PT  - JOURNAL ARTICLE
AU  - EUN YOUNG KIM
AU  - JIN YOUNG SHIN
AU  - YOUNG-JA PARK
AU  - AN KEUN KIM
TI  - Equol Induces Mitochondria-mediated Apoptosis of Human Cervical Cancer Cells
DP  - 2014 Sep 01
TA  - Anticancer Research
PG  - 4985--4992
VI  - 34
IP  - 9
4099  - http://ar.iiarjournals.org/content/34/9/4985.short
4100  - http://ar.iiarjournals.org/content/34/9/4985.full
SO  - Anticancer Res2014 Sep 01; 34
AB  - Background/Aim: The present study aimed to investigate anticancer properties of equol and demonstrate its underlying mechanisms of action in human cervical cancer HeLa cells. Materials and 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. Conclusion: Equol is a potential anticancer agent against HeLa, with possible mechanisms involved in ROS generation and mitochondrial membrane alteration.