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首页> 外文期刊>Journal of Cellular Physiology >Insulin-like growth factor 1 stimulation of androgen receptor activity requires beta(1A) integrins.
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Insulin-like growth factor 1 stimulation of androgen receptor activity requires beta(1A) integrins.

机译：胰岛素样生长因子1的刺激雄激素受体活动需要β(1)整合蛋白。

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Despite the findings that beta1 integrins play a vital role in the regulation of cell proliferation and survival, the mechanisms through which they operate and lead to cancer progression remain elusive. Previously, our laboratory has shown that beta(1A) integrins support insulin-like growth factor 1 (IGFI)-mediated mitogenic and transforming activities. Here, we report that beta(1A) integrins regulate basal levels of IGF-IR, although they are not critical for maintaining cancer cell morphology. Upon transfection of beta(1A) siRNA and consequent downregulation of IGF-IR, we show inhibition of anchorage-independent growth of prostate cancer cells, a function which is dependent on IGF-IR expression. In addition, we demonstrate that IGFI-mediated activation of androgen receptor (AR), known to occur in prostate cancer cells, requires expression of beta(1A) integrins as evaluated by luciferase reporter assays and immunoblotting analysis. Since beta(1A) integrin levels are increased by R1881 or dihydrotestosterone (DHT), our results imply that beta(1A) integrins support an androgen-enhanced feedback loop that regulates the expression of IGF-IR. beta(1A) integrins also regulate inducible levels of IGF-IR in cells stimulated by androgen or by a combination of androgen and IGFI, as evaluated by flow cytometric analysis and immunoblotting. Furthermore, upon transfection of beta(1A) siRNA and consequent downregulation of IGF-IR, neither activation of AKT, an effector of IGF-IR, nor AR levels are affected. We conclude that beta(1A) integrin expression is critical for maintaining the regulatory crosstalk between IGF-IR and AR.
机译：尽管发现beta1整合蛋白发挥在调节细胞至关重要的作用增殖和生存机制通过操作和导致癌症发展仍然是难以捉摸的。实验表明,β(1)整合蛋白胰岛素样生长因子1的支持(IGFI)介导促有丝分裂的转变活动。整合蛋白调节基底IGF-IR水平,虽然他们不维护的关键癌症细胞的形态。小干扰rna的差别和由此产生的对这些β(1 a)IGF-IR,我们显示抑制anchorage-independent前列腺癌的生长细胞,一个函数依赖IGF-IR表达式。IGFI-mediated雄激素受体的激活(AR),发生在前列腺癌细胞,需要表达的β(1)整合蛋白荧光素酶报告分析和评估免疫印迹分析。增加了R1881或水平二氢睾酮(DHT),我们的研究结果暗示β(1)整合蛋白支持androgen-enhanced反馈回路,调节的表达IGF-IR。诱导细胞刺激的IGF-IR水平雄性激素和雄激素或组合IGFI,如通过流仪分析评估和免疫印迹。转染β(1)核和结果downregulation IGF-IR,既不激活一种蛋白激酶,IGF-IR的效应,也不是基于“增大化现实”技术的水平受到影响。表达对维护至关重要监管IGF-IR之间的串扰和基于“增大化现实”技术。

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