Aberrant expression of miR-511 is involved in the development of cancer,but the role of miR-511 in hepatocellular carcinoma (HCC) is not well documented.In this study,we explored the molecular mechanisms of miR-511 in hepatocarcinogenesis.Our results of bioinformatics analysis suggested that B cell translocation gene 1 (BTG1),a member of anti-proliferative gene family,was one of the putative targets of miR-511.The expression levels of miR-511 were significantly higher in 30 clinical HCC tissues than in corresponding peritumor tissues,and were negatively correlated with those of BTG1 in the HCC tissues (r=-0.6105,P＜O.01).In human hepatoma cell lines HepG2 and H7402,overexpression of miR-511 dose-dependently inhibited the expression of BTG1,whereas knockdown of miR-511 dose-dependently increased the expression of BTG1.Luciferase reporter gene assays verified that miR-511 targeted the 3’UTR of BTG1 mRNA.In the hepatoma cells,overexpression of miR-511 significantly decreased BTG1-induced G1 phase arrest,which was rescued by overexpression of BTG1.Furthermore,overexpression of miR-511 promoted the proliferation of the hepatoma cells,which was rescued by overexpression of BTG1.Conversely,knockdown of miR-511 inhibited cell proliferation,which was reversed by knockdown of BTG1.In conclusion,miR-511 promotes the proliferation of human hepatoma cells in vitro by targeting the 3’UTR of BTG1 mRNA.