CDKN2/p16基因5′-CpG岛SmaI位点甲基化与肺癌的关系  

Correlation between methylation on SmaI locus of the CDKN2/p16 gene CpG island and lung cancer

作　　者：苏长青[1] 叶玉坤[1] 汪栋[1] 张卫兵[1] 张志敏[1] 邱红[1] 单祥年[2] 

机构地区：[1]解放军第八一医院全军肿瘤研究中心,南京210002 [2]南京师范大学生命科学学院

出　　处：《中华肿瘤杂志》2000年第6期471-473,共3页Chinese Journal of Oncology

基　　金：国家“九五”重点科技攻关资助项目(969060118);国家自然科学基金资助项目(39670714)

摘　　要：目的　研究CDKN2 /p16基因 5′端调控序列CpG岛甲基化的状态与肺癌发生发展的关系。方法　采用对甲基化敏感的核酸内切酶SmaⅠ ,酶切基因组DNA的方法 ,对 89例肺癌标本和 10例正常肺组织的CDKN2 /p16基因进行Southern杂交分析。结果　 89例肺癌中 ,CDKN2 /p16基因甲基化者 15例 ,甲基化频率为 16 .9%。 42例p16蛋白阴性的肺癌患者中 ,有 12例发生甲基化 ,甲基化频率为 2 8.6 % ;另有 47例p16蛋白阳性患者中仅有 3例发生甲基化。 10例正常肺组织中均未发现CDKN2 /p16基因有甲基化现象。结论　CDKN2 /p16基因 5′端CpG岛甲基化是该基因失活的重要机制 ,是肺癌细胞区别于正常细胞的分子事件之一 。Objective To study the relationship between the status of methylation of the CDKN2/p16 gene 5′ CpG island and lung cancer. Methods Genomic DNA was digested with methylation sensitive enzyme SmaI and Southern blotting was applied to analyze the status of methylation of the CDKN2/p16 in 89 cases of lung cancer and 10 cases of normal lung tissue.Results Of the 89 cases of lung cancer studied, the CDKN2/p16 gene was shown to be methylated in 15 cases (16.9%). It occurred in 12 of 42 p16 protein negative cases (28.6%), and in 3 of 47 p16 protein positive cases. The CDKN2/p16 gene was not shown to be methylated in 10 cases of normal lung tissue.Conclusion Methylation of the CDKN2/p16 gene 5′ CpG island may be an important mechanism for gene inactivation in lung cancer progression.

关 键 词：肺肿瘤 CDKN2/P16基因 甲基化 核酸内切酶 

分 类 号：R734.2[医药卫生—肿瘤]