舒林酸经survivin/Aurora B途径对人胰腺癌细胞分裂的阻断效应
The inhibitory effect of Sulindac on human pancreatic cancer cells' proliferation by targeting survivin/ Aurora B pathway
摘要目的 观察舒林酸处理胰腺癌细胞BxPC3后对survivin、Aurora B表达及细胞周期和增殖的影响,探讨舒林酸的作用机制.方法 应用MTT法检测舒林酸对BxPC3细胞的增殖抑制作用,RT-PCR法检测survivin mRNA、Aurora B mRNA的表达,Western blot法检测survivin蛋白表达及Aurora BThr-232磷酸化水平,流式细胞仪检测细胞周期变化.结果 舒林酸呈时间和剂量依赖性抑制BxPC3细胞增殖.经500μmoL/L舒林酸作用细胞48 h后,survivin mRNA和Aurora B mRNA表达量分别从1.56和0.66下降到0.44和0.11(P<0.01);survivin蛋白表达从1.27下降到0.21(P<0.01),Aurora BThr-232磷酸化水平从0.47下降到0.25(P<0.01);G0/G1期细胞比例从(56.65±1.93)%升高到(70.58±3.21)%(P<0.01).结论 舒林酸通过下调survivin表达,降低Aurora B的活性,从而影响染色体过客复合物蛋白(CPC)对细胞染色体的排列和分离作用,使大量细胞停滞在G0/G1期,从而抑制细胞的有丝分裂.
更多相关知识
abstractsObjective To observe the expression of survivin and Aurora B in human pancreatic cancer BXPC3 cells after the treatment of sulindac and to explore the potential mechanism. Methods MTr assay was used to determine the effect of sulindac on the proliferation of the BXPC3 cells. RT-PCR was used to detect the expression of mRNA level of survivin and Aurora B, western blot was used to detect protein expression of survivin and Aurora B Thr-232. Cell cycle and apoptosis were detected by flow eytometry (FCM). Results The BXPC3 cells were inhibited by sulindac in a dose and time-dependent manner; the expression of mRNA of survivin and Aurora B were both significantly decreased from 1.5644 and 0.6554 to 0. 4372 and 0.1132 (P< 0.01), the expression of survivin protein and the phosphorylation of Aurora B Thr-232 were also decreased from 1.2735 and 0.4680 to 0.2126 and 0.2546 (P<0.01); the proportion of cells in the G0/G1 phase was increased from (56.65±1.93)% to (70.58±3.21)% (P<0.01). Conclusions Sulindac had inhibitory effects on the growth of BXPC3 cells, the possible mechanism was via decreasing the expression of survivin which depressed the activity of Aurora B, then the CPC was influenced. The most of the cells were blocked in the G0/G1 phase, and the cells' mitosis was inhibited.
More相关知识
- 浏览279
- 被引1
- 下载1
相似文献
- 中文期刊
- 外文期刊
- 学位论文
- 会议论文