Paterson H, Reeves B, Brown R, Hall A, Furth M, Bos J, Jones P, Marshall C
Institute of Cancer Research, Chester Beatty Laboratories, London, U.K.
Cell. 1987 Dec 4;51(5):803-12. doi: 10.1016/0092-8674(87)90103-6.
To investigate whether the activated N-ras oncogene of HT1080 human fibrosarcoma cells contributes to the expression of the transformed phenotype, we have isolated flat revertants. In two independent revertant lines, an increase in chromosomal ploidy occurred without a concomitant increase in the number of copies of the N-ras transforming allele. Immunoprecipitation confirms that the level of the mutant N-ras p21 gene product in the revertants is correspondingly lower than in HT1080. Analysis of sporadic tumors derived from the revertant cells reveals an increased dosage of the transforming allele. The revertants also retransform after transfection of cloned activated ras oncogenes. These results imply direct participation of an N-ras oncogene in maintaining the transformed phenotype of a human tumor cell line.
为了研究HT1080人纤维肉瘤细胞中激活的N-ras癌基因是否有助于转化表型的表达，我们分离出了扁平回复突变体。在两个独立的回复突变体系中，染色体倍性增加，而N-ras转化等位基因的拷贝数没有相应增加。免疫沉淀证实，回复突变体中突变型N-ras p21基因产物的水平相应低于HT1080细胞。对来自回复突变体细胞的散发性肿瘤分析显示，转化等位基因的剂量增加。回复突变体在转染克隆的激活型ras癌基因后也会再次转化。这些结果表明，N-ras癌基因直接参与维持人肿瘤细胞系的转化表型。
