Physiological concentrations of genistein and 17β-estradiol inhibit MDA-MB-231 breast cancer cell growth by increasing BAX/BCL-2 and reducing pERK1/2.

Aim: The aim of the present study was to identify the mechanism by which genistein and 17β-estradiol inhibit proliferation of MDA-MB-231 breast cancer cells.

Materials And Methods: The expression of cell signaling proteins involved in cell apoptosis, proliferation, and survival (BCL-2 associated X protein, BAX; B-cell lymphoma 2, BCL-2; extracellular signal regulated kinase, pERK1/2; and protein kinase B, pAKT) were examined by western blotting, and tested whether these effects correlated with cell proliferation and apoptosis.

Results: Compared to the control, 1 μM genistein plus 1 nM 17β-estradiol significantly increased apoptosis, and the BAX/BCL-2 ratio, with a concomitant decrease in ERK1/2 phosphorylation.

Effect of genistein on p90RSK phosphorylation and cell proliferation in T47D breast cancer cells.

Background: The molecular mechanisms of genistein's proliferative effects on breast cancer cells are largely unknown. This study aimed to examine estrogen-receptor (ER)-related signaling molecules involved in genistein-associated cell proliferation and survival (ERK1/2, p90RSK, JNK, Akt and NFκB) and to correlate these results to cell proliferation.

Materials And Methods: The effect of genistein on cell-signaling molecules was determined in T47D breast cancer cells by a Bioplex phosphoprotein detection kit.

Genistein in the presence of 17beta-estradiol inhibits proliferation of ERbeta breast cancer cells.

Background/aim: Genistein, a soy component, has been shown to have a biphasic proliferative effect in breast cancer cells, inhibiting in vitro cell proliferation at high concentrations (>10 micromol/l), while stimulating cell proliferation at lower concentrations (<10 micromol/l). However, epidemiological studies have shown an inverse correlation between the intake of genistein and the incidence of breast cancer. One of the possible reasons for this discrepancy could be the differing status of the estrogen receptor (ERalpha and/or ERbeta).