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Titolo:
Fibroblast growth factor and insulin-like growth factor differentially modulate the apoptosis and G1 arrest induced by anti-epidermal growth factor receptor monoclonal antibody
Autore:
Liu, BL; Fang, M; Lu, Y; Mendelsohn, J; Fan, Z;
Indirizzi:
Univ Texas, MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 ept Expt Therapeut, Houston, TX 77030 USA
Titolo Testata:
ONCOGENE
fascicolo: 15, volume: 20, anno: 2001,
pagine: 1913 - 1922
SICI:
0950-9232(20010405)20:15<1913:FGFAIG>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE PATHWAY; EPITHELIAL-CELLS; G(1) ARREST; BAD PHOSPHORYLATION; CARCINOMA-CELLS; INHIBITION; ACTIVATION; SURVIVAL; ALPHA; AKT;
Keywords:
EGF receptor; monoclonal antibody; apoptosis; cell cycle arrest; bFGF; IGF-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Fan, Z Univ Texas, MD Anderson Canc Ctr, Dept Expt Therapeut, Box 36,1515 Holcombe Blvd, Houston, TX 77030 USA Univ Texas Box 36,1515 Holcombe Blvd Houston TX USA 77030 77030 USA
Citazione:
B.L. Liu et al., "Fibroblast growth factor and insulin-like growth factor differentially modulate the apoptosis and G1 arrest induced by anti-epidermal growth factor receptor monoclonal antibody", ONCOGENE, 20(15), 2001, pp. 1913-1922

Abstract

DiFi human colon carcinoma cells are stimulated by the transforming growthfactor-alpha (TGF-alpha)/epidermal growth factor (EGF) receptor autocrine loop. Exposure of DiFi cells to monoclonal antibody (mAb) 225, which blocksligand-induced activation of the EGF receptor, induces G1 arrest and subsequent cell death via apoptosis, We investigated the signal pathways by which basic fibroblast growth factor (bFGF) and insulin-like growth factor-1 (IGF-1) modulate mAb 225-induced G1 arrest and apoptosis in DiFi cells. Both bFGF and IGF-1 activated the mitogen-activated protein kinase (MAPK) kinase(MEK) pathway in DiFi cells, Additionally, IGF-1 activated the phosphoinositide 3-kinase (PI-3K)/Akt pathway. Both bFGF and IGF-1 inhibited mAb 225-induced apoptosis; however, bFGF provided sustained protection against apoptosis, while the protection by IGF-1 was only temporary. Also, bFGF reversedthe mAb 225-induced increase in the p27(Kip1) level, inhibition of cyclin-dependent kinase-2 (CDK-2) activity, dephosphorylation of the retinoblastoma (Rb) protein and the resultant G1 arrest of the cells. In contrast, IGF-1did not reverse such effects by mAb 225, The prevention of mAb 225-inducedG1 arrest and apoptosis in DiFi cells by bFGF was sensitive to the MEK/MAPK inhibitor PD98059 but not to the PI-3K inhibitor LY294002. In contrast, inhibition of apoptosis by IGF-1 in DiFi cells was sensitive only to LY294002 and not to PD98059, These results further our understanding of how mAb 225 induces apoptosis in DiFi cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/10/20 alle ore 00:11:14