AR and neoplasm: PARP-1 can be recruited to the site of AR and can regulate the AR function; PARP-1 activity is increased in CRPC and can regulate the AR activity in castration-resistant states; (2) PARP inhibition can suppress the AR function, increase the sensitivity of PC cells to genotoxic damage, and synergize with anti-androgen therapy to inhibit cell proliferation, thereby suppressing tumor growth and delaying the development of the castration-resistant state.