Spandidos A, Wilkie N M
Beatson Institute for Cancer Research, Bearsden, Glasgow, UK.
Br J Cancer Suppl. 1988 Dec;9:67-71.
The altered morphology and tumorigenic phenotypes of rat 208F fibroblasts transformed with the human T24 H-ras1 oncogene is suppressed by transfection with the human normal H-ras1 gene. In the suppressed cells, both the normal and mutant T24 ras gene products are expressed although the normal p21 is expressed at a higher level. Rare transformants or tumours derived from suppressed cells possess reduced expression of normal ras p21. Our findings suggest that transforming ras alleles do not behave in a dominant manner and that elevated expression of the normal allele could cause suppression of the morphologically transformed and tumorigenic phenotypes.
用人T24 H-ras1癌基因转化的大鼠208F成纤维细胞的形态改变和致瘤表型,可通过转染人正常H-ras1基因而受到抑制。在被抑制的细胞中,正常和突变的T24 ras基因产物均有表达,尽管正常的p21表达水平更高。源自被抑制细胞的罕见转化体或肿瘤,其正常ras p21的表达降低。我们的研究结果表明,具有转化作用的ras等位基因并非以显性方式发挥作用,正常等位基因的表达升高可导致形态转化和致瘤表型受到抑制。