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HGF — SRC
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
HGF(dimer)/MET(dimer) complex (MET-HGF)
→
Src (SRC)
(modification, activates)
Kanda et al., Biochem Biophys Res Commun 2006*, Rush et al., Exp Cell Res 2007*, Ponzetto et al., Cell 1994
Evidence: assay, physical interaction
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
Src (SRC)
→
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
(modification, activates)
Chan et al., J Biol Chem 2003*, Chan et al., Oncogene 2010
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
Src (SRC)
→
HGF(dimer)/MET(dimer)/GAB1/SHP2 complex (MET-GAB1-PTPN11-HGF)
(modification, activates)
Chan et al., J Biol Chem 2003*, Chan et al., Oncogene 2010
Evidence: mutant phenotype, assay
Text-mined interactions from Literome
Manganini et al., Oncogene 2000
:
Indeed, TGF beta2 inhibited HGF effects because it prevented
HGF induced MAP kinase activation and tyrosine phosphorylation of
Src
Hung et al., J Biol Chem 2001
(Mammary Neoplasms, Experimental) :
Expression of activated
c-Src in SP1 cells
increased transcription from the
HGF promoter and expression of HGF mRNA and protein, while dominant negative c-Src had the opposite effect ... Coexpression of activated
c-Src and Stat3 synergistically
induced strong
HGF promoter activity in SP1 cells, as well as in a nonmalignant epithelial cell line, HC11 ( HGF negative )
Elliott et al., Can J Physiol Pharmacol 2002
(Breast Neoplasms...) :
We have recently demonstrated that sustained activation or hyper-activation of
c-Src and Stat3, which occurs in invasive breast cancer, can
stimulate strong expression of
HGF in carcinoma cells
Pongchairerk et al., World J Gastroenterol 2005
(Cholangiocarcinoma) :
Autophosphorylated
Src ,
induced by
HGF , mediates Src kinase activation, which subsequently phosphorylates its substrate, FAK, and signals to cell proliferation and invasion
Kanda et al., Biochem Biophys Res Commun 2006
:
Stable expression of kinase-inactive Src in MSS31 cells inhibited
HGF induced activation of
Src as well as capillary morphogenesis ... These results suggest that
HGF induces capillary morphogenesis of endothelial cells through
Src
Sam et al., Molecular cancer 2007
(Breast Neoplasms) :
A novel activating
role of
SRC and STAT3 on
HGF transcription in human breast cancer cells ...
Src/Stat3 expression did
activate HGF transcription in OVCAR3 cells, but this effect was not mediated by the Stat3 site at nt-95 ... These results suggest that human breast cells are a uniquely permissive environment for
HGF transactivation by
Src/Stat3 which may allow for the inappropriate activation of HGF transcription during the early stages of breast transformation
Watanabe et al., Mol Cancer Res 2009
(Sarcoma, Synovial) :
In
response to
hepatocyte growth factor stimulation, Crk prominently induced the tyrosine phosphorylation of Grb2 associated binder 1 through activation of
Src and focal adhesion kinase, and the Src family kinase inhibitor PP2 almost completely inhibited the proliferation of SYO-1 cells
Singhal et al., Int J Biochem Cell Biol 2011
:
Inhibition of I?B kinase is mediated by
hepatocyte growth factor induced activation of
c-Src ... Proximal signaling events induced in dendritic cells by hepatocyte growth factor include a physical association of c-Src with the
hepatocyte growth factor receptor c-MET and concomitant
activation of
c-Src ... Notably,
hepatocyte growth factor stimulated
c-Src activation results in induction of phosphatidylinositol 3-kinase complexes p85a/p110a and p85a/p110d, which is required for activation of mammalian target of rapamycin, and consequent inhibition of I?B kinase and nuclear factor-?B activation
Singhal et al., J Biol Chem 2011
:
Notably, Btk activation is necessary for
HGF induced association of
c-Src and PI3K with c-MET
Chen et al., PloS one 2012
:
Hepatocyte growth factor increases osteopontin expression in human osteoblasts through PI3K, Akt,
c-Src , and AP-1 signaling pathway ... Stimulation of osteoblasts with
HGF enhanced PI3K, Akt, and
c-Src activation
Grano et al., Proc Natl Acad Sci U S A 1996
(Bone Neoplasms...) :
In osteoclasts,
HGF receptor activation is
followed by increase in intracellular Ca2+ concentration and by activation of the
pp60c-Src kinase
Rahimi et al., J Biol Chem 1998
(Mammary Neoplasms, Experimental) :
Taken together, our data strongly suggest that
HGF induced association of
c-Src with Met and c-Src activation play a critical role in HGF induced cell motility and anchorage independent growth of mammary carcinomas and further support the notion that the presence of paracrine and autocrine HGF loops contributes significantly to the transformed phenotype of carcinoma cells