Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Mar 25;13:2491–2510. doi: 10.2147/OTT.S231257

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 Liang and Wang.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

Major Mechanism of MET/HGF axis dysregulation. The extracellular portion of c-MET consists of a four immunoglobulin (Ig)-like modules, a cysteine-rich, MET-related sequence domain, and a Sema domain (homologous to semaphorin) responsible for binding to HGF. The intracellular portion of c-MET consists of the paramembrane domain, the Catalytic domain, and the Docking site responsible for signal transduction. Various mechanisms of MET/HGF axis addiction in NSCLC, including MET/HGF overexpression, and MET gene alterations (including point mutations, amplification, and fusion). A number of drugs targeting MET (small molecule TKIs, MET antibody, and HGF antibody) have been studied. MET, c-mesenchymal-epithelial transition factor; HGF, hepatocyte growth factor; NSCLC, non-small cell lung cancer.