Cross-communication between the Met receptor tyrosine kinase and the epidermal growth
factor receptor (EGFR) has been proposed to involve direct association of both receptors
and EGFR kinase-dependent phosphorylation. Here, we demonstrate that in human
hepatocellular and pancreatic carcinoma cells the Met receptor becomes tyrosine
phosphorylated not only upon EGF stimulation but also in response to G protein-coupled
receptor (GPCR) agonists. Whereas specific inhibition of the EGFR kinase activity blocked …