The human T24 Ha-ras1 oncogene: a study of the effects of overexpression of the mutated ras gene product in rodent cells.
The human T24 Ha-ras1 oncogene was inserted into a high expression vector which carried the aminoglycoside phosphotransferase (aph) gene as a selectable market. This recombinant was introduced into early passage rodent cells by the calcium-phosphate technique. Under the selection pressure of geneticin foci appeared of morphologically altered cells which became immortalized, anchorage independent and tumourigenic. These cells overexpressed the p21 product of the T24 Ha-ras1 oncogene. It was concluded that p21 is not toxic to these cells. In reconstruction experiments, where transformed and normal cells were plated together at various cell densities, normal cells, at high cell density and in the absence of selection, suppressed the transformed phenotype.
D000818:Animals; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D006224:Cricetinae; D005260:Female; D006801:Humans; D009154:Mutation; D009363:Neoplasm Proteins / Q000096:biosynthesis*; D015689:Oncogene Protein p21(ras); D009857:Oncogenes; D010641:Phenotype; D051381:Rats; D014158:Transcription, Genetic
D009363:Neoplasm Proteins; D015689:Oncogene Protein p21(ras)