Transformation of NIH 3T3 cells by cotransfection with c-src and nuclear oncogenes - PubMed (original) (raw)
Transformation of NIH 3T3 cells by cotransfection with c-src and nuclear oncogenes
D Shalloway et al. Mol Cell Biol. 1987 Oct.
Abstract
pp60c-src, the cellular homolog of the Rous sarcoma virus transforming protein, does not completely transform cells even when present at high levels, but has been shown to be involved in polyomavirus-induced transformation when activated by polyomavirus middle T (pmt)-antigen binding. Here we show that cotransfection, but not solo transfection, of expression plasmids for c-src and either adenovirus E1A, v-myc, c-myc, or the 5' half of polyomavirus large T (pltN) antigen into NIH 3T3 cells induces anchorage-independent growth, enhanced focus formation, and, for pltN cotransfection, tumorigenicity in adult NFS mice. Enhancement of transformation was not observed with polyomavirus small t (pst) antigen. Cotransfection of c-src with pltN induced modification of pp60c-src that altered its electrophoretic mobility and in vivo phosphorylation state and stimulated its in vitro kinase activity. Similar alterations were not seen after c-src-E1A cotransfection, suggesting that at least two different mechanisms of enhancement are involved.
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References
- J Mol Appl Genet. 1982;1(4):327-41 - PubMed
- J Virol. 1987 May;61(5):1593-601 - PubMed
- J Virol. 1983 Jan;45(1):462-5 - PubMed
- Cell. 1983 Mar;32(3):881-90 - PubMed
- Proc Natl Acad Sci U S A. 1983 May;80(9):2519-23 - PubMed
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