title: Daidzein induces MCF-7 breast cancer cell apoptosis via the mitochondrial pathway.
abstract: BACKGROUND
  In order to study the anticancer effects and cellular apoptosis pathways induced by daidzein.
  
  
  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.
  
  
  CONCLUSIONS
  Accordingly, daidzein could induce breast cancer cell apoptosis through the mitochondrial caspase-dependent cell death pathway.
authors.affiliation: Department of Oncology, The Third College Hospital of Harbin Medical University, Harbin, People's Republic of China.
authors.forename: S
authors.initials: S
authors.lastname: Jin
authors.affiliation: Department of Oncology, The Third College Hospital of Harbin Medical University, Harbin, People's Republic of China. Electronic address: zhma19650210@126.com.
authors.forename: Q Y
authors.initials: QY
authors.lastname: Zhang
authors.affiliation: Department of Oncology, The Third College Hospital of Harbin Medical University, Harbin, People's Republic of China.
authors.forename: X M
authors.initials: XM
authors.lastname: Kang
authors.affiliation: Department of Oncology, The Third College Hospital of Harbin Medical University, Harbin, People's Republic of China.
authors.forename: J X
authors.initials: JX
authors.lastname: Wang
authors.affiliation: Department of Oncology, The Third College Hospital of Harbin Medical University, Harbin, People's Republic of China.
authors.forename: W H
authors.initials: WH
authors.lastname: Zhao
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D005260:Female; D006801:Humans; D007529:Isoflavones / Q000494:pharmacology*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D048789:Phytoestrogens / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D007529:Isoflavones; D048789:Phytoestrogens; D017382:Reactive Oxygen Species; C004742:daidzein