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首页> 外文期刊>Biochemical and Biophysical Research Communications >Estradiol regulates the insulin-like growth factor-I (IGF-I) signalling pathway: A crucial role of phosphatidylinositol 3-kinase (PI 3-kinase) in estrogens requirement for growth of MCF-7 human breast carcinoma cells
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Estradiol regulates the insulin-like growth factor-I (IGF-I) signalling pathway: A crucial role of phosphatidylinositol 3-kinase (PI 3-kinase) in estrogens requirement for growth of MCF-7 human breast carcinoma cells

机译：雌二醇调节胰岛素样生长因子-I（IGF-1）信号通路：磷脂酰肌醇3激酶（PI 3激酶）在雌激素对MCF-7人乳腺癌细胞生长的需求中起着至关重要的作用

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Estrogens can stimulate the proliferation of estrogen-responsive breast cancer cells by increasing their proliferative response to insulin-like growth factors. With a view to investigating the molecular mechanisms implicated, we studied the effect of estradiol on the expression of proteins implicated in the insulin-like growth factor signalling pathway. Estradiol dose- and time-dependently increased the expression of insulin receptor substrate-1 and the p85/p110 subunits of phosphatidylinositol 3-kinase but did not change those of ERK2 and Akt/PKB. ICI 182,780 did not inhibit estradiol-induced IRS-1 and p85 expression. Moreover, two distinct estradiol-BSA conjugate compounds were as effective as estradiol in inducing IRS-1 and p85/p110 expression indicating the possible implication of an estradiol membrane receptor. Comparative analysis of steroids-depleted and steroids-treated cells showed that IGF-1 only stimulates cell growth in the latter condition. Nevertheless, expression of a constitutively active form of PI 3-kinase in steroid-depleted cells triggers proliferation. These results demonstrate that estradiol positively regulates essential proteins of the IGF signalling pathway and put in evidence that phosphatidylinositol 3-kinase plays a central role in the synergistic pro-proliferative action of estradiol and IGF-1. (c) 2006 Elsevier Inc. All rights reserved.
机译：雌激素可以通过增加它们对胰岛素样生长因子的增殖反应来刺激雌激素反应性乳腺癌细胞的增殖。为了研究涉及的分子机制，我们研究了雌二醇对胰岛素样生长因子信号通路中涉及的蛋白质表达的影响。雌二醇剂量和时间依赖性地增加了胰岛素受体底物1的表达和磷脂酰肌醇3激酶的p85 / p110亚基，但并未改变ERK2和Akt / PKB的表达。 ICI 182,780没有抑制雌二醇诱导的IRS-1和p85表达。此外，两种不同的雌二醇-BSA共轭化合物在诱导IRS-1和p85 / p110表达方面与雌二醇同样有效，表明可能存在雌二醇膜受体。对类固醇缺乏和类固醇处理的细胞进行的比较分析表明，IGF-1仅在后一种情况下刺激细胞生长。然而，在类固醇缺乏的细胞中PI 3激酶的组成型活性形式的表达会触发增殖。这些结果表明雌二醇正调控IGF信号通路的必需蛋白，并证明磷脂酰肌醇3-激酶在雌二醇和IGF-1的协同增生作用中起着核心作用。 （c）2006 Elsevier Inc.保留所有权利。

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