C-MET as a new therapeutic target for the development of novel anticancer drugs.
MET is a tyrosine kinase receptor that, upon binding of its natural ligand, the hepatocyte growth factor (HGF), is phosphorylated and subsequently activates different signalling pathways involved in proliferation, motility, migration and invasion. MET has been found to be aberrantly activated in human cancer via mutation, amplification or protein overexpression. MET expression and activation have been associated with prognosis in a number of tumour types and predict response to MET inhibitors in preclinical models. Here we review the HGF/MET signalling pathway, its role in human cancer and the different inhibitory strategies that have been developed for therapeutic use.
Cañadas
I
I
Molecular Therapeutics and Biomarkers in Cancer Laboratory, Institut Municipal d'Investigacions Mediques, Hospital del Mar, Barcelona, Spain.
Rojo
F
F
Arumí-Uría
M
M
Rovira
A
A
Albanell
J
J
Arriola
E
E
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D019859:Proto-Oncogene Proteins c-met / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
D000970:Antineoplastic Agents; D019859:Proto-Oncogene Proteins c-met
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