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cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance

In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also...

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Autores principales: Van Der Steen, Nele, Pauwels, Patrick, Gil-Bazo, Ignacio, Castañon, Eduardo, Raez, Luis, Cappuzzo, Federico, Rolfo, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491670/
https://www.ncbi.nlm.nih.gov/pubmed/25815459
http://dx.doi.org/10.3390/cancers7020556
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author Van Der Steen, Nele
Pauwels, Patrick
Gil-Bazo, Ignacio
Castañon, Eduardo
Raez, Luis
Cappuzzo, Federico
Rolfo, Christian
author_facet Van Der Steen, Nele
Pauwels, Patrick
Gil-Bazo, Ignacio
Castañon, Eduardo
Raez, Luis
Cappuzzo, Federico
Rolfo, Christian
author_sort Van Der Steen, Nele
collection PubMed
description In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors. In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism.
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spelling pubmed-44916702015-07-06 cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance Van Der Steen, Nele Pauwels, Patrick Gil-Bazo, Ignacio Castañon, Eduardo Raez, Luis Cappuzzo, Federico Rolfo, Christian Cancers (Basel) Review In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors. In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism. MDPI 2015-03-25 /pmc/articles/PMC4491670/ /pubmed/25815459 http://dx.doi.org/10.3390/cancers7020556 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Van Der Steen, Nele
Pauwels, Patrick
Gil-Bazo, Ignacio
Castañon, Eduardo
Raez, Luis
Cappuzzo, Federico
Rolfo, Christian
cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title_full cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title_fullStr cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title_full_unstemmed cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title_short cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
title_sort cmet in nsclc: can we cut off the head of the hydra? from the pathway to the resistance
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491670/
https://www.ncbi.nlm.nih.gov/pubmed/25815459
http://dx.doi.org/10.3390/cancers7020556
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