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Titolo:
Involvement of focal adhesion kinase in hepatocyte growth factor-induced scatter of Madin-Darby canine kidney cells
Autore:
Lai, JF; Kao, SC; Jiang, ST; Tang, MJ; Chan, PC; Chen, HC;
Indirizzi:
Natl Chung Hsing Univ, Dept Zool, Taichung 40227, Taiwan Natl Chung Hsing Univ Taichung Taiwan 40227 Zool, Taichung 40227, Taiwan Natl Cheng Kung Univ, Coll Med, Dept Physiol, Tainan 70101, Taiwan Natl Cheng Kung Univ Tainan Taiwan 70101 t Physiol, Tainan 70101, Taiwan
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 11, volume: 275, anno: 2000,
pagine: 7474 - 7480
SICI:
0021-9258(20000317)275:11<7474:IOFAKI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR TYROSINE KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; EPITHELIAL-CELLS; C-MET; INTEGRIN EXPRESSION; PROTEIN-KINASE; GRB2 BINDING; MDCK CELLS; 3T3 CELLS; V-SRC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Chen, HC Natl Chung Hsing Univ, Dept Zool, Taichung 40227, Taiwan Natl Chung Hsing Univ Taichung Taiwan 40227 chung 40227, Taiwan
Citazione:
J.F. Lai et al., "Involvement of focal adhesion kinase in hepatocyte growth factor-induced scatter of Madin-Darby canine kidney cells", J BIOL CHEM, 275(11), 2000, pp. 7474-7480

Abstract

Focal adhesion kinase (FAK) has been implicated to play a critical role inintegrin-mediated control of cell behavior. However, it is unclear whetherFAK also participates in the regulation of growth factor-elicited. cellular functions. In this study, we have demonstrated that although overexpression of FAK in Madin-Dardy canine kidney cells did not alter their growth property or ability to form tubules within collagen gel upon hepatocyte growthfactor (HGF) stimulation, it apparently enhanced HGF-induced cell scattering This enhancement was largely because of an increase in the third phase (i.e. cell migration) of cell scattering rather than the first two phases (i.e. cell spreading and cell-cell dissociation). Conversely, the expression of FAR-related nonkinase significantly (similar to 60%) inhibited HGF-induced cell migration. Moreover, we have found that the effect of FAK on promoting HGF-induced cell motility was greatly dependent on cell-matrix interactions. We showed that HGF treatment selectively increased the expression of integrins alpha(2) and, to a lesser extent, alpha(3) in Madin-Dardy canine kidney cells and that a monoclonal antibody against integrin alpha(2) efficiently blocked HGF-enhanced cell migration on collagen. In our efforts to determine the mechanism. by which FAK promotes HGF-induced cell migration, we found that FAK mutants deficient in phosphatidylinositol 3-kinase or p130(Cas) binding failed to promote HGF-induced cell migration, Interestingly, cells expressing a FAK mutant defective in Grb2 binding exhibited a rate ofmigration similar to 50% lower than that of cells expressing wild type FAKin response to HGF stimulation, Taken together, our results suggest a linkbetween HGF-increased integrin expression, FAK activation, and enhanced cell motility and implicate a role for FAK in the facilitation of growth factor-induced cell motility.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 14:54:15