A Mutant p53 Protein is Required for Maintenance of the Transformed Phenotype in Cells Transformed with p53 Plus Ras cDNAs

Mutant p53 and activated ras cDNA clones cooperate to fully transform primary rat embryo fibroblasts in cell culture, whereas neither cDNA alone results in the full transformation of these cells. The mutant p53 protein may be required to initiate the transformation event with ras. Alternatively, mut...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1992-05, Vol.89 (9), p.3952-3956
Main Authors: Zambetti, Gerard P., Olson, David, Labow, Mark, Levine, Arnold J.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell culture techniques
Cell Division
Cell growth
Cell lines
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cell Transformation, Neoplastic - genetics
Cells, Cultured
Cellular biology
Complementary DNA
Cultured cells
Deoxyribonucleic acid
DNA
Fundamental and applied biological sciences. Psychology
Gene Expression
Gene expression regulation
Genes, p53
Genes, ras
Immunoprecipitation
In Vitro Techniques
Molecular and cellular biology
Mutation
p53 genes
Phenotypes
Proteins
Proto-Oncogene Proteins p21(ras) - physiology
Rats
Rodents
Transfection
Transformed cell line
Tumor Suppressor Protein p53 - physiology
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Summary:Mutant p53 and activated ras cDNA clones cooperate to fully transform primary rat embryo fibroblasts in cell culture, whereas neither cDNA alone results in the full transformation of these cells. The mutant p53 protein may be required to initiate the transformation event with ras. Alternatively, mutant p53 gene expression may be required to maintain the properties of the transformed phenotype. To distinguish between these possibilities, primary rat embryo fibroblasts were transformed with mutant p53 plus ras cDNAs, where the expression of the p53 gene was regulated by an isopropyl β-D-thiogalactoside-responsive promoter. When expression of the mutant p53 cDNA was inhibited and no detectable exogenous p53 protein was produced, both the growth rate and the morphology of the cells reverted to a normal phenotype. These results demonstrate that a mutant p53 protein is required for the maintenance of the transformed phenotype in cells transformed with p53 plus ras cDNAs.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.89.9.3952