Androgen plays a significant role in the development and progression of prostate cancer (PCa), one of the commonest malignancies in the male urogenital system. Castration-resistant PCa (CRPC) is the end-result of the majority of prostate cancer cases treated by androgen deprivation therapy (ADT). Furthermore, the androgen axis is reactivated due to adaptive intratumoral androgen biosynthesis, which can be driven by adrenal androgens and /or by changes in the androgen receptor (AR) including AR gene amplification. At present, drugs targeting the androgen axis, such as abiraterone and enzalutamide, et al, are used for the first-line therapy for CRPC. Nevertheless, drug resistance and disease progression occur during the treatment of CRPC by anti-androgen therapy. Therefore, an insight into the mechanisms of drug resistance in anti-androgen therapy for CRPC may help surmount the drug reistance and improve the prognosis of the malignancy.
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