Prostate cancer is the most common non-cutaneous malignancy in American men and the second greatest cause of cancer-related death. Development of effective therapeutic modalities for the treatment of this cancer relies heavily on understanding the molecular alterations that result in the initiation and progression of the tumorigenic process. Increasing evidence indicates that impaired ability to undergo apoptosis plays an important role in the evolution from androgen-dependent to androgen-independent prostate cancer. In this review, we address recent progress toward the central objectives of understanding the molecular events that contribute to prostate cancer progression. We focus on some key regulatory molecules, including the pro-apoptotic regulators p53, PTEN, caspases and Par-4, and the anti-apoptotic molecules Bcl-2, NF-κB and Akt, to discuss their roles in prostate cancer progression and their therapeutic implications in human prostate carcinoma.

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