title: Equol induces mitochondria-mediated apoptosis of human cervical cancer cells.
abstract: OBJECTIVE
  The present study aimed to investigate anticancer properties of equol and demonstrate its underlying mechanisms of action in human cervical cancer HeLa cells.
  
  
  METHODS
  Inhibition of cell viability was examined by 3-(4,5-dimethylthiazoly-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was evaluated by observation of apoptotic cell morphology, and an increase of annexin-V(+) cells. Western blotting was used to examine apoptosis-related proteins. Flow cytometry was used to measure mitochondrial membrane potential (MMP) and reactive oxygen species (ROS).
  
  
  RESULTS
  Equol treatment inhibited HeLa cell proliferation in dose- and time-dependent manner. Equol-induced apoptotic cell death was accompanied by the activation of caspases, and alteration of MMP and mitochondrial membrane proteins; equol also rapidly triggered ROS production. Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.
  
  
  CONCLUSIONS
  Equol is a potential anticancer agent against HeLa, with possible mechanisms involved in ROS generation and mitochondrial membrane alteration.
authors.affiliation: College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
authors.forename: Eun Young
authors.initials: EY
authors.lastname: Kim
authors.affiliation: College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
authors.forename: Jin Young
authors.initials: JY
authors.lastname: Shin
authors.affiliation: College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
authors.forename: Young-Ja
authors.initials: YJ
authors.lastname: Park
authors.affiliation: College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea akkim@sookmyung.ac.kr.
authors.forename: An Keun
authors.initials: AK
authors.lastname: Kim
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D060754:Equol / Q000494:pharmacology*; D005260:Female; D006367:HeLa Cells; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D002583:Uterine Cervical Neoplasms / Q000378:metabolism* / Q000473:pathology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D060754:Equol; D020169:Caspases
keywords: Equol; apoptosis; caspase; cervical cancer cells; mitochondria