摘要Background:MicroRNAs (miRNAs) function as essential posttranscriptional modulators ofgene expression,and are involved in a wide range of physiologic and pathologic states,including cancer.Numerous miRNAs are deregulated in hepatocellular carcinoma (HCC).This study aimed to investigate the role of miR-27a in the development of HCC.Methods:The expression of MiR-27a was measured by quantitative real-time polymerase chain reaction (qRT-PCR).3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to examine changes in the viability of HepG2,Bel-7402,Bel-7404 hepatoma cell lines associated with up-regulation or down-regulation of miR-27a.A dual-luciferase activity assay was used to verify a target gene of miR-27a.Immunohistochemistry,qRT-PCR,Western blotting analysis,and cell cycle and apoptosis flow cytometric assays were used to elucidate the mechanism by which miR-27a modulates liver cancer cell proliferation.Results:The expression of miR-27a was significantly increased in HCC tissues and HepG2,Bel-7402,Bel-7404 hepatoma cell lines (P ＜ 0.05).We also found that the down-regulation of miR-27a in HepG2 cells dramatically inhibited proliferation,blocked the G1 to S cell cycle transition and induced apoptosis (P ＜ 0.05).In addition,miR-27a directly targeted the 3'-untranslated region of peroxisome proliferator-activated receptor γ (PPAR-γ),and ectopic miR-27a expression suppressed PPAR-γ expression on the mRNA and protein levels.The rosiglitazone-induced overexpression of PPAR-γ attenuated the effect of miR-27a in HCC cells.Conclusions:Our findings suggested that miRNA-27a promoted HCC cell proliferation by regulating PPAR-γ expression.MiR-27a may provide a potential therapeutic strategy for HCC treatment.