Differential responses of MET activations to MET kinase inhibitor and neutralizing antibody.

ABSTRACT:

Background

Aberrant MET tyrosine kinase signaling is known to cause cancer initiation and progression. While MET inhibitors are in clinical trials against several cancer types, the clinical efficacies are controversial and the molecular mechanisms toward sensitivity remain elusive.

Methods

With the goal to investigate the molecular basis of MET amplification (MET^amp) and hepatocyte growth factor (HGF) autocrine-driven tumors in response to MET tyrosine kinase inhibitors (TKI) and neutralizing antibodies, we compared cancer cells harboring MET^amp (MKN45 and MHCCH97H) or HGF-autocrine (JHH5 and U87) for their sensitivity and downstream biological responses to a MET-TKI (INC280) and an anti-MET monoclonal antibody (MetMab) in vitro, and for tumor inhibitio

SUBMITTER: Kou J 

PROVIDER: S-EPMC6134500 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature