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.
出处
《现代生物医学进展》
CAS
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)
