Department of Biological Sciences, DePaul University, Chicago, IL 60614, USA.
Anticancer Res. 2012 Apr;32(4):1181-91.
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.
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.
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. High concentrations of genistein (100 μM) both in the presence and absence of 17β-estradiol also increased apoptosis; however, these changes were not correlated with the BAX/BCL-2 ratio or with phosphorylation of ERK1/2.
These results suggest that different concentrations of genistein elicit cell responses through different signaling mechanisms. These results are especially relevant in premenopausal women with breast cancer who are on a soy diet.
本研究旨在确定金雀异黄素和 17β-雌二醇抑制 MDA-MB-231 乳腺癌细胞增殖的机制。
通过 Western blot 检测参与细胞凋亡、增殖和存活的细胞信号蛋白（BCL-2 相关 X 蛋白、BAX；B 细胞淋巴瘤 2、BCL-2；细胞外信号调节激酶、pERK1/2；蛋白激酶 B、pAKT）的表达，并检测这些效应是否与细胞增殖和凋亡相关。
与对照组相比，1 μM 金雀异黄素加 1 nM 17β-雌二醇显著增加细胞凋亡和 BAX/BCL-2 比值，同时 ERK1/2 磷酸化减少。高浓度金雀异黄素（100 μM）在存在和不存在 17β-雌二醇的情况下也增加细胞凋亡；然而，这些变化与 BAX/BCL-2 比值或 ERK1/2 磷酸化无关。
这些结果表明，不同浓度的金雀异黄素通过不同的信号机制引起细胞反应。这些结果对于处于绝经前且正在进行大豆饮食的乳腺癌妇女尤其相关。
