摘要
目的:探讨去甲基化药物5-氮杂-2’-脱氧胞苷(5-Aza-2’-deoxycytidine,5-Aza-CdR)对人肝癌细胞株SMMC7721细胞增殖以及对死亡相关蛋白激酶(Death-associated protein kinase,DAPK)基因mRNA表达水平的影响。方法:用不同浓度(0.5,5.0,50.0μmol/L)的5-Aza-CdR对SMMC7721细胞处理后,采用MTT法检测细胞的增殖情况;半定量RT-PCR法检测各组细胞DAPK mRNA的表达水平。结果:5-Aza-CdR对肝癌细胞株SMMC7721生长有明显抑制作用,并且存在剂量依赖性反应关系(F=242.40,P<0.01);半定量RT-PCR结果显示,MMC7721细胞中DAPK mRNA表达水平很弱,采用不同浓度5-Aza-CdR处理SMMC7721细胞72h后,SMMC7721细胞中DAPK mRNA表达水平呈剂量依赖性逐渐升高(F=360.41,P<0.01)。结论:5-Aza-CdR可诱导MMC7721细胞DAPK mRNA表达,并抑制SMMC7721细胞增殖。
Objective： To explore the effect of DNA methylation inhibitor 5-Aza-2＇-deoxycytidine（5-Aza-CdR） on the proliferation of human hepatoma cell line SMMC7721 cells and the expression of tumor suppressor gene DAPK mRNA.Methods： Human hepatoma cell line SMMC7721 cells were treated with different concentrations（0.5,5.0,50.0 μmol/L） of 5-Aza-2＇-deoxycytidine.The cell proliferation and the expression of DAPK mRNA in SMMC7721 cells were detected using a MTT cell proliferation assay and a real-time reverse transcription polymerase chain reaction（RT-PCR） assay,respectively.Results： The proliferation of SMMC7721 cells was significantly inhibited in a dose-dependent manner（F=242.40,P0.01）.The expression of DAPK mRNA was very weak in SMMC7721 cells.However,after SMMC7721 cells were treated with5-Aza-CdR for 72 hours,the expression levels of DAPK mRNA were gradually increased in a dose-dependent manner（F=360.40,P0.01）.Conclusion： 5-Aza-CdR inhibited SMMC7721 cell proliferation,and induced the expresseion of DAPK mRNA in SMMC7721 cells.
出处
《广西医科大学学报》
CAS
2012年第1期13-16,共4页
Journal of Guangxi Medical University
基金
广西自然科学基金(No.0832288)
国家自然科学基金(30660162)
国家自然科学基金(30860247)
广西自然科学基金(No.0991126
0832017Z)
广西科学研究与技术开发项目(桂科攻No.0719006-2-13
0993003D-4)
广西大型仪器协作网测试补助(668-2008-081)
