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本研究以恶性程度不同的两种前列腺癌细胞PC-3和DU-145为模型,研究了具有降糖活性的钒化合物metavanadate、VO(acac)_2和VO(ma)_2的增殖抑制效应及机制。结果表明,在两种细胞中,三种钒化合物均可诱导细胞阻滞于G2/M期,表现在Cdc2的第15位酪氨酸的磷酸化水平升高。结果还显示,钒化合物能够引起ROS水平升高,且抗氧化剂N-乙酰半胱氨酸能恢复由于钒化合物诱导下降的Cdc25C蛋白水平,这说明活性氧在钒化合物引起的周期阻滞中起到调节作用。此外,研究表明钒化合物对PTEN缺失且ROS本底水平较高的PC-3的抑制作用强于对DU-145细胞,这提示PTEN可作为生物标记物而为患者抗肿瘤方案的选择提供依据。由于所研究的钒化合物已被证实具有抗糖尿病活性,因此其在抑制前列腺癌细胞的作用中可能具有独特的优势。
In this study, two kinds of prostate cancer cell lines PC-3 and DU-145 with different degrees of malignancy were used as models to study the inhibitory effects and mechanism of the proliferation inhibition of vanadium compounds metavanadate, VO (acac) _2 and VO (ma) _2 . The results showed that in both cells, three kinds of vanadium compounds can induce cell arrest in the G2 / M phase, showing an increase in tyrosine phosphorylation at position 15 of Cdc2. The results also show that vanadium compounds can cause an increase in ROS levels and that the antioxidant N-acetylcysteine can restore the Cdc25C protein levels induced by vanadium compounds, indicating that reactive oxygen species plays a role in the cycle retardation caused by vanadium compounds Regulatory effect. In addition, studies have shown that vanadium compounds have a stronger inhibitory effect on DU-145 cells than PC-3 cells lacking PTEN and higher background levels of ROS, suggesting that PTEN may serve as a biomarker for the selection of anti-tumor options in patients. Since the vanadium compounds studied have been shown to have anti-diabetic activity, they may have unique advantages in inhibiting the action of prostate cancer cells.