摘要
背景与目的:启动子区CpG岛高甲基化是导致基因转录水平下调的重要表观遗传学机制,我们前期的研究发现EphA7基因在部分胃癌中表达下调。本研究探讨EphA7基因下调的机制及其临床意义。方法:检测6株胃癌细胞及62例胃癌标本中EphA7基因甲基化状态。采用同位素掺入方法对胃癌细胞系的EphA7基因表达进行半定量RT-PCR测定;利用亚硫酸氢钠处理DNA后,进行DNA测序和甲基化特异性PCR检测。结果:对胃癌细胞系亚硫酸氢钠修饰后DNA测序发现,在EphA7基因启动子区内CpG岛存在超甲基化现象,利用甲基化特异性PCR检测胃癌标本证实,在部分胃癌组织中存在高甲基化。高甲基化与胃癌细胞的分化程度有关(P=0.03)。结论:高甲基化是导致该基因下调的机制之一。EphA7基因在胃癌的发生过程中可能发挥一定作用。
Background and purpose： Hypermethylation of CpG island in the promoter region is an important epigenetic mechanism that can lead to down-regulation of genes. We previously found there was down-regulation of EphA7 transcript in parts of gastric cancer. Our aim was to study the mechanism of down-regulation of EphA7 and its clinical significances. Methods： We detected hypermethylaiton of EphA7 using bisulfite sequencing and methylation specific PCR in gastric cancer cell lines and gastric carcinoma specimens. We used semiquantitative RT-PCR with isotope to detect expression of EphA7 in gastric cancer cell lines. Methylation status of EphA7 in gastric cancer cell lines and gastric carcinoma samples was analyzed using bisulfite sequencing and methylation specific PCR. Results： We detected hypermethylation of CpG island of EphA7 in gastric cell lines using bisulfite sequencing, and confirmed it in gastric carcinoma specimens using specific methylation PCR. Methylation status is significantly related to differentiation（ P = 0.03）. Conclusions： Hypermethylation is one of the mechanisms that lead to down-regulation of EphA7 in gastric carcinoma. EphA7 may play a role in the development of gastric carcinoma.
出处
《中国癌症杂志》
CAS
CSCD
2007年第6期457-460,共4页
China Oncology
基金
全国博士后科学基金(No:2005038578)
江苏省博士后基金
南京军区医学科学技术研究"十一五"计划重点课题(No:06Z37)
关键词
EPHA7
胃癌细胞系
胃癌
高甲基化
EphA7
gastric cancer cell line
gastric carcinoma
hypermethylation
