Kendal W S, Frost P
Cancer Res. 1986 Dec;46(12 Pt 1):6131-5.
To investigate the hypothesis that increased malignant potential correlates with increased genetic instability, we measured spontaneous mutation rates for the production of ouabain-resistant mutants in two benign (nonmetastatic) murine cell lines and their recently induced metastatic variants. Metastatic variants of the NIH 3T3 and CBA SP-1 cells were induced by transfection with the h-ras oncogene. Metastatic variants were also induced from the CBA SP-1 cell line by treatment with either 2'-deoxy-5-azacytidine or hydroxyurea. Mutation rates for the parent NIH 3T3 cells and their metastatic variants were less than 3 X 10(-8) variants per cell per generation, with no significant differences between them. Rates for the CBA SP-1 line and its variants ranged from 9 X 10(-9) to 8 X 10(-8) variants per cell generation, again without statistically significant differences. We conclude that in the cell lines studied the rate of spontaneous mutation for ouabain resistance was unrelated to the acquisition of the metastatic phenotype. This conclusion was based on the view that the generation of ouabain-resistant mutants is a reflection of the overall stability of the genome. Since the spontaneous mutation rate for ouabain resistance was unchanged in cells that had recently acquired the ability to metastasize, other genetic or epigenetic events were probably responsible for progression to the malignant (metastatic) phenotype.
为了研究恶性潜能增加与基因不稳定性增加相关的假说,我们测量了两种良性(非转移性)小鼠细胞系及其最近诱导产生的转移性变体中哇巴因抗性突变体产生的自发突变率。NIH 3T3和CBA SP-1细胞的转移性变体通过用h-ras癌基因转染诱导产生。CBA SP-1细胞系的转移性变体也通过用2'-脱氧-5-氮杂胞苷或羟基脲处理诱导产生。亲代NIH 3T3细胞及其转移性变体的突变率低于每细胞每代3×10⁻⁸个变体,它们之间无显著差异。CBA SP-1细胞系及其变体的突变率范围为每细胞代9×10⁻⁹至8×10⁻⁸个变体,同样无统计学显著差异。我们得出结论,在所研究的细胞系中,哇巴因抗性的自发突变率与转移性表型的获得无关。这一结论基于这样的观点,即哇巴因抗性突变体的产生反映了基因组的整体稳定性。由于在最近获得转移能力的细胞中,哇巴因抗性的自发突变率没有变化,其他遗传或表观遗传事件可能是导致向恶性(转移性)表型进展的原因。