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Targeting stromal androgen receptor suppresses prolactin-driven benign prostatic hyperplasia (BPH).

Journal article
Authors Kuo-Pao Lai
Chiung-Kuei Huang
Lei-Ya Fang
Kouji Izumi
Chi-Wen Lo
Ronald Wood
Jon Kindblom
Shuyuan Yeh
Chawnshang Chang
Published in Molecular endocrinology (Baltimore, Md.)
Volume 27
Issue 10
Pages 1617-31
ISSN 1944-9917
Publication year 2013
Published at Institute of Clinical Sciences, Department of Oncology
Pages 1617-31
Language en
Links dx.doi.org/10.1210/me.2013-1207
Subject categories Cancer and Oncology, Endocrinology and Diabetes

Abstract

Stromal-epithelial interaction plays a pivotal role to mediate the normal prostate growth, the pathogenesis of benign prostatic hyperplasia (BPH), and prostate cancer development. Until now, the stromal androgen receptor (AR) functions in the BPH development, and the underlying mechanisms remain largely unknown. Here we used a genetic knockout approach to ablate stromal fibromuscular (fibroblasts and smooth muscle cells) AR in a probasin promoter-driven prolactin transgenic mouse model (Pb-PRL tg mice) that could spontaneously develop prostate hyperplasia to partially mimic human BPH development. We found Pb-PRL tg mice lacking stromal fibromuscular AR developed smaller prostates, with more marked changes in the dorsolateral prostate lobes with less proliferation index. Mechanistically, prolactin mediated hyperplastic prostate growth involved epithelial-stromal interaction through epithelial prolactin/prolactin receptor signals to regulate granulocyte macrophage-colony stimulating factor expression to facilitate stromal cell growth via sustaining signal transducer and activator of transcription-3 activity. Importantly, the stromal fibromuscular AR could modulate such epithelial-stromal interacting signals. Targeting stromal fibromuscular AR with the AR degradation enhancer, ASC-J9(®), led to the reduction of prostate size, which could be used in future therapy.

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