Gamou S, Shimosato Y, Merlino G T, Shimizu N
Department of Molecular Biology, Keio University School of Medicine, Tokyo.
Jpn J Cancer Res. 1988 Sep;79(9):989-95. doi: 10.1111/j.1349-7006.1988.tb00065.x.
The methylation status of the epidermal growth factor receptor (EGFR) gene was compared in cell lines from four major types of lung carcinoma, small cell lung carcinoma (SCLC), large cell lung carcinoma, squamous cell carcinoma and adenocarcinoma, in order to examine whether DNA methylation is responsible for the suppression of EGFR gene in SCLC cells. Southern blot analysis revealed that the structural region of the EGFR gene is methylated to various degrees regardless of the expression of EGF receptor on the surface. An 8-kilobase EcoRI fragment which contains the EGFR gene promoter region is readily digested with various methylation-sensitive restriction enzymes in all types of cells, indicating that the EGFR gene 5' region is barely methylated. Thus, a mechanism other than DNA methylation appears to control EGFR gene expression and the lack of EGFR gene expression in SCLC cells may be caused by a paucity of some transcription regulatory factor(s).
比较了四种主要类型肺癌（小细胞肺癌、大细胞肺癌、鳞状细胞癌和腺癌）细胞系中表皮生长因子受体（EGFR）基因的甲基化状态，以研究DNA甲基化是否与小细胞肺癌细胞中EGFR基因的抑制有关。Southern印迹分析显示，无论表皮生长因子受体在表面的表达情况如何，EGFR基因的结构区域均存在不同程度的甲基化。包含EGFR基因启动子区域的一个8千碱基的EcoRI片段在所有类型的细胞中都能被各种甲基化敏感的限制性内切酶轻易切割，表明EGFR基因的5'区域几乎没有甲基化。因此，除DNA甲基化之外的其他机制似乎控制着EGFR基因的表达，小细胞肺癌细胞中EGFR基因表达的缺失可能是由于某些转录调节因子的缺乏所致。
