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ERK/MAPK Regulation of the Androgen Responsiveness of Breast Cancer Cells

机译：ERK / MAPK调节乳腺癌细胞的雄激素反应性

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The androgen receptor (AR) is the most widely expressed steroid hormone receptor in human breast cancers and androgens including 5a-dihydrotestosterone are potent inhibitors of breast cancer cell proliferation. The extracellular signal-regulated mitogen activated protein kinase (ERK/MAPK) pathway is hyperactivated in a proportion of breast tumors and can interact with steroid hormone receptor signaling by altering receptor phosphorylation, turnover, ligand, and cofactor interactions. To examine the effects of ERK/ MAPK hyperactivity on AR levels, MCF-7 cells were stably transfected with a plasmid encoding a constitutively active MEK1 protein to create MCF-7-AMEK1 cells. Treatment of MCF-7-AMEK1 with androgens caused a transient increase in AR protein levels, similar to that observed in untransfected MCF-7 cells treated with androgens. Androgens also inhibited the proliferation of MCF-7-AMEK1 cells by 50-60% following 8 days of treatment in association with increased accumulation of cells in the Gl phase of the cell cycle. These results indicate that although ERK/MAPK hyperactivation in breast cancer cells is associated with reduced estrogen receptor (ERa) levels and antiestrogen resistance, AR levels are maintained and breast cancer cells remain susceptible to the growth inhibitory effects of androgens.
机译：雄激素受体（AR）是人乳腺癌中最广泛表达的类固醇激素受体，包括5a-Dihydrottoronne是乳腺癌细胞增殖的有效抑制剂。细胞外信号调节的丝裂型蛋白激酶激酶（ERK / MAPK）途径在乳腺肿瘤的比例中偏振，并且可以通过改变受体磷酸化，周转，配体和辅因子相互作用与类固醇激素受体信号传导相互作用。为了检查ERK / MAPK多动对AR水平的影响，用编码组成型活性MEK1蛋白的质粒稳定地转染MCF-7细胞以产生MCF-7-AMEK1细胞。用雄激素治疗MCF-7-AMEK1导致Ar蛋白水平的瞬时增加，类似于在用雄激素处理的未转化的MCF-7细胞中观察到的瞬时增加。雄激素还抑​​制MCF-7-AMEK1细胞的增殖在治疗后8天的治疗后80-60％，与细胞周期的GL阶段的GL阶段增加的增加。这些结果表明，虽然乳腺癌细胞中的ERK / MAPK多动激活与雌激素受体（时代）水平降低和抗雌激素相关，但维持AR水平，并且乳腺癌细胞仍然易于雌激素的生长抑制作用。

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