Benign prostatic hyperplasia (BPH), a non-cancerous enlargement of the prostate, affects about half of men between 51 and 60 years of age, and nine of ten men older than 80. How BPH happens, however, is still open for debate. In a paper published online on September 1, 2016 in Molecular Cell, researchers at Baylor College of Medicine, together with colleagues, report a new mechanism that can explain the development of BPH and suggest strategies to improve the response to androgen-targeting therapies, which are usually used to treat prostate cancer and BPH. The article is titled “Non-Cell-Autonomous Regulation of Prostate Epithelial Homeostasis by Androgen Receptor.” "Scientists have considered that inflammation can cause BPH. But how inflammation initiates in human prostate tissues and promotes BPH remains unclear," said senior author Dr. Li Xin (photo), Associate Professor of Molecular and Cellular Biology at Baylor. "Our study provides molecular insights to answer these questions." In the beginning, "we were investigating the role of the androgen receptor in prostate epithelial cell homeostasis, or how these cells balance their functions to work properly," said first author Dr. Boyu Zhang, a postdoctoral associate in Dr. Xin's lab. In particular, the scientists were studying the role that the androgen receptor plays in prostate homeostasis by deleting the androgen receptor in luminal epithelial cells. The androgen receptor allows cells to respond to androgens, which are hormones that affect how the male reproductive system develops. Most prostate luminal epithelial cells need androgen to survive. Dihydrotestosterone is the most active androgen. Although other research groups had already studied the role of androgen receptor in the prostate by deleting the receptor in prostate epithelial cells, Dr.
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