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 hum...

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Bibliographic Details
Published in:Clinical & translational oncology 2010-04, Vol.12 (4), p.253-260
Main Authors: Cañadas, Israel, Rojo, Federico, Arumí-Uría, Montserrat, Rovira, Ana, Albanell, Joan, Arriola, Edurne
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - pharmacology
Educational Series
Humans
Medicine
Medicine & Public Health
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Oncology
Proto-Oncogene Proteins c-met - genetics
Proto-Oncogene Proteins c-met - metabolism
Signal Transduction - physiology
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Summary: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.
ISSN:1699-048X
1699-3055
DOI:10.1007/s12094-010-0501-0