关键词：脂肪酸；前列腺癌；氨基酸；雄激素
摘 要：Although prostate cancers are initially responsive to androgen deprivation therapy, castration resistant prostate cancer demands alternative treatment options. It has been reported that the apoptotic protease, caspase 2 (C2) is critical for prostate cancer cell death in several settings. Several reports have also indicated that fatty acid synthesis is critical for maintaining prostate cancer cell viability and that inhibition of fatty acid synthesis can lead to apoptosis. Finally, C2 is suppressed by high intracellular NADPH and this is not due to the redox effects of NADPH, suggesting that the synthetic role of NADPH (e.g., in fatty acid synthesis) may account for its ability to suppress apoptosis. Our new data suggest that manipulating metabolism, particularly inhibiting fatty acid synthesis, can alter chemosensitivity in prostate cancer cells.