Mechanisms of oncogene cooperation: activation and inactivation of a growth antagonist.

Ragozzino MM, Kuo A, DeGregori J, Kohl N, Ruley HE
Environ Health Perspect. 1991 93: 97-103

PMID: 1837777 · PMCID: PMC1568054 · DOI:10.1289/ehp.919397

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.

MeSH Terms (26)

Adenovirus Early Proteins Animals Antigens, Polyomavirus Transforming Cell Line Cell Line, Transformed Cell Transformation, Neoplastic Cricetinae Epistasis, Genetic Fibroblasts Gene Expression Regulation, Neoplastic Genes, ras Genes, Retinoblastoma Genetic Complementation Test Hybrid Cells Mesocricetus Mice Mice, Nude Neoplasms, Experimental Oncogene Proteins, Viral Oncogenes Phenotype Platelet-Derived Growth Factor Proto-Oncogene Proteins Proto-Oncogene Proteins c-sis Proto-Oncogene Proteins p21(ras) Rats

Connections (1)

This publication is referenced by other Labnodes entities:

Links