中国肿瘤生物治疗杂志2011，Vol.18Issue(2)：139-143,5.DOI:10.3872/j.issn.1007-385X.2011.02.004
CHFR基因CpG岛甲基化对食管癌Eca109细胞增殖和凋亡的影响
Effect of CHFR CpG island methylation status on proliferation and apoptosis of esophageal cancer Eca109 cells
摘要
Abstract
Objective:To study the relationship of CHFR CpG island methylation status on proliferation and apoptosis of esophageal cancer Eca109 cells.Methods: Eca109 cells were treated with different concentrations (2, 5, and 10 μmol/L) of 5-Aza-2'-deoxycytidine (5-Aza-CdR), and untreated Eca109 cells were used as control.Methylation-specific PCR (MSP) analysis was used to evaluate the CpG island methylation status of CHFR gene, and RT-PCR was used to detect the CHFR mRNA expression in Eca109 cells.MTT and flow cytometery were used to determine the proliferation and apoptosis of Eca109 cells treated with different concentrations of 5-Aza-CdR.Results: CHFR CpG island was hypermethylated in the untreated Eca109 cells, and methylated CHFR CpG was demethylated to different degrees in 5-Aza-CdR treatment groups.No expression of CHFR mRNA was found in untreated Eca109 cells, but the relative expression of CHFR mRNA was remarkably increased in 5-Aza-CdR (2, 5, and 10 μmol/L) treatment groups (0.174 ±0.010, 0.221 ±0.013, and 0.356 ±0.014).Different concentrations of 5-Aza-CdR inhibited the proliferation ( [30.87 ± 0.74]％, [44.60 ± 0.79]％, and [56.67 ± 0.35]％ ), and promoted apoptosis of Eca109 cells ( [7.46 ± 1.46]％, [16.27 ± 1.61]％, [25.29 ± 2.25]％ vs [1.83 ± 0.411％, P ＜ 0.01 ).Conclusion: 5-Aza-CdR can partly demethylate CHFR CpG island in esophageal cancer Eca109 cells, inducing CHFR mRNA expression, inhibiting proliferation and promoting apoptosis of Ecal09 cells.关键词
CHFR基因/甲基化/食管癌/Eca109细胞/增殖/凋亡分类
医药卫生引用本文复制引用
朱应超,田辉,岳韦名,高存,亓磊,司立博..CHFR基因CpG岛甲基化对食管癌Eca109细胞增殖和凋亡的影响[J].中国肿瘤生物治疗杂志,2011,18(2):139-143,5.基金项目
国家自然科学基金资助项目(No.30571844) （No.30571844）
山东省科技攻关项目(No.2009GG10002007) （No.2009GG10002007）
山东省自然科学基金项目(No.ZR2009CM090). （No.ZR2009CM090）
