Gwin John, Drews Neil, Ali Syed, Stamschror Justin, Sorenson Matthew, Rajah Talitha T
Department of Biological Sciences, DePaul University, Chicago, IL 60614, USA.
Anticancer Res. 2011 Jan;31(1):209-14.
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.
The effect of genistein on cell-signaling molecules was determined in T47D breast cancer cells by a Bioplex phosphoprotein detection kit. These results were confirmed by Western blotting and were correlated to cell proliferation by MTT assay.
Low and high concentrations of genistein induced an ERK1/2-independent decrease in phosphorylated p90RSK. This effect was accompanied by decreased cell proliferation at high concentrations and an increased response at low concentrations of genistein following a 48-hour exposure.
Concentration-dependent actions of genistein in T47D cells may be due to differential activation of signaling molecules.
金雀异黄素对乳腺癌细胞增殖作用的分子机制在很大程度上尚不清楚。本研究旨在检测参与金雀异黄素相关细胞增殖和存活的雌激素受体（ER）相关信号分子（细胞外信号调节激酶1/2、p90核糖体S6激酶、应激活化蛋白激酶、蛋白激酶B和核因子κB），并将这些结果与细胞增殖相关联。
通过生物芯片磷蛋白检测试剂盒在T47D乳腺癌细胞中测定金雀异黄素对细胞信号分子的影响。这些结果通过蛋白质免疫印迹法得到证实，并通过MTT法与细胞增殖相关联。
低浓度和高浓度的金雀异黄素均诱导磷酸化p90RSK出现不依赖细胞外信号调节激酶1/2的降低。这种效应伴随着高浓度时细胞增殖的降低以及48小时暴露后低浓度金雀异黄素时反应的增加。
金雀异黄素在T47D细胞中的浓度依赖性作用可能归因于信号分子的不同激活。
