硫化砷对人结肠癌细胞株HCT116生长及迁移能力的影响  被引量:5

Arsenic Sulfide Inhibits the Proliferation and Migration Ability of HCT116 Cells in Vitro

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作  者:田玮[1] 丁文评[1] 金星镜[1] 张莲[1] 陈思宇[1] 

机构地区:[1]上海交通大学附属新华医院肿瘤科,上海200092

出  处:《现代生物医学进展》2013年第19期3615-3618,共4页Progress in Modern Biomedicine

基  金:国家自然科学基金项目(81274142;30300139);上海市科委自然基金项目(11ZR1423400);上海市教委重点项目(07zz43)

摘  要:目的:研究硫化砷对人结肠癌细胞株HCT116迁移能力的影响及其作用机制。方法:以HCT116细胞为研究对象,通过MTT法观察硫化砷对肿瘤细胞活性及增殖能力的影响,通过划痕实验观察硫化砷处理后细胞的迁移能力。Western Blot、Real-time PCR检测硫化砷处理前后细胞内E-钙粘素、P53、Notch1蛋白的表达及相应mRNA水平的变化。结果:硫化砷对HCT116细胞有抑制增殖的作用,此作用随着剂量的增加而增强。选取无毒剂量的硫化砷(1μM)处理HCT116细胞24 h后,细胞的迁移能力降低了52.00%±7.55%。Western Blot及Real-time PCR结果显示,硫化砷处理后,HCT116细胞内的E-钙粘素蛋白水平及mRNA水平均明显升高,P53蛋白水平增高,但对Notch1蛋白及mRNA水平无明显影响。结论:一定剂量范围的硫化砷能抑制HCT116细胞增殖,并能降低其迁移能力。硫化砷降低HCT116细胞的迁移能力,其机制可能是通过上调P53蛋白的水平,从而增高E-钙粘素的表达实现的。Objective: To investigate the role ofrealgar (As4S4) on regulating migration ability ofHCT116 cells in vitro. Methods: The cytotoxicity effect of As4S4 on HCT116 cells was observed by MTT assay. The effect of As454 on migration ability was observed by cell migration test. Expression of E-cadherin, P53 and Notchl protein and mRNA levels was determined by western blot assay and Real- time PCR assay. Results: The proliferation ofHCT116 cells was inhibited by AsaS4 in a dose -dependent manner. 1 IxM As454 showed no significant proliferation inhibition effect on HCTll6 cells. With this dose, As4S4 reduced the migration ability of HCTll6 cells by 52.00%+ 7.55%. AsaS4 treatment up-regulated the protein and mRNA levels of E-cadherin, up-regulated the protein level of P53, but showed no effect on Notchl. Conclusion: A$454 reduced the proliferation and migration ability ofHCT116 cells. Inhibition of the migra- tion ability probably caused by the up-regulation of P53 and E-cadherin.

关 键 词:硫化砷 雄黄 HCT116 E-钙粘素 P53 迁移 

分 类 号:R735.35[医药卫生—肿瘤] R285.5[医药卫生—临床医学]

 

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