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Prostate cancer is an extremely common disease that affects one in every seven men in their lifetime. The standard care for late-stage cancer is designed to inhibit the activation of androgen receptor (AR). While this therapeutic approach is initially efficient, the cancer almost always develops resistance and gives rise to castration-resistant prostate cancer (CRPC). When therapy fails, the median survival of patients who suffer from CRPC is 12-16 months. It is critical to understand the mechanism of CRPC better to ameliorate the outcome of late-stage prostate cancer patients.

AR is a transcription factor that consists of an N-terminal domain (NTD), a DNA binding domain (DBD) and a ligand binding domain (LBD). Upon activation by androgen, an intramolecular interaction between NTD and LBD occurs. The AR translocates into the nucleus where it forms a homodimer. It binds to the promoter and enhancer elements of …