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

Cancers

Nele Van Der Steen³  Patrick Pauwels³  Ignacio Gil-Bazo¹  Eduardo Castañon¹  Luis Raez²  Federico Cappuzzo²  Christian Rolfo³ 

[1] Department of Oncology, Clínica Universidad de Navarra, Pamplona 31008, Spain; E-Mails:;Thoracic Oncology Program, Memorial Cancer Institute, Memorial Health Care System, Pembroke Pines, FL 33024, USA; E-Mail:;Center for Oncological Research Antwerp, University of Antwerp, Universiteitsplein 1, Wilrijk 2610, Belgium; E-Mails:

关键词: cMET;    NSCLC;    targeted therapies;   

DOI  :  10.3390/cancers7020556

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.