Equol induces mitochondria-mediated apoptosis of human cervical cancer cells.

Abstract

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.

• Authors: Eun Young Kim, Jin Young Shin, Young-Ja Park, An Keun Kim
• Journal: Anticancer research (Anticancer Res) Vol. 34 Issue 9 Pg. 4985-92 (Sep 2014) ISSN: 1791-7530 [Electronic] Greece
• PMID: 25202081 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.

Chemical References

• Proto-Oncogene Proteins c-bcl-2
• Reactive Oxygen Species
• Equol
• Caspases

Topics

• Apoptosis (drug effects)
• Caspases (metabolism)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Dose-Response Relationship, Drug
• Equol (pharmacology)
• Female
• HeLa Cells
• Humans
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (drug effects, metabolism)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (drug effects)
• Uterine Cervical Neoplasms (metabolism, pathology)