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Titolo:
Bombesin and gastrin releasing peptide increase tyrosine phosphorylation of focal adhesion kinase and paxillin in non-small cell lung cancer cells
Autore:
Leyton, J; Garcia-Marin, LJ; Tapia, JA; Jensen, RT; Moody, TW;
Indirizzi:
NCI, Med Branch, Rockville, MD 20850 USA NCI Rockville MD USA 20850NCI, Med Branch, Rockville, MD 20850 USA NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA NIDDK Bethesda MD USA 20892 igest Dis Branch, NIH, Bethesda, MD 20892 USA
Titolo Testata:
CANCER LETTERS
fascicolo: 1, volume: 162, anno: 2001,
pagine: 87 - 95
SICI:
0304-3835(20010110)162:1<87:BAGRPI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SWISS 3T3 CELLS; GROWTH-FACTORS; RECEPTOR ANTAGONIST; PROTEIN; STIMULATION; ACTIN; PROLIFERATION; NEUROPEPTIDES; CYTOSKELETON; VASOPRESSIN;
Keywords:
bombesin/gastrin releasing peptide; focal adhesion kinase; non-small cell lung cancer; antisense;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Moody, TW NCI, Med Branch, Bldg KWC,Rm 300,9610 Med Ctr Dr, Rockville, MD 20850 USA NCI Bldg KWC,Rm 300,9610 Med Ctr Dr Rockville MD USA 20850 0 USA
Citazione:
J. Leyton et al., "Bombesin and gastrin releasing peptide increase tyrosine phosphorylation of focal adhesion kinase and paxillin in non-small cell lung cancer cells", CANCER LETT, 162(1), 2001, pp. 87-95

Abstract

The effects of some oncogenes, growth factors and neuropeptides are mediated by tyrosine phosphorylation of focal adhesion kinase (p125(FAK)) and paxillin cytoskeletal proteins. In this study the ability of bombesin/gastrin releasing peptide (BB/GRP) to stimulate tyrosine phosphorylation of p125(FAK) and paxillin in non-small cell lung cancer (NSCLC) H1299 cells was investigated. BB, 100 nM caused increased p125(FAK) and paxillin tyrosine phosphorylation maximally after 1 min. The effect of BB on p125(FAK) and paxillintyrosine phosphorylation was concentration-dependent being half maximal at4-8 nM. Also, 100 nM GRP, GRP(14-27) but not GRP(1-16) increased p125(FAK)and paxillin tyrosine phosphorylation indicating that the C-terminal of GRP is essential. BW2258U89, a GRP receptor antagonist, caused a dose-dependent inhibition of BB-stimulated p125(FAK) and paxillin tyrosine phosphorylation with an IC50 value of 3 muM. Cytochalasin D (0.3 muM), which inhibits actin polymerization, reduced the ability of BB to stimulate tyrosine phosphorylation of p125FAK and paxillin. Genistein (50 muM) and H-7 (50 muM), which are kinase inhibitors, reduced the tyrosine phosphorylation of p125(FAK)and paxillin stimulated by BB. Also, treatment of NCI- H1299 cells with FAK antisense resulted in decreased FAK tyrosine kinase activity and proliferation. These results suggest that p125(FAK) is,important enzyme for NSCLC proliferation. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 11:45:03