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The simian virus 40 large tumor antigen activates cSrc and requires cSrc for full neoplastic transformation.

AIM
To investigate the role of the cellular protooncogene product, cSrc, in neoplastic transformation by the large tumor antigen of simian virus 40 (TAg), the ability of TAg to increase cSrc activity was examined.


MATERIALS AND METHODS
cSrc activity was measured in cells expressing wild-type or mutant TAg and compared to the parental line.


RESULTS
The results indicated that TAg expression in mouse 3T3 fibroblasts causes a dramatic increase in cSrc activity, a finding which establishes TAg as a cSrc activator. This ability depended upon a TAg, intact retinoblastoma-susceptibility gene product (Rb) family-binding site. In addition, genetic ablation of pRb in mouse fibroblasts increased cSrc activity, suggesting that pRb inactivation by TAg might be responsible for the observed cSrc activation. Furthermore, down-regulation or genetic ablation of cSrc alone, or together with the Src family members, Yes and Fyn, caused a dramatic reduction in the ability of TAg to transform mouse fibroblasts.


CONCLUSION
Taken together, these findings suggest for the first time that cSrc is part of an important pathway emanating from TAg and leading to neoplastic conversion.