食管癌前病变DLEC1基因启动子区的甲基化状态研究

Methylation status of DLEC1 gene promoter region of esophageal precancerous lesions

目的研究食管癌及癌前病变中DLEC1基因启动子区的高甲基化状态,并进一步观察食管重度非典型增生/原位癌组织(EDYSⅢ/CIS)病变在内镜微创治疗后甲基化状态的改变。方法采用甲基化特异性PCR(MSP)方法检测食管鳞状细胞癌组织(ESCC),EDYSⅢ/CIS,食管轻、中度非典型增生粘膜组织(EDYSⅠ~Ⅱ),食管正常粘膜组织(ENT)启动子区甲基化率并比较之间的差异,同时进一步比较EDYSⅢ/CIS病变在内镜治疗前后甲基化率的改变。结果所有标本均成功进行了MSP检测,将完全甲基化及半甲基化归为甲基化进行统计。ESCC甲基化率为75.0%,与EDYSⅢ/CIS 61.11%相比差异无统计学意义(P>0.05);EDYSⅢ/CIS组织甲基化率明显高于EDYSⅠ~Ⅱ34.62%及食管重度非典型增生/原位癌经内镜下切除修复后组织(EDYSⅢ/CISAR)9.52%,差异有统计学意义(P<0.05);EDYSⅠ~Ⅱ组织甲基化率高于ENT组织7.69%,差异有统计学意义(P<0.05)。结论 DLEC1启动子区甲基化状态可能参与食管鳞癌的发生、发展。

Objective To investigate the methylation status of DLEC1 gene promoter region after endoscopic minimally invasive treatment of esophageal precancerous lesions. Methods A methylmion specific PCR（MSP）method was applied to examine the CPG methylation of the DLEC1 gene in esophageal normal tissue（ENT）, esophageal mild or moderate dysplasia tissue（EDYSⅠ~Ⅱ）, esophageal severe dysplasia/carcinoma in situ tissue（EDYSⅢ/CIS）and esophageal squamous cell cancer（ESCC）tissues,and then compared the differences among them before and after treatment. Results All specimens were successfully detected by MSP,with a total of 4 cases,the complete methylation and semi-methylation were classified as methylation.Methylation was detected in 7.69% of ENT, in 34.62% of EDYSⅠ~Ⅱ, in 61.11% of EDYSⅢ/CIS, in 75.0% of ESCC and in 9.52% of esophageal severe dysplasia/carcinoma in situ after resection tissue（EDYS Ⅲ/CISAR）. The difference in methylation rates of EDYSⅢ/CIS and ESCC were not statistically significant（P〉0.05）. The methylation rate of EDYSⅢ/CIS was significantly higher than that of EDYSⅠ~Ⅱand EDYSⅢ/CISAR（P〈0.05）. The methylation rate of EDYSⅠ~Ⅱ was significantly higher than that of ENT（P〈0.05）. Conclusion The methylation status of DLEC1 gene promoter region may be used to diagnose ESCC.