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非基因组雄激素作用调控基质细胞的增殖/迁移信号。

Non-genomic androgen action regulates proliferative/migratory signaling in stromal cells.

机构信息

Department of Biochemistry, Biophysics and General Pathology, II University of Naples , Naples , Italy.

出版信息

Front Endocrinol (Lausanne). 2015 Jan 19;5:225. doi: 10.3389/fendo.2014.00225. eCollection 2014.

Abstract

Prostate cancer (PCa) is the major cause of cancer-related death among the male population of Western society, and androgen-deprivation therapy (ADT) represents the first line in PCa treatment. However, although androgen receptor (AR) expression is maintained throughout the various stages of PCa, ADT frequently fails. Clinical studies have demonstrated that different androgen/AR signaling pathways operate in target tissues. AR stimulates growth and transformation of target cells, but under certain conditions slows down their proliferation. In this review, we discuss the role of AR in controlling different functions of mesenchymal and transformed mesenchymal cells. Findings here presented support the role of AR in suppressing proliferation and stimulating migration of stromal cells, with implications for current approaches to cancer therapy.

摘要

前列腺癌(PCa)是西方社会男性人群中癌症相关死亡的主要原因,而雄激素剥夺疗法(ADT)是 PCa 治疗的一线方法。然而,尽管雄激素受体(AR)在 PCa 的各个阶段都保持表达,但 ADT 经常失败。临床研究表明,不同的雄激素/AR 信号通路在靶组织中发挥作用。AR 刺激靶细胞的生长和转化,但在某些条件下会减缓其增殖。在这篇综述中,我们讨论了 AR 在控制间充质和转化间充质细胞的不同功能中的作用。这里提出的研究结果支持 AR 在抑制基质细胞增殖和刺激其迁移中的作用,这对当前的癌症治疗方法具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7495/4298220/a59655027a9a/fendo-05-00225-g001.jpg

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