Fangchinoline induces cell apoptosis via the mitochondrial apoptotic pathway in gastric cancer cells

The aim of this study was to explore the effect of fangchinoline (FCL), a bioactive compound derived from traditional Chinese herb Stephaniatetrandra S. Moore (Fen Fang Ji), on the proliferation of gastric cancer cells, and to define the related mechanisms. MTT assay, PI staining/flow cytometry, Annexin V-PI staining and western blot assays were conducted to validate the effect of FCL in gastric cancer cells. Our data demonstrated that FCL significantly inhibited cell growth of human gastric cancer HGC-27 and SGC-7901 cells and stimulated cell cycle arrest at G0/G1 phase. Furthermore, FCL induced cell apoptosis in gastric cancer HGC-27 and SGC-7901 cells, and apoptosis induced by FCL was reversed by total caspase inhibitor Z-VAD-FMK or caspase 3 inhibitor Ac-DEVD-CHO. The following western blotting results indicated that FCL down-regulated the expression of Bcl-2, caspase 3, upregulated the expression of Bax, cleaved caspase 3 and stimulated the release of cytochrome C from mitochondria into cell cytoplasm in gastric cancer cells. In addition, incubating gastric cancer cells with FCL resulted in the suppression of pAkt and pNF-kB. Collectively, these results suggest that FCL promotes apoptosis in gastric cancer cells via inhibition of mitochondrial capacity.