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为研究偏钒酸钠对人前列腺癌细胞DU145的增殖抑制作用及其机制,我们检测了偏钒酸钠对细胞活力、细胞周期、活性氧水平和细胞周期调节蛋白活性的影响。结果显示偏钒酸钠能显著降低调控Cdc2的主要磷酸酯酶Cdc25C的蛋白水平,导致Cdc2 Tyr-15位磷酸化水平升高,引起DU145细胞发生G2/M周期阻滞和增殖活力抑制。而抗氧化剂N-乙酰半胱氨酸能降低偏钒酸钠诱导升高的活性氧水平并能恢复偏钒酸钠导致的Cdc25C蛋白水平降低和Cdc2磷酸化水平(Tyr-15)的升高。这证实偏钒酸钠能导致DU145细胞发生G2/M周期阻滞从而引起细胞增殖活力抑制,且这种抑制可能是通过偏钒酸钠所诱导的活性氧水平升高引起的Cdc25C蛋白降解实现的。
To study the inhibitory effect of sodium metavanadate on proliferation of human prostate cancer cell DU145 and its mechanism, we examined the effect of sodium metavanadate on cell viability, cell cycle, ROS level and cell cycle regulatory protein activity. The results showed that sodium metavanadate could significantly reduce the protein level of Cdc25C, which is the major phosphatase regulating Cdc2, resulting in an increase of phosphorylation of Tyr-15 at Cdc2 level, resulting in G2 / M cycle arrest and inhibition of proliferation in DU145 cells. The antioxidant N-acetylcysteine decreased sodium metavanadate induced elevated ROS and restored the reduction of Cdc25C protein and Cdc2 phosphorylation (Tyr-15) induced by sodium metavanadate. This confirms that sodium metavanadate can lead to G2 / M cycle arrest in DU145 cells and lead to inhibition of cell proliferation activity, and this inhibition may be achieved through the degradation of Cdc25C protein induced by the elevated level of reactive oxygen species induced by sodium metavanadate .