摘要
目的:探讨胃癌组织中runx3的变化机制及胃癌中runx3甲基化改变和p53突变的区别及意义。方法:采用聚合酶链反应-单链多态性(PCR—SSCP)检测runx3的2~4外显子及p53基因5~8外显子在胃癌中的突变情况,采用甲基化特异性聚合酶链反应(MSP)技术对30例胃癌组织甲基化状态进行检测,对runx3甲基化率和p53突变率进行分析。结果:2例胃癌标本在runx3的第3外显子发现突变,第2、4外显子未发现突变改变。87%(26/30)胃癌标本runx3基因检测到甲基化改变,53.3%(16/30)胃癌标本p53基因发现突变,runx3甲基化率高于p53突变率(P〈0.05)。结论:runx3突变不是胃癌的遗传易感因素,runx3启动子区CpG岛的高甲基化是胃癌中runx3的主要改变机制。与p53突变率比较,runx3高频甲基化改变更具有胃癌的遗传学特异性,可能是引起胃癌的关键性基因。
Objective To observe the mechanism of the change in runx3 in gastric carcinoma its difference and with p53 mutation. Methods A total of 30 cases of gastric carcinoma were taken from clinical operation. PCR-SSCP method was used to detect mutations in exons 2, 3, 4 of runx3 gene in the gastric carcinoma. The methylation status of runx3 gene was examined by methylation-specific polymerase chain reaction (MS-PCR), PCR-SSCP method was used to detect mutations in exons 5, 6, 7, 8 of p53 gene in the gastric carcinoma. Results Two cases with mutation were found , methylation of runx3 promoter region was confirmed in 87% (26/30) specimens of gastric carcinoma, 53.3 % (16/30) cases were confirmed with mutation in the p53 gene. The rate of methylation of runx3 was higher than the rate of mutation of p53 (P〈0. 05). Conclusion The gene mutation of runx3 is not the change of the molecular biology of gene in the gastric carcinoma. High frequent methylation in the promoter region of runx3 is primary change in the gastric carcinoma; compared with the mutation in the p53 gene, high frequent methylation in the promoter region of runx3 has genetic specificity and runx3 is pivotal gene in the development of gastric carcinoma.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2006年第6期1074-1076,共3页
Journal of Jilin University:Medicine Edition
基金
吉林省科技厅科技发展计划项目资助课题(20000133)