丹参酮IIA对肾癌786-O细胞生长抑制作用及其分子机制

目的 研究丹参酮IIA对肾癌细胞生长抑制作用及其分子机制.方法 MTT法检测丹参酮IIA对肾癌细胞活力影响；流式细胞分析检测丹参酮IIA对肾癌细胞周期阻滞；免疫印迹检测细胞周期阻滞相关靶蛋白蛋白表达水平；激光共聚焦观察核仁蛋白Nucleophosmin (NPM)/B23定位的变化.结果 丹参酮能够呈浓度依赖方式显著抑制肾癌细胞生长活力(P＜0.05)；细胞周期分析表明丹参酮IIA处理的肾癌细胞阻滞在S期；免疫印迹结果证明丹参酮IIA处理肾癌细胞,cyclin A,p53及其下游基因p21显著上调；激光共聚焦结果表明在丹参酮IIA作用下,NPM蛋白定位从核仁移位到核浆.结论 丹参酮IIA作用786-O细胞导致细胞周期S阻滞,其机制可能与NPM移位促使其相互作用靶蛋白p53和p21蛋白水平上调有关.

Inhibitive Effect and Molecular Mechanism of Tanshinone IIA on Growth of Renal Carcinoma Cell 786-O

Objective To explore the inhibitive effect and molecular mechanism of Tanshinone IIA(Tan IIA) on the growth of renal carcinoma cell 786-O.Methods MTT assay was used to detect the vitality of 786-O cells after treatment with Tan IIA.Flow Cytometry was employed to examine the cell cycle distribution in 786-O cells induced by Tan IIA.Immunoblotting method was utilized to determine the expression level of target proteins related to cell cycle arrest.The translocation of Nucleophosmin(NPM)/B23 after Tan IIA treatment was observed by confocal microscopy.Results Tan IIA remarkably inhibited 786-O cells vitality in dose-dependent manner(P < 0.05).The results of cell cycle analysis indicated that 786-O cells were arrested in S phase after Tan IIA treatment.Furthermore,the upregulation of cyclin A,p53 and its downstream gene p21 in 786-O cells was shown by Immunoblotting.Translocation of NPM from nucleolus to nucleoplasm was found under confocal microscopy.Conclusion Treatment with Tan IIA can induce 786-O cell cycle S arrest,and the underlying mechanism might relate to the translocation of NPM and to the upregulation of p53 and p21.