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Titolo:
The monoclonal antibody 225 activates caspase-8 and induces apoptosis through a tumor necrosis factor receptor family-independent pathway
Autore:
Liu, BL; 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: 28, volume: 20, anno: 2001,
pagine: 3726 - 3734
SICI:
0950-9232(20010621)20:28<3726:TMA2AC>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPIDERMAL GROWTH-FACTOR; FAS-MEDIATED APOPTOSIS; CYTOCHROME-C RELEASE; ANTICANCER DRUGS; CD95 FAS/APO-1; DEATH DOMAIN; CANCER-CELLS; G(1) ARREST; LIGAND; FADD;
Keywords:
apoptosis; caspase; TNF receptor family; EGF receptor; monoclonal antibody;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
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 e Z. Fan, "The monoclonal antibody 225 activates caspase-8 and induces apoptosis through a tumor necrosis factor receptor family-independent pathway", ONCOGENE, 20(28), 2001, pp. 3726-3734

Abstract

We previously reported that the anti-epidermal growth factor (EGF) receptor monoclonal antibody (mAb) 225 induces DiFi colon cancer cells to undergo apoptosis, and this apoptosis was accompanied by activation of the two apoptosis initiation caspases, caspase-8 and caspase-9, In the current study, we found that pretreatment of DiFi cells with the caspase-8-specific inhibitor z-IETD-fmk but not pretreatment with the caspase-9-specific inhibitor z-LEHD-fmk inhibited mAb 225-induced apoptosis, indicating that caspase-8 plays an essential role in initiating mAb 225-induced apoptosis, Because caspase-8 is activated primarily by the members of the tumor necrosis factor (TNF) receptor family, such as Fas, TNF receptor-1 (TNFR1), or receptors for TNF-related apoptosis-inducing ligand (TRAIL), we investigated whether mAb 225 activated caspase-8 by regulating one or more of these known pathways, Exposure of DiFi cells to TNF alpha or TRAIL activated caspase-8 and inducedapoptosis in the cells. A TNFR1-antagonistic mAb or a TRAIL decoy receptorinhibited the activation of caspase-8 and the subsequent apoptosis inducedby TNF alpha or TRAIL, respectively, in the cells. However, neither the TNFR1-antagonistic mAb nor the TRAIL decoy receptor inhibited mAb 225-inducedactivation of caspase-8 and apoptosis in DiFi cells, DiFi cells express detectable level of Fas but are not sensitive to the treatment by the Fas-agonistic mAb CH-II, A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonisticmAb CH-ll-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells. Taken together, our results suggest that mAb 225 does not interact with or regulate these known deathreceptor pathways, An exploration is therefore warranted for a novel mechanism by which mAb 225 activates caspase-8 and triggers apoptosis in DiFi cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 20:56:22