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EGFR — MET
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Jo et al., J Biol Chem 2000
(Carcinoma, Hepatocellular...) :
The increase of
c-Met phosphorylation by TGFalpha in A431 cells was
inhibited by neutralizing antibodies against TGFalpha and/or EGFR and by the
EGFR-specific inhibitor tyrphostin AG1478 ... These results indicate that constitutive
c-Met phosphorylation, and the increase of c-Met phosphorylation by TGFalpha or EGF, in tumor cell lines is the
result of the activation via
EGFR
Nath et al., J Cell Sci 2001
(MAP Kinase Signaling System) :
We show that
epidermal growth factor (EGF) receptor activation, either directly by EGF or indirectly via the G-protein coupled receptor ( GPCR ) agonist lysophosphatidic acid (LPA),
induces cleavage of
Met through activation of the Erk MAP kinase signalling cascade
Bonine-Summers et al., Cancer Biol Ther 2007
(Breast Neoplasms...) :
In the present study it was shown that the
epidermal growth factor receptor (EGFR) plays a significant role in
HGF/c-Met mediated biological activities indicative of advanced tumor pathology, including enhanced proliferation and invasion ... Our analyses indicated that
EGFR inhibition significantly
blocked HGF activation of
c-Met and EGFR and that inhibition of these pathways mitigated HGF induced proliferation and motility ... The data indicate that this inhibition was not through a direct effect of gefitinib on c-Met, but that
EGFR is
necessary for
c-Met activation in the assays performed
Siegfried et al., Mol Pharmacol 2007
(Carcinoma, Non-Small-Cell Lung...) :
The addition of PGE ( 2 ) to NSCLC cells also led to rapid phosphorylation of
c-Met in the absence of HGF, which was
blocked by
epidermal growth factor receptor (EGFR) inhibition
Mueller et al., Cancer Res 2008
(Breast Neoplasms) :
Stimulating
Met kinase activity in SUM149 cells with hepatocyte growth factor
increased EGFR tyrosine phosphorylation and cell growth in the presence of EGFR TKIs
Ichihara et al., Cancer Res 2009
(Adenocarcinoma...) :
Note that phospho-MET in PC-9/VanR was suppressed following EGFR inhibition by an irreversible EGFR-TKI, indicating that
MET signaling of PC-9/VanR was
dependent on
EGFR signaling and that MET amplification was not the primary mechanism of resistance to vandetanib
Milligan et al., Clin Cancer Res 2009
(Carcinoma, Non-Small-Cell Lung...) :
EGCG also completely inhibited ligand induced
c-Met phosphorylation and partially
inhibited EGFR phosphorylation
Rho et al., Mol Cancer Res 2009
(Carcinoma...) :
In addition, hepatocyte growth factor was found to block the ability of
EGFR-TKIs to
inhibit MET activation
Xu et al., Oncogene 2010
(Carcinoma, Non-Small-Cell Lung...) :
Epidermal growth factor receptor regulates
MET levels and invasiveness through hypoxia-inducible factor-1alpha in non-small cell lung cancer cells ...
EGFR regulation of
MET levels in cell lines occurred through the hypoxia-inducible factor (HIF)-1alpha pathway in a hypoxia independent manner
Mueller et al., Journal of molecular signaling 2010
:
Here we have found that
EGFR phosphorylation and cell proliferation is in part
regulated by
Met expression
Yue et al., Eur J Cancer 2011
(Carcinoma, Hepatocellular...) :
DCP was found to bind to the cell surface receptor Met, resulting in
Met phosphorylation and subsequent
activation of the
epidermal growth factor receptor (EGFR)
Gusenbauer et al., Oncogene 2013
(Neoplasms) :
However, only little is known about the
HGF/Met induced
EGFR TKI resistance mechanism in other human cancer types
Stabile et al., Clin Cancer Res 2013
(Head and Neck Neoplasms) :
Inhibiting
EGFR resulted in minimal reduction of
phospho-Met in DA-Src cells, whereas complete phospho-Met inhibition was achieved by inhibiting c-Src
Breindel et al., Cancer Res 2013
:
However, promiscuous interactions between MET and ERBB family members have made it difficult to evaluate the
effects of
MET on
EGFR signaling, both independent of drug treatment and in the context of drug resistance ... Using this model, we determined that
EGFR signaling is
sufficient to induce
MET phosphorylation, although MET activation is enhanced by coexpression of ERBB3