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Equol induced the apoptosis via cell cycle arrest in MDA‐MB‐453 but not in MCF‐7 cells

To investigate the effects of equol on cell cycle distribution and apoptosis in human breast cancer cells, we first determined the antiproliferative effects of various concentrations of equol (1nM‐100μM) in MCF‐7 and MDA‐MB‐453 cells exposed for 24, 48, or 72h. Equol significantly inhibited proliferation in MDA‐MB‐453 cells in a dose‐ and time‐dependent manner. In contrast, equol at low concentrations (<1μM) stimulated proliferation in MCF‐7 cells, with increased expression of PCNA, and equol inhibited proliferation only at a high concentration (100uM). Similarly, equol treatment of MDA‐MB‐453 cells resulted in significant cell cycle arrest at the G1/S transition and in G2/M phase, whereas equol caused a slight cell cycle arrest of MCF‐7 cells in G2/M phase after 72h of treatment. Also, when cells were treated with 50 and 100μM equol for 72h, equol affected cell cycle regulatory proteins more significantly in MDA‐MB‐453 than in MCF‐7 cells. During equol‐induced apoptosis, equol increased the number of cells in sub‐G0 phase and enhanced the level of p53. The expressions of Bax and cytochrome c, downstream targets of p53, were markedly increased by treatment with higher concentrations of equol. Equol‐induced cell cycle arrest and apoptosis apparently involves a p53‐dependent pathway in different types of breast cancer cells.