Anoctamin 1 (TMEM16A) is essential for testosterone-induced prostate hyperplasia

Significance Benign prostatic hyperplasia (BPH) is characterized by an enlargement of the prostate gland, a common disease in elderly men. Excessive testosterone is considered to cause BPH. However, its etiologic mechanisms are elusive. We found that ANO1, a Ca 2+ -activated Cl − channel, is essential for the testosterone-induced BPH. ANO1 was highly expressed in dihydrotestosterone (DHT)-treated prostate epithelial cells. The selective knockdown of ANO1 suppressed DHT-induced cell proliferation. Surprisingly, we found that there were three androgen-response elements in the ANO1 promoter region, which were relevant for the DHT-dependent induction of ANO1. Intraprostate treatment of Ano1 siRNA inhibited the prostate enlargement in vivo. Thus, ANO1 appears essential for the development of prostate hyperplasia and becomes a useful target for treating BPH.