Objective:To explore the role of miR-214 in the progression of hepatocellular carcinoma(HCC) and its inhibitory mechanisms in depressing the signaling pathway of j3-catenin.this study was conducted.Methods:We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2.Differences between the two cell lines were compared in cell growth,proliferation,colony forming ability and cell cycles.RT-PCR method was applied for the quantification of β-catenin mRNA expression.Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets(ie.Cyclin D1,c-Myc and TCF-1).The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression.Results:In comparison with negative(Lv-control-HepG2) and blank(HepG2) control,a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48~72h of cell culture experiments(P<0.05).The miR-214 treatment resulted in a colony forming efficiency of(23.28±3.26)%,which was significantly lower than that of negative control[(51.31±3.97)%](P<0.05).According to FCM results,the experimental group,compared with control,showed a higher proportion of cells in G_0/G_1 phase[(70.32±3.12)%]but a lower proportion in S phase[(18.42±2.90)%](P<0.05).The MTT assay demonstrated a significant inhibition of the proliferation and β-catenin expression of HCC cells compared with control(P<0.05).while no significant difference was observed after HCC cells being transfected withβ-catenin overexpression plasmid(P>0.05).By comparing to the RT-PCR and Western-blot results of control,the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression(P>0.05).but an extremely inhibition in the protein level of β-catenin and its downstream targets Cyclin Dl,c-Myc.and TCF-1(P<0.05).Conclusions:miR-214 functions as a suppressor during the progression of HCC,and its inhibitory role was achieved by downregulating β-catenin signaling pathway. Objective: To explore the role of miR-214 in the progression of hepatocellular carcinoma (HCC) and its inhibitory mechanisms in depressing the signaling pathway of j3-catenin. This study was conducted. Methods: We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2.Differences between the two cell lines were compared in cell growth, proliferation, colony forming ability and cell cycles. RT-PCR method was applied for the quantification of β-catenin mRNA expression. Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets (ie. Cyclin D1, c-Myc and TCF-1). The effect of miR- was further explored through RNA interference and restoring of miR-214 expression. Results: a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48 (Lv-control-HepG2) and blank ~ 72h of cell culture experiments (P <0.05 ). The miR-214 treatment resulted in a colony forming efficiency of (23.28 ± 3.26)%, which was significantly lower than that of negative control [(51.31 ± 3.97)%] (P <0.05) experimental group, compared with control, showed a higher proportion of cells in G_0 / G_1phase [(70.32 ± 3.12)%] but a lower proportion in S phase [(18.42 ± 2.90)%] (P <0.05) demonstrated a significant inhibition of the proliferation and β-catenin expression of HCC cells compared with control (P <0.05) .while no significant difference was observed after HCC cells were transfected with β-catenin overexpression plasmid (P> 0.05) .By comparing to the RT-PCR and Western-blot results of control, the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression (P> 0.05) .but an extremely inhibition in the protein level of β-catenin and its lower targets Cyclin Dl, c-Myc.and TCF-1 (P <0.05) .Conclusions: miR-214 functions as a suppressor during the progression of HCC, and its inhibitory role wasachieved by downregulating β-catenin signaling pathway.