Activation of Stat3 by v-Src is through a Ras-independent pathway.
V-Src induces tyrosine phosphorylation of various cellular proteins and activates a number of signaling molecules including the Jak family of proteins tyrosine kinases and Stat (signal transducers and activators of transcription) proteins. Many cellular effects elicited by v-Src are mediated through Ras, a molecular switch linking growth factor receptors and non-receptor tyrosine kinases to many downstream effectors. In this report, we demonstrated that v-H-Ras and v-Src both induced cellular transformation. However, the activation of Jak1 and Stat3 were only observed in v-Src transformed cells. Using reporter gene assays, we further showed that activation of Stat3 and possibly of Jak1 by v-Src were mediated through a Ras-independent pathway. As Stat3 activation has recently been shown to be required for cellular transformation by v-Src, our results suggest that activation of the Jak-Stat pathway may serve as a modulator in some but not all transformation processes.[1]References
- Activation of Stat3 by v-Src is through a Ras-independent pathway. Liu, J.J., Nakajima, K., Hirano, T., Yang-Yen, H.F. J. Biomed. Sci. (1998) [Pubmed]
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