Expression And Functional Study Of MicroRNA-122 In Hepatocellular Carcinoma

'Objective:To investigate the expression level of microRNA-122 (miR-122) in hepatocellular carcinoma(HCC) tissues and cell lines, analysis the potential relationship between miR-122 expression and clinicopathologic parameters in HCC patients, explore the biological functions of miR-122 and provide a basis for the targeting treatment of HCC.Methods:The expression level of miR-122 in hepatocellular carcinoma tissues and cell lines were quantified by using TaqMan MicroRNA Assays-based real-time RT-PCR. The correlations of clinicalpathologic parameters with the miR-122 expression level in cancerous tissues were analyzed by using independent-Samples T Test respectively. MiR-122 Agomir was transfected into HepG2 hepatocellular carcinoma cell to overexpress miR-122. The effect of over-expression miR-122 on HepG2 cell proliferation and apoptosis were evaluated by using CCK-8 kit and flow cytometer respectively. All the data were expressed as means±SD and analyzed by using SPSS 16.0 for Windows. Student t and ANOVA were used to compare the differences between corresponding groups. P<0.05 was regarded as statistically significant.Results:The expression level of miR-122 in HCC tissues was significantly decreased than the expression in paracancerou tissues (P<0.01). Compared to Chang liver cell, the expression level of miR-122 was significantly decreased in all HCC cell lines except for Huh-7 (P<0.01). The highly metastatic variant, MHCC97-H and HCCLM3 had a lower miR-122 expression than the low metastatic potential variant, MHCC97-L (P< 0.01). The expression level of miR-122 was significantly correlated with the HCC differentiation grade (P<0.01). However, no significant correlation was observed between other clinicalpathologic parameters and the expression level of miR-122 in HCC patients respectively (P>0.05). In vitro experiment, over-expression of miR-122 significantly inhibited the proliferation(P<0.01), and prbmoted the apoptosis of HepG2 cell (P<0.01), compared to the HepG2-negative group and the HepG2-control group cells.Conclusions:The expression level of miR-122 was significantly down-regulated in HCC tissues and cell lines, and its down-regulation was correlated with poor differentiation of hepatocellular carcinoma. Over expression of miR-122 could inhibit HepG2 cell growth and promote the cell apoptosis.