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

Abstract

BackgroundIn order to study the anticancer effects and cellular apoptosis pathways induced by daidzein. Materials and methodsWe 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. ResultsOur 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. ConclusionAccordingly, daidzein could induce breast cancer cell apoptosis through the mitochondrial caspase-dependent cell death pathway.