Prostate cancer is a major cause of cancer-related deaths in American men. The development and growth of prostate cancer depends on the androgen receptor (AR) and its high-affinity binding of dehydrotestosterone (DHT), which derives from testosterone (T). Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. The AR, a member of the steroid receptor family that is activated by testicular androgens, is the major regulatory transcription factor in normal prostate growth and development and in the growth of androgen-dependent prostate cancer. Recent evidence suggests that the AR may also contribute to prostate cancer growth during its recurrence in the androgen-deprived patient. A role for AR-mediated gene activation in recurrent prostate cancer is supported by its expression together with the expression of androgen-regulated genes. This review highlights the different mechanisms of the available androgen deprivation therapies and also focuses on the novel targeted therapies in advanced or metastatic prostate cancer. Furthermore, we provide a molecular basis for the AR and its role in activation and progression in recurrent or castration resistant prostate cancer.