Daidzein induces MCF-7 breast cancer cell apoptosis via the mitochondrial pathway.

BACKGROUND In order to study the anticancer effects and cellular apoptosis pathways induced by daidzein. MATERIALS AND METHODS We used the human MCF-7 breast cancer cell line as a model and examined the apoptosis by Hoechst-propidium iodide staining fluorescence imaging and flow cytometry. RESULTS Our data indicated that daidzein induces antiproliferative effects in a concentration- and time-dependent manner. We demonstrated that daidzein-induced apoptosis in MCF-7 cells was initiated by the generation of reactive oxygen species (ROS). Furthermore, we showed that this daidzein-induced ROS generation was accompanied by disruption of mitochondrial transmembrane potential, down-regulation of bcl-2, and up-regulation of bax, which led to the release of cytochrome C from the mitochondria into the cytosol, which, in turn, resulted in the activation of caspase-9 and caspase-7, and ultimately in cell death. The induction of the mitochondrial caspase-dependent pathway was confirmed by pretreatment with pan-caspase inhibitor z-VAD-fmk and antioxidant N-acetyl-L-cysteine. CONCLUSION Accordingly, daidzein could induce breast cancer cell apoptosis through the mitochondrial caspase-dependent cell death pathway.