Regulation of alternative polyadenylation by androgen receptor inhibition

Prostate cancer (PC) onset and progression relies on the androgen receptor (AR) signaling. Anti-androgenic hormonal therapy (HT) is initially efficacious, but most patients evolve to a castration resistant stage (CRPC) for which no cure is currently available. Most proposed mechanisms of acquired resistance to HT focus on the transcriptional activity in CRPC cells. In this study, however, we have uncovered a new role of AR in alternative cleavage and polyadenylation (APA) regulation.