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MET promotes cell motility

Stable Identifier
R-HSA-8875878
Type
Pathway
Species
Homo sapiens
Locations in the PathwayBrowser
Summation

Direct and indirect interactions of MET with integrins, focal adhesion kinase PTK2 (FAK1), tensin-4 (TNS4) and GTPases RAP1 and RAC1, induce morphological changes that promote cell motility and play an important role in HGF-induced invasiveness of cancer cells (Weidner et al. 1993, Beviglia et al. 1999, Sakkab et al. 2000, Parr et al. 2001, Trusolino et al. 2001, Lamorte et al. 2002, Chen and Chen 2006, Watanabe et al. 2006, Muharram et al. 2014, Murray et al. 2014).

Literature References
PubMed ID Title Journal Year
8384622 The Met receptor tyrosine kinase transduces motility, proliferation, and morphogenic signals of scatter factor/hepatocyte growth factor in epithelial cells J. Cell Biol. 1993
10521801 HGF induces FAK activation and integrin-mediated adhesion in MTLn3 breast carcinoma cells Int. J. Cancer 1999
11478803 The HGF/SF-induced phosphorylation of paxillin, matrix adhesion, and invasion of prostate cancer cells were suppressed by NK4, an HGF/SF variant Biochem. Biophys. Res. Commun. 2001
24518591 Guanine nucleotide exchange factor Dock7 mediates HGF-induced glioblastoma cell invasion via Rac activation Br. J. Cancer 2014
24814316 Tensin-4-dependent MET stabilization is essential for survival and proliferation in carcinoma cells Dev. Cell 2014
16849525 Adaptor molecule Crk is required for sustained phosphorylation of Grb2-associated binder 1 and hepatocyte growth factor-induced cell motility of human synovial sarcoma cell lines Mol. Cancer Res. 2006
10753869 Signaling of hepatocyte growth factor/scatter factor (HGF) to the small GTPase Rap1 via the large docking protein Gab1 and the adapter protein CRKL J. Biol. Chem. 2000
16782899 Direct interaction of focal adhesion kinase (FAK) with Met is required for FAK to promote hepatocyte growth factor-induced cell invasion Mol. Cell. Biol. 2006
12006644 Crk adapter proteins promote an epithelial-mesenchymal-like transition and are required for HGF-mediated cell spreading and breakdown of epithelial adherens junctions Mol. Biol. Cell 2002
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