Activation of Stat3 by v-Src is through a Ras-independent pathway

V-Src induces tyrosine phosphorylation of various cellular proteins and act ivates a number of signaling molecules including the Jak family of proteins tyrosine kinases and Stat (signal transducers and activators of transcript ion) proteins. Many cellular effects elicited by v-Src are mediated through Ras, a molecular switch linking growth factor receptors and non-receptor t yrosine kinases to many downstream effecters. In this report, we demonstrat ed that v-H-Ras and v-Src both induced cellular transformation. However, th e activation of Jak1 and Stat3 were only observed in v-Src transformed cell s. Using reporter gene assays, we further showed that activation of Stat3 a nd possibly of Jak I by v-Src were mediated through a Ras-independent pathw ay. As Stat3 activation has recently been shown to be required for cellular transformation by v-Src, our results suggest that activation of the Jak-St at pathway may serve as a modulator in some but not all transformation proc esses.