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机构地区:[1]第二军医大学长海医院妇产科,上海200433 [2]第二军医大学基础医学部病理生理学教研室,上海200433
出 处:《第二军医大学学报》2005年第9期1015-1017,共3页Academic Journal of Second Military Medical University
摘 要:目的:观察不同浓度的地塞米松(Dex) 对人乳腺癌细胞系(MCF-7) 细胞增殖、细胞周期分布及P21/WAF1表达的影响.方法:以不同浓度Dex(10-10~10-6 mol/L)处理细胞,采用活细胞计数法观察细胞增殖情况;测定碱性磷酸酶(AKP)活性;通过流式细胞仪技术,测定Dex作用后其细胞周期分布;通过蛋白印迹分析的方法检测Dex对p21/WAF1表达的影响.结果:Dex对MCF-7细胞的增殖有明显抑制作用, 10-7mol/L Dex作用5 d后活细胞计数为对照组的70%,细胞在G0/G1期停滞; Dex还可使MCF-7 细胞AKP活性增高,这种作用具有时间和剂量依赖性;Dex对p21/WAF1表达无明显影响.结论:Dex对MCF-7细胞有明显的增殖抑制作用,细胞在G0/G1期停滞.Objective:To study the effects of dexamethasone (Dex), a synthetic glueoeortieoid, on the proliferation and cell cycle of human breast carcinoma cell line MCF-7. Methods: MCF-7 cells were treated with different concentrations of Dex (10^-10 10^-6 mol/L). Cell proliferation was evaluated by viable cell count and alkaline phosphatase(AKP) activity was also determined. The cell cycle was examined with flow cytometry and p21/WAF1 expression was detected with Western blot analysis. Results: Dex inhibited the proliferation of MCF 7 cells, with the cell number being 70% of the control group 5 d after treatment with Dex(10^-7 mol/L). Dex also induced G0/G1 arrest of MCF-7 cells phase. AKP activity increased significantly af ter treatment with Dex in a time and dose-dependent manner. Dex had no obvious effect on p21/WAF1 expression. Conclusion: Glucocortocoids can obviously inhibit the proliferation of MCF-7 cells and induce G0/G1 phase arrest.
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