C-Met, the tyrosine kinase receptor of hepatocyte growth factor (HGF), influences behaviour of several cancer types by controlling growth, morphogenesis, angiogenesis, invasion and metastasis.Its overexpression correlates closely with metastatic tendency and poor prognosis.In addition, several germline and somatic missense mutations of cMet, which lead to increased tyrosine kinase activity, have been reported in various tumours.We aim to understand c-Met compartmental signalling and to elucidate if this is a mechanism for receptor deregulation in human cancers.In previous work, we provided evidence that c-Met endocytosis controls ERK1/2 temporal and spatial regulation to stimulate cell migration.It will be shown here that c-Met endomembrane traffic controls HGF dependent STAT3 nuclear uptake.This is an active process that is predicted to be more efficient than simple diffusion.Further data on trafficking and signalling of c-Met will be presented.