Low miR-29c expression is a prognostic marker in hepatocellular carcinoma.

A previous study has revealed that miR-29c functions as a tumor suppressor in hepatocellular carcinoma (HCC), but the clinical significance and prognostic value of miR-29c in HCC have not been investigated. Paired human HCC tissues and adjacent noncancerous tissues were obtained from 91 patients, between 2008 to 2014. Quantitative real-time PCR (qRT-PCR) was used to analyze miR-29c expression. Kaplan-Meier survival plots and log-rank tests were used to assess differences in the overall survival of different subgroups of HCC patients. It was observed that miR-29c expression was remarkably decreased in HCC tissues relative to that in normal hepatic tissues (P < 0.001). The low miR-29c level was significantly associated with histologic grade (P = 0.001), microvascular invasion (P = 0.005), and tumor stage (P < 0.001). Kaplan-Meier analysis showed that decreased miR-29c expression correlated with shorter overall survival (P = 0.002). Multivariate Cox regression analysis showed that decreased miR-29c expression (hazard ratio = 2.19, 95%CI = 1.361-6.779, P = 0.025) was independently associated with poor survival in HCC. Our findings demonstrate that miR-29c expression is significantly downregulated in HCC patients and that miR-29c can act as an independent predictor of unfavorable clinical outcome.

microRNA15b induced SMCC7721 apoptosis via down-regulation of XIAP.

OBJECTIVE: microRNA can regulate cell growth, proliferation, and death; also, it can promote or inhibit cell growth and proliferation through regulation of apoptotic proteins. XIAP is a newly discovered pro-apoptotic protein, but how is XIAP regulated remains unclear. This study investigated the role of microRNA-15b in liver cancer cells' proliferation and apoptosis. MATERIALS AND METHODS: microRNA15b and control microRNA (miRNA) were purchased and transfected with hepatoma SMCC7721 cells using liposomal transfection techniques. MTT assay, caspase-3 activity assay, and flow cytometry were used to investigate the effects of micorRNA-15b on growth, proliferation, and apoptosis of SMCC7721 cells. SiRNA of XIAP and control siRNA were purchased and transfected into SMCC7721 cells. microRNA15b and control microRNA were then transfected into siRNA of XIAP or control siRNA transfected SMCC7721 cells. Western blot analysis was used to detect the expression levels of XIAP and apoptotic proteins. XIAP plasmid and control vector were purchased and transfected into SMCC7721 cells followed by transfection of microRNA15b and control microRNA. Expression levels of XIAP and apoptosis of SMCC7721 cells were analyzed. RESULTS: Transfection of microRNA15b reduced the growth of SMCC7721 cells, increased phosphatidylserine eversion, activated caspase-3, and decreased the expression levels of XIAP. Silence of XIAP enhanced microRNA15b-induced apoptosis of SMCC7721 cells. Overexpression of XIAP inhibited microRNA15b-induced apoptosis of SMCC7721 cells. microRNA15b inhibited the growth of SMCC7721 cells. CONCLUSIONS: microRNA15b induced apoptosis of SMCC7721 cells via down-regulation of XIAP.