Anti-proliferation effects of trifolirhizin on MKN45 cells and possible mechanism.

Trifolirhizin is a compound isolated from Sophora flavescens. It has been shown to exert cytotoxicity on several cancer cell lines. However, the underlying mechanism remains unknown. MKN45 cells were used as a research model. We assessed the cytotoxicity of trifolirhizin to MKN45 by MTT. Hoechst staining and TUNEL method were used to demonstrate apoptosis. Flow cytometry was used to determine cell cycle and ratio of apoptosis. Caspase activity assay was used to examine the activation of caspase cascade pathways. Western blotting was used to explore the protein levels. Consistently, trifolirhizin inhibited MKN45 xenograft tumor growth in vivo. Trifolirhizin caused a significantly decreased proliferation of MKN45 cells in a time- and dose-dependent manner, with IC50 values of 33.27±2.06 µg/ml at 48 h. Western blot assay manifested that trifolirhizin activated the EGFR-MAPK signaling pathways. This study indicated that trifolirhizin may be a therapeutic application in human gastric cancer therapy.