类固醇受体共激活因子2:黄体酮诱导的子宫和乳腺形态发生的重要共调节因子。

A Mukherjee, P Amato, D Craig-Allred, F J DeMayo, B W O'Malley, J P Lydon
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引用次数: 3

摘要

在女性生殖和乳腺生物学中,孕激素受体(PR)在孕激素信号转导中的重要性已经确立;然而,PR在这些系统中优先招募的共调节因子尚未得到全面的研究。利用一种创新的遗传方法,在表达PR的小鼠细胞系中特异性地消除基因功能,类固醇受体共激活因子2 (SRC-2,也称为TIF-2或GRIP-1)在子宫和乳腺的孕激素依赖性反应中发挥了有效的共调节特性。PR阳性的子宫细胞(但缺乏SRC-2)导致胚胎着床早期阻滞,这是SRC-1或SRC-3基因敲除所没有的表型。以乳腺为例,在缺乏SRC-2的情况下,孕激素依赖性分支形态形成和肺泡形成无法发生,从而确立了SRC-2在该组织中由孕激素启动的细胞增殖程序中的关键协同激活因子作用。重要的是,最近在人类子宫内膜和乳房中检测到SRC-2表明,这种共调节因子可能为未来女性生殖健康和/或乳腺癌的管理提供新的临床靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Steroid receptor coactivator 2: an essential coregulator of progestin-induced uterine and mammary morphogenesis.

The importance of the progesterone receptor (PR) in transducing the progestin signal is firmly established in female reproductive and mammary gland biology; however, the coregulators preferentially recruited by PR in these systems have yet to be comprehensively investigated. Using an innovative genetic approach, which ablates gene function specifically in murine cell-lineages that express PR, steroid receptor coactivator 2 (SRC-2, also known as TIF-2 or GRIP-1) was shown to exert potent coregulator properties in progestin-dependent responses in the uterus and mammary gland. Uterine cells positive for PR (but devoid of SRC-2) led to an early block in embryo implantation, a phenotype not shared by knockouts for SRC-1 or SRC-3. In the case of the mammary gland, progestin-dependent branching morphogenesis and alveologenesis failed to occur in the absence of SRC-2, thereby establishing a critical coactivator role for SRC-2 in cellular proliferative programs initiated by progestins in this tissue. Importantly, the recent detection of SRC-2 in both human endometrium and breast suggests that this coregulator may provide a new clinical target for the future management of female reproductive health and/or breast cancer.

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