"ET-1, as well as PGE2, induced HEY and OVCA433 cells revealed a significant increase in the level of phosphorylated EGFR. Pretreatment of HEY cells with the specific EGFR kinase inhibitor, AG1478, as well as with the Src tyrosine kinase inhibitor, PP2 significantly reduced both ET-1 and PGE2 induced EGFR phosphorylation, indicating that activation of Src is essential for ET-1- and PGE2 induced EGFR transactivation. The interruption of EGFR signaling induced by AG1478, as well as by PP2, resulted in a concomitant reduction of PGE2 secretion, as well as of VEGF expression at protein and mRNA levels, indicating that Src mediated EGFR transactivation is involved in ET-1 induced PGE2 and VEGF production."
"The constitutively activated Src allele did not initially enhance growth of EGFRvIII expressing tumors, but eventually conferred a modest growth enhancement once the tumors had become very large (XREF_FIG, p = 0.03)."
"Indeed, this treatment increases EGFR expression, induces Src activation and caveolae mediated EGFR endocytosis."
"Consistent with these findings, siRNA silencing of Src also effectively reduced in vitro invasion of EGFR expressing LN229 glioblastoma cells (XREF_FIG)."