» Articles » PMID: 25815459

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

Overview
Journal Cancers (Basel)
Publisher MDPI
Specialty Oncology
Date 2015 Mar 28
PMID 25815459
Citations 18
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Design, synthesis and biological evaluation of thienopyridine derivatives as c-Met kinase inhibitors.

Xie T, Hu W, You L, Wang X Mol Divers. 2024; .

PMID: 39356364 DOI: 10.1007/s11030-024-10998-3.


Combined inhibition of MET and VEGF enhances therapeutic efficacy of EGFR TKIs in EGFR-mutant non-small cell lung cancer with concomitant aberrant MET activation.

Huang S, Long Y, Gao Y, Lin W, Wang L, Jiang J Exp Hematol Oncol. 2024; 13(1):97.

PMID: 39354638 PMC: 11443824. DOI: 10.1186/s40164-024-00565-9.


Genomic instability in congenital lung malformations in children.

Rodrigues de Moura R, Patrizi S, Athanasakis E, Schleef J, Pederiva F, dAdamo A Pediatr Surg Int. 2024; 40(1):248.

PMID: 39237666 DOI: 10.1007/s00383-024-05835-5.


Savolitinib: A Promising Targeting Agent for Cancer.

Lee T, Kim J, Lee M, Cho I, Paik W, Ryu J Cancers (Basel). 2023; 15(19).

PMID: 37835402 PMC: 10571651. DOI: 10.3390/cancers15194708.


Targeting Amplification: Opportunities and Obstacles in Therapeutic Approaches.

Kumaki Y, Oda G, Ikeda S Cancers (Basel). 2023; 15(18).

PMID: 37760522 PMC: 10526812. DOI: 10.3390/cancers15184552.


References
1.
Kopitz C, Gerg M, Bandapalli O, Ister D, Pennington C, Hauser S . Tissue inhibitor of metalloproteinases-1 promotes liver metastasis by induction of hepatocyte growth factor signaling. Cancer Res. 2007; 67(18):8615-23. DOI: 10.1158/0008-5472.CAN-07-0232. View

2.
Elia G, Ren Y, Lorenzoni P, Zarnegar R, Burger M, Rusciano D . Mechanisms regulating c-met overexpression in liver-metastatic B16-LS9 melanoma cells. J Cell Biochem. 2001; 81(3):477-87. DOI: 10.1002/1097-4644(20010601)81:3<477::aid-jcb1061>3.0.co;2-b. View

3.
Tyner J, Fletcher L, Wang E, Yang W, Rutenberg-Schoenberg M, Beadling C . MET receptor sequence variants R970C and T992I lack transforming capacity. Cancer Res. 2010; 70(15):6233-7. PMC: 2913476. DOI: 10.1158/0008-5472.CAN-10-0429. View

4.
Wang R, Kobayashi R, Bishop J . Cellular adherence elicits ligand-independent activation of the Met cell-surface receptor. Proc Natl Acad Sci U S A. 1996; 93(16):8425-30. PMC: 38687. DOI: 10.1073/pnas.93.16.8425. View

5.
Parachoniak C, Luo Y, Abella J, Keen J, Park M . GGA3 functions as a switch to promote Met receptor recycling, essential for sustained ERK and cell migration. Dev Cell. 2011; 20(6):751-63. PMC: 3115551. DOI: 10.1016/j.devcel.2011.05.007. View