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.

Authors in the journal PNAS found that ANO1, a Ca2+-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, they 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.