FH535 inhibits the proliferation of HepG2 cells via downregulation of the Wnt/β-catenin signaling pathway

Hepatocellular carcinoma (HCC) is a primary cancer of the liver. Target therapy may improve prognosis of HCC. In the present study, we evaluated the inhibition of the Wnt/beta-catenin pathway as a potential therapeutic approach. HepG2 cells were treated with the beta-catenin inhibitor FH535. beta-catenin protein expression was semi-quantitatively assessed using western blot analysis. Cell proliferation was examined with a 3-(4,5-dimethyl-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt (MTS) assay. The mRNA expression of nitric oxide synthase (iNOS) was detected by reverse transcription polymerase chain reaction. The Griess assay was used to determine nitric oxide (NO) concentration. FH535 inhibited the proliferation of HepG2 cells and decreased beta-catenin protein expression. mRNA expression of iNOS, a target gene of the Wnt/beta-catenin pathway, was decreased in FH535-treated HepG2 cells compared to the control group. NO production was also reduced by FH535. In conclusion, the beta-catenin inhibitor FH535 may inhibit HCC cell proliferation via downregulation of the Wnt/beta-catenin pathway. Thus, targeting this pathway may be useful in HCC therapy.