Polly P, Nicholson R C
Carcinogenesis Research Unit, School of Pathology, University of New South Wales, Sydney, Australia.
Cancer Lett. 1994 Jan 30;76(2-3):87-92. doi: 10.1016/0304-3835(94)90382-4.
A cell culture model of mouse lung alveologenic carcinoma, consisting of type 2 pneumocyte-related cells, known to contain an A to G transition in the second base position of codon 61 of the c-Ki-ras gene has been examined for molecular changes affecting nuclear oncogenes. A small, twofold increase in c-myc mRNA levels and transcription levels was observed in malignant cell lines (C4SE9 and NULB5) compared with non-malignant cells (C4E10). Interestingly, the transcriptional level of the c-myc gene in C4E10 cells was very high relative to any other gene examined. Similar high levels of c-myc gene expression levels were also observed in type 2 pneumocytes obtained from normal mouse lung tissue. No major DNA rearrangements or amplifications were detected between C4E10 cells and either C4SE9 or NULB5 cell lines. These data suggest that high levels of c-myc gene expression occurred prior to the activating point mutation of the c-Ki-ras gene and may predispose the type 2 pneumocyte to transformation.
一种由2型肺上皮细胞相关细胞组成的小鼠肺泡源性癌细胞培养模型，已知其c-Ki-ras基因第61密码子的第二个碱基位置存在A到G的转换，已对影响核癌基因的分子变化进行了检测。与非恶性细胞（C4E10）相比，在恶性细胞系（C4SE9和NULB5）中观察到c-myc mRNA水平和转录水平有小幅两倍的增加。有趣的是，相对于所检测的任何其他基因，C4E10细胞中c-myc基因的转录水平非常高。在从正常小鼠肺组织获得的2型肺上皮细胞中也观察到了类似的高水平c-myc基因表达。在C4E10细胞与C4SE9或NULB5细胞系之间未检测到主要的DNA重排或扩增。这些数据表明，c-myc基因的高水平表达发生在c-Ki-ras基因的激活点突变之前，并且可能使2型肺上皮细胞易于发生转化。
