肺癌E-cadherin基因启动子CpG岛甲基化的研究

The Study of CpG Island Methylation of E-cadherin Gene Promoter in Lung Cancer

目的检测肺癌组织、相应的癌旁组织及正常肺组织中E-cadherin基因启动子CpG岛甲基化水平,探讨肺癌的发病机制。方法采用甲基化特异性PCR技术检测22例肺癌组织、相应的癌旁组织和9例正常肺组织中E-cad-herin基因启动子CpG岛甲基化水平。结果肺癌中E-cadherin基因启动子CpG岛完全甲基化率为13.6%(3/22),部分甲基化率为27.3%(6/22),总甲基化率为40.9%(9/22),显著高于相应癌旁组织中该基因的甲基化率9.1%(2/22)。9例正常肺组织中该基因未发生甲基化。此外,E-cadherin基因启动子CpG岛异常甲基化与患者性别、年龄无关,甲基化的发生率随着肿瘤的分期早晚有上升的趋势。结论E-cadherin基因启动子CpG岛的异常甲基化是肺癌发生中的常见分子事件,可能参与了肺癌的发生发展过程。

Objective To detect the CpG island methylation status of E-cadherin gene promoter in lung cancer , paired adjacent cancerous tissues and normal lung tissues, and to explore the mechanism of lung carcinogenesis. Methods The tissue specimens from 22 cases of lung cancer,adjacent cancerous tissues and 9 cases of normal lung tissues were examined CpG island methylation of E-cadherin gene promoter by methylation specific PCR. Results The positive rate of E-cadherin hypermethylation in lung tumor tissues was significantly higher than that in the adjacent cancerous tissues（40.9% vs 9.1%, P 〈0.05 ）. The incidence of promoter hypermethylation was not examined in 9 normal lung tissues. Anymore, hypermethylation of E-cadheHn was not associated with gender and age. The incidence ratio of promoter hypermethylation of E-cadherin is ascendant with the carcinomas becoming much later. Conclusion Methylation of E-cadherin gene is a common molecule event in lung cancer and play a role in the development and progression of lung cancer.