阿托伐他汀调控上皮间质转化抑制结肠癌细胞生长的机制研究

目的:探讨阿托伐他汀调控上皮间质转化（EMT）对人结肠癌SW480细胞侵袭和迁移的影响。方法:0.1、1、10、100 μmol/L的阿托伐他汀处理SW480细胞24 h、48 h和72 h，MTT检测细胞活力。100 μmol/L的阿托伐他汀处理细胞48 h，Transwell小室检测细胞侵袭能力及迁移能力，Western blotting检测EMT相关蛋白E-cadherin、β-catenin和Twist及PI3K/AKT信号通路PI3K、AKT和p-AKT蛋白表达。结果:随着阿托伐他汀浓度升高，作用时间延长，对SW480细胞活力抑制越明显，各浓度阿托伐他汀组与对照组比较差异具有统计学意义（P<0.05），同一实验组不同时间点间比较差异具有统计学意义（P<0.05）。与对照组比较，阿托伐他汀组细胞侵袭及迁移能力均明显降低，E-cadherin蛋白表达明显升高，β-catenin、Twist、PI3K和p-AKT蛋白表达明显降低（P<0.05）。结论:阿托伐他汀可抑制结肠癌细胞的侵袭和迁移能力，机制可能与抑制EMT及PI3K/AKT信号通路有关。

Mechanism of atorvastatin regulating epithelial mesenchymal transition inhibiting colon cancer growth

Objective:To investigate the effect of atorvastatin on invasion and migration of human colon cancer SW480 cells by regulating EMT.Methods:0.1,1,10,100 μmol/L atorvastatin treated SW480 cells with 24 h,48 h and 72 h,and cell viability was detected by MTT.when 100 μmol/L atorvastatin treated cell for 48 h,Transwell assay was used to detect cell invasiveness and migration.EMT associated protein E-cadherin,β-catenin and Twist and PI3K/AKT signaling pathways PI3K,AKT and p-AKT protein expression were detected by Western blotting.Results:As the concentration of atorvastatin increased and the time of action was prolonged,the inhibition of SW480 cell viability was more obvious,and the difference between the atorvastatin group and the control group was statistically significant (P<0.05),and the difference between the same experimental group at different time points was statistically significant (P<0.05).Compared with the control group,the cell invasion and migration ability in atorvastatin group decreased significantly,the expression of E-cadherin protein increased significantly,and the expression of β-catenin,Twist,PI3K and p-AKT protein decreased significantly (P<0.05).Conclusion:Atorvastatin can inhibit the invasion and migration of colon cancer cells,which may be related to the inhibition of EMT and PI3K/AKT signaling pathway.