TSA对食管癌细胞系EC9706细胞周期作用及分子机制的探讨

The molecular mechanism of TSA to esophagus cancer cell line EC9706 mitotic cycle function

目的研究去乙酰化酶抑制剂曲古菌素A(TSA)对食管癌细胞EC9706细胞周期的作用及机制。方法将浓度为0.5、1.0、1.5μmol/L TSA作用EC9706细胞24 h,用MTT观察不同浓度TSA对EC9706细胞的生长抑制作用;流式细胞仪检测细胞生长及周期;Western Blot检测TSA对食管癌细胞周期相关基因的表达。结果 1.0μmol/L浓度的TSA对EC9706细胞有明显的生长抑制作用,并呈现一定的量效关系,在1.0μmol/L浓度之上可明显诱导食管癌细胞EC9706细胞周期阻滞,明显增强p21、p27基因的表达,明显降低CCND1、CDK4D基因的表达。结论一定剂量的TSA可抑制食管癌EC9706细胞的生长,通过调控多个细胞周期相关基因诱导食管癌细胞细胞周期阻滞,细胞阻滞的发生与p21、p27基因表达的增加及CCND1、CDK4D基因表达的减少相关。

Objective To study the deacetylase inhibitor TSA on the esophageal cancer cell EC9706 cell cycle effect and its mechanism.Methods 0.5,1.0,1.5 μmol/L TSA actin EC9706 cells 24 hours,the effects of different concentrations of TSA on EC9706 cell growth inhibition were observed by MTT,flow cytometry measured cell growth and cycle;TSA on esophageal cancer cell cycle-related genes expression by Western Blot test.Results 1.0 μmol/L concentration of TSA on the EC9706 inhibited the growth of cells and showed a definite dose-effect relationship,above 1.0 μmol/L concentration could significantly induce cell cycle arrest of esophageal cancer cell EC9706 could significantly enhance the p21,p27 gene expression,decreased CCND1,CDK4D gene expression.Conclusion The dose of TSA inhibite the growth of esophageal cancer EC9706 cells by regulating multiple cell cycle-related genes induced by esophageal cancer cells in cell cycle arrest,cell block occurrence revelant with p21,p27 gene expression increase and CCND1,CDK4D expression gene reduction.