期刊
CHEMICO-BIOLOGICAL INTERACTIONS
卷 177, 期 1, 页码 7-11出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2008.09.031
关键词
Apoptosis; Caspase cascade; Cell proliferation; Equol; Human breast caner cells
资金
- Korea Research Foundation
- Korean Government [MOEHRD, KRF-2006311-1700127]
This study investigated the role of the caspase activation cascade in extrinsic and intrinsic apoptosis induced by equol in human breast cancer MDA-MB cells. First, the antiproliferative effect of equol was determined in cells treated with 1-100 mu M equol for 24, 48, and 72 h. Equol significantly inhibited cell proliferation in a dose-dependent manner (p < 0.05). Exposure to 50 or 100 mu M equol for 72 h strongly promoted apoptosis. Under the same conditions, remarkable cytochrome c release was observed. Subsequently, caspase-9, which acts in mitochondria-mediated apoptosis, was cleaved by equol at high concentrations, but caspase-8 activation of receptor-mediated apoptosis was not observed. At both equol concentrations, the caspase-8 and -9 activity assays showed similar patterns. In addition, equol treatment activated caspase-3, which is downstream from caspase-9, and this was accompanied by the cleavage of capase-6 and -7. Activation of these caspases leads to increased activation of PARP, lamin, and ICAD. This study suggests that equol induces the intrinsic pathway of apoptosis via caspase-9 and cytochrome c, independent of caspase-8, in human breast cancer MDA-MB-453 cells. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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