Hydrogen sulfide suppresses H 2 O 2 -induced proliferation and migration of HepG2 cells through Wnt/β-catenin signaling pathway.

Both H 2 S and H 2 O 2 affect many cellular events, such as cell differentiation, cell proliferation and cell death. However, there is some controversy about the roles of H 2 S and H 2 O 2, since the detailed mechanisms they are involved remain unclear. In this study, low concentration of H 2 O 2 (40 μM) increased the viability of hepatocellular carcinoma cells HepG2, while both H 2 S and high concentration of H 2 O 2 decreased the cell viability in a dose-dependent manner. Wound healing assay indicated that 40 μM H 2 O 2 promoted migration of HepG2 cells, which was suppressed by exogenous H 2 S. Further analysis revealed that administration of exogenous H 2 S and H 2 O 2 changed the redox status of Wnt3a in HepG2 cells. Altered expression of proteins including Cyclin D1, TCF-4, and MMP7, which are downstream of the Wnt3a/β-catenin signaling pathway, were found after treatment with exogenous H 2 S and H 2 O 2 . Compared with H 2 S, low concentration of H 2 O 2 showed opposite effects on these protein expression levels in HepG2 cells. These results suggest that H 2 S suppressed H 2 O 2 -induced proliferation and migration of HepG2 through regulating Wnt3a/β-catenin signaling pathway.