Anticancer Research, 2012, 32(4):1181-91.

Physiological Concentrations of Genistein and 17β-Estradiol Inhibit MDA-MB-231 Breast Cancer Cell Growth by Increasing BAX/BCL-2 and Reducing pERK1/2

Talitha T Rajah, Kevin J Peine, Nga Du, et al

Department of Biological Sciences, DePaul University, Chicago, IL 60614, USA

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. 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.

CONCLUSION:

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.

希腊《抗癌研究》，2012年4月

生理浓度的金雀异黄素和 17β-雌二醇通过提高 BAX/bcl-2 和减少p ERK1/2抑制MDA-MB-231 乳腺癌细胞的生长

塔莉莎 T 让佳，凯文 J 派尼，尼雅 杜，等

美国芝加哥保罗大学生物学院

目的︰

本研究旨在确认金雀异黄素和 17β- 雌二醇抑制 MDA-MB-231 乳腺癌细胞增殖的作用机制。

材料和方法︰

细胞信号转导蛋白包括凋亡、 增殖和生存 (BCL-2 关联 X 蛋白，BAX；B 细胞淋巴瘤 2，BCL-2；细胞外信号调节激酶，pERK1/2；和蛋白激酶 B，pAKT）的表达由免疫印迹法检测，并验证这些作用是否与细胞增殖和凋亡有关。

结果︰

与对照相比，1 μM 金雀异黄素加 1 nM 17 β-雌二醇明显提高了细胞凋亡，并且 BAX/BCL-2 的比率，与 ERK1/2 磷酸化同时减少。高浓度的金雀异黄素 (100μM) 在17β- 雌二醇缺席或存在的情况下均增加了细胞凋亡；然而，这些改变与BAX/BCL-2 的比例或ERK1/2的磷酸化无关。

结论︰

这些结果表明，不同浓度的金雀异黄素通过不同的信号转导机制引起细胞的反应。这些结果与以大豆为食的绝经前乳腺癌女性患者有关。