Naragoni Srivatcha, Sankella Shireesha, Harris Kinesha, Gray Wesley G
Department of Environmental Toxicology, Southern University and A&M College, Baton Rouge, Louisiana, USA.
J Cell Physiol. 2009 Jun;219(3):584-94. doi: 10.1002/jcp.21699.
Phytoestrogens (PEs) are non-steroidal ligands, which regulate the expression of number of estrogen receptor-dependent genes responsible for a variety of biological processes. Deciphering the molecular mechanism of action of these compounds is of great importance because it would increase our understanding of the role(s) these bioactive chemicals play in prevention and treatment of estrogen-based diseases. In this study, we applied suppression subtractive hybridization (SSH) to identify genes that are regulated by PEs through either the classic nuclear-based estrogen receptor or membrane-based estrogen receptor pathways. SSH, using mRNA from genistein (GE) treated MCF-7 cells as testers, resulted in a significant increase in GNB1 mRNA expression levels as compared with 10 nM 17beta estradiol or the no treatment control. GNB1 mRNA expression was up regulated two- to fivefold following exposure to 100.0 nM GE. Similarly, GNB1 protein expression was up regulated 12- to 14-fold. GE regulation of GNB1 was estrogen receptor-dependent, in the presence of the anti-estrogen ICI-182,780, both GNB1 mRNA and protein expression were inhibited. Analysis of the GNB1 promoter using ChIP assay showed a PE-dependent association of estrogen receptor alpha (ERalpha) and beta (ERbeta) to the GNB1 promoter. This association was specific for ERalpha since association was not observed when the cells were co-incubated with GE and the ERalpha antagonist, ICI. Our data demonstrate that the levels of G-protein, beta-1 subunit are regulated by PEs through an estrogen receptor pathway and further suggest that PEs may control the ratio of alpha-subunit to beta/gamma-subunits of the G-protein complex in cells. J. Cell. Physiol. 219: 584-594, 2009. (c) 2009 Wiley-Liss, Inc.
植物雌激素(PEs)是一类非甾体配体,可调节许多雌激素受体依赖性基因的表达,这些基因参与多种生物学过程。阐明这些化合物的分子作用机制非常重要,因为这将增进我们对这些生物活性化学物质在预防和治疗雌激素相关疾病中所起作用的理解。在本研究中,我们应用抑制性消减杂交(SSH)技术来鉴定通过经典的基于核的雌激素受体或基于膜的雌激素受体途径受PEs调控的基因。以染料木黄酮(GE)处理的MCF-7细胞的mRNA作为检测子进行SSH,结果显示与10 nM 17β-雌二醇或未处理对照相比,GNB1 mRNA表达水平显著增加。暴露于100.0 nM GE后,GNB1 mRNA表达上调了2至5倍。同样,GNB1蛋白表达上调了12至14倍。GE对GNB1的调节依赖于雌激素受体,在抗雌激素ICI-182,780存在的情况下,GNB1 mRNA和蛋白表达均受到抑制。使用染色质免疫沉淀(ChIP)分析GNB1启动子表明,雌激素受体α(ERα)和β(ERβ)与GNB1启动子存在PE依赖性结合。这种结合对ERα具有特异性,因为当细胞与GE和ERα拮抗剂ICI共同孵育时未观察到结合。我们的数据表明,G蛋白β1亚基的水平通过雌激素受体途径受PEs调控,并且进一步表明PEs可能控制细胞中G蛋白复合物α亚基与β/γ亚基的比例。《细胞生理学杂志》219: 584 - 594, 2009。(c)2009威利 - 利斯公司。