Published online Nov 24, 2014. doi: 10.5410/wjcu.v3.i3.264
Revised: June 26, 2014
Accepted: July 27, 2014
Published online: November 24, 2014
Processing time: 204 Days and 18.9 Hours
Prostate cancer is the most common male malignant neoplasm. Androgens and the androgen receptor (AR) play a key role in the onset and progression of prostate cancer. The expression of the AR is still preserved in the majority of patients with castration-resistant prostate cancer (CRPC). CRPC is considered to be induced by the following mechanisms: (1) sustained AR activation by enhancing intracellular conversion of adrenal androgens to dehydrotestosterone via a de novo route; (2) AR hypersensitivity; (3) promiscuous activation of AR signaling; and (4) outlaw pathways. Recent advances in the treatment of CRPC include novel medicines targeting AR signaling pathways. In addition, functional molecular studies have shown that some of the AR-regulated genes and AR coregulators are prognostic markers and potential therapeutic targets for prostate cancer, particularly in the castration-resistant state. Therefore, identification of the AR signaling pathways responsible for establishment of CRPC is critical for developing new strategies for the treatment of CRPC.
Core tip: Prostate cancer is the most common male malignant neoplasm. Androgens and the androgen receptor (AR) play a key role in the onset and progression of prostate cancer. The expression of the AR is still preserved in the majority of patients with castration-resistant prostate cancer (CRPC). Therefore, identification of the AR signaling pathways responsible for establishment of CRPC is critical for developing new strategies for the treatment of CRPC.