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姜黄素诱导肾癌786-O细胞G2/M期阻滞及其分子机制的研究 被引量:6

Studies on Curcumin Inducing Renal Carcinoma 786-O Cell G2/M Phase Arrest and Its Molecular Mechanism
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摘要 目的研究姜黄素对肾癌786-O细胞生长抑制作用及其分子机制。方法 MTT(四甲基偶氮唑盐)法检测姜黄素对肾癌细胞786-O生长影响;流式细胞术分析姜黄素对786-O细胞周期的影响;免疫印迹检测细胞周期相关靶基因表达水平。结果姜黄素能够呈浓度依赖方式显著抑制肾癌786-O细胞生长活力;细胞周期分析表明姜黄素对786-O细胞具有G2/M期阻滞效应;免疫印迹结果证明姜黄素处理后786-O细胞P53、P21蛋白均上调表达,相应Cyclin B1蛋白表达维持较低水平。结论姜黄素作用于786-O细胞导致细胞周期G2/M期阻滞,其机制可能依赖于P53和P21蛋白信号通路。 Objective To explore the growth-inhibition effects and molecular mechanism of curcumin(Cur) on 786-0 cells. Methods MTI' assay was used to detect the vitality of 786-0 cells treated with curcumin; flow cytometry was employed to examine the cell cycle distribution in 786-0 cells induced by curcumin, and immunoblotting was utilized to determine the expression level of target proteins related to cell cycle. Results Curcumin remarkably inhibited 786-0 cell vitality in dose-dependent manner. Cell cycle analysis results indicated that 786-0 cells were arrested in G2/M phase following curcumin treatment. Furthermore, immunoblotting results indicated the up-regulation of P53 and P21, and down-regulation of its downstream target gene CyclinB1 in 786-0 cells treated with curcumin. Conclusion Curcumin treatment causes 786-0 cell cycle G2/M arrest whose underlying mechanism might depend on P53/P21 signal pathway.
出处 《中药新药与临床药理》 CAS CSCD 北大核心 2015年第4期460-463,共4页 Traditional Chinese Drug Research and Clinical Pharmacology
基金 广东省中医药管理局基金(20122157)
关键词 姜黄素 肾癌 细胞周期 P53 P21 CYCLINB1 Curcumin(Cur) Renal carcinoma Cell cycle P53 P21 CyclinB1
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参考文献11

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