Induction of Solasonine on Apoptosis of Human Breast Cancer Bcap-37 Cells through Mitochondria-Mediated Pathway

ObjectiveTo study the in vitro antiproliferative effect and probable mechanism of solasonine on human breast cancer Bcap-37 cells, meanwhile, make comparison with solamargine.MethodsThe cytotoxicity was evaluated by MTT assay. The cell damage and type of cell death were examined through Hoechst33342/PI and Annexin V/PI staining, respectively. Mitochondrial membrane potential was detected by JC-1 staining. The expression of Bcl-2, Bcl-xL, Bax, and cytochrome c was determined by immunoblot method, and the activation of caspase-3 was analyzed by immunocytochemistry method.ResultsSolasonine showed the different extents of cytotoxicity on eight human tumor cell lines as well as four human normal cell lines, and the IC50 values of solasonine ranged from 12.73 to 37.15 μmol/L. Cell apoptosis and mitochondria depolarization were observed in Bcap-37 cells after treatment with solasonine for 24 h, respectively. In immunoblot and immunocytochemistry analysis, solasonine obviously induced the up-regulation of Bax and down-regulation of Bcl-2 and Bcl-xL, caused the release of cytochrome c from mitochondria into cytosol, and increased the expression of both pro- and cleaved caspase-3. Solamargine exhibited stronger antipoliferative activity than solasonine, but the similar mechanism in Bcap-37 cells in this study.ConclusionSolasonine possesses the antiproliferative effect on tumor cells. Regulation of the levels of Bcl-2, Bcl-xL, Bax, and activation of mitochondria cytochrome c-dependent apoptosis pathway might be one of its main antitumor mechanisms against breast cancer cells. In view of the cytotoxic effect of solasonine and solamargine also shown on normal cells, the safety needs concern when the antitumor activity is studied.