1. Mechanisms of oncogene cooperation: activation and inactivation of a growth antagonist
- Author
-
N E Kohl, H E Ruley, James DeGregori, A Kuo, and M M Ragozzino
- Subjects
Platelet-derived growth factor ,Oncogene Proteins ,Health, Toxicology and Mutagenesis ,Antigens, Polyomavirus Transforming ,Mice, Nude ,Biology ,Hybrid Cells ,Cell Line ,Proto-Oncogene Proteins p21(ras) ,chemistry.chemical_compound ,Mice ,Cricetinae ,Proto-Oncogene Proteins ,Animals ,Genes, Retinoblastoma ,Cell Line, Transformed ,Regulation of gene expression ,Platelet-Derived Growth Factor ,Oncogene ,Mesocricetus ,Adenovirus Early Proteins ,Genetic Complementation Test ,Public Health, Environmental and Occupational Health ,Epistasis, Genetic ,Neoplasms, Experimental ,Oncogene Proteins, Viral ,Oncogenes ,Proto-Oncogene Proteins c-sis ,Fibroblasts ,Phenotype ,Rats ,Gene Expression Regulation, Neoplastic ,Cell Transformation, Neoplastic ,Genes, ras ,chemistry ,Cell culture ,Cancer research ,Research Article - Abstract
Gene transfer experiments have defined limitations with regard to the ability of individual oncogenes to transform cultured cells to a tumorigenic state. The stable transformation of REF52 cells by either the ras or sis oncogenes requires the continuous expression of a second collaborating oncogene, such as adenovirus-5 E1A or SV40 large T-antigen. Our studies suggest that the function of the nuclear collaborators is to antagonize dominant growth controls which limit the ability of REF52 cells to proliferate in response to mitogenic stimuli.
- Published
- 1991