p16基因甲基化在非小细胞肺癌发病中的研究

Research on methylation of p16 gene in non-small cell lung cancer

目的研究p16基因甲基化在非小细胞肺癌(NSCLC)发病过程中的作用及其影响因素,为探索肺癌发病机制提供依据。方法采用甲基化特异性PCR(MSP)技术检测47例NSCLC患者肺癌组织和47例对应癌旁组织中DNA的p16基因甲基化状况,同时收集吸烟等环境暴露资料。结果肺癌组织中p16基因甲基化率44·7%,高于癌旁组织的17%(P<0·01),p16基因甲基化好发于鳞癌(P<0·05),在鳞癌中肺癌组织p16基因甲基化率明显高于癌旁组织,差异有显著性(P<0·01),且p16甲基化和吸烟在鳞癌中高度相关(P<0·01)。结论p16基因甲基化可能参与鳞癌的形成,且与吸烟高度相关。

Objective To study the effect of p16 gene methylation in non-small cell lung cancer and correlative factors and to explore the mechanism of lung cancer. Methods The methylation-specific PCR（MSP） was used to test the methylation status of DNA from 47 lung cancer tissues and corresponding nomalignant tissues, meanwhile data of environment exposure such as smoking was collected. Results The total frequency of p16 methylation was 44.7% in lung cancer tissues, significantly higher than that in the nomalignant tissues 17% （P 〈 0. 01 ）, p16 methylation was more seen in squamous cell carcinomas （ P 〈 0. 05 ）, there was a statistic difference of methylation frequency between lung cancer tissues and nomalignant tissues in squamous cell carcinomas （P 〈 0. 01 ）, and methylation significantly correlated with smoking in squamous cell carcinomas （ P 〈 0. 01 ）. Conclusion Methylation of p16 gene may be involved in the progress of squamous cell carcinomas,and be related with smoking/side effect.