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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 study the effect of arsenic sulfide on the migration of human colon carcinoma cell line HCT116 and its mechanism. Methods: HCT116 cells were used as research objects. The effects of arsenic sulfide on activity and proliferation of tumor cells were observed by MTT assay. The migration ability of arsenic sulfide treated cells was observed by scratch test. Western Blot and Real-time PCR were used to detect the expression of E-cadherin, P53, Notch1 and the corresponding mRNA levels before and after treated with arsenic sulfide. Results: As4S inhibited the proliferation of HCT116 cells, and its effect increased with the increase of dose. The cytotoxicity of HCT116 cells was reduced by 52.00% ± 7.55% after treated with non-toxic dose of arsenic sulfide (1μM) for 24 h. The results of Western Blot and Real-time PCR showed that the E-cadherin and mRNA levels of HCT116 cells were significantly increased and the level of P53 protein was increased after treatment with As 2 S 4, but no significant effect on Notch 1 protein and mRNA levels was observed. Conclusion: Arsenic sulfide at a dose range can inhibit the proliferation of HCT116 cells and decrease its migration ability. Arsenic sulfide reduces HCT116 cell migration, the mechanism may be through the increase of P53 protein levels, thereby increasing E-cadherin expression achieved.