosis.
Keywords: miR-124, BIRC3, Hepatocellular carcinoma, migration, NF-κB signal pathway