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Titolo:
Treatment-induced expression of anti-apoptotic proteins in WSU-CLL, a human chronic lymphocytic leukemia cell line
Autore:
Wall, NR; Beck, FWJ; Al-Katib, AM; Mohammad, RM;
Indirizzi:
Wayne State Univ, Sch Med, Inst Canc, Dept Internal Med,Div Hematol & Oncol, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 atol & Oncol, Detroit, MI 48201 USA
Titolo Testata:
JOURNAL OF DRUG TARGETING
fascicolo: 5, volume: 9, anno: 2001,
pagine: 329 - 339
SICI:
1061-186X(2001)9:5<329:TEOAPI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; CYTOCHROME-C; CLINICAL UPDATE; KINASE-C; B-CLL; BRYOSTATIN-1; FLUDARABINE; INHIBITORS; 2-CHLORODEOXYADENOSINE; PHOSPHORYLATION;
Keywords:
apoptosis; Bcl-2/Bax; bryostatin 1; CLL; 2-CdA; IAPs;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Mohammad, RM Karmanos Canc Inst, Room 724 HWCRC,4100 John R, Detroit, MI 48201 USA Karmanos Canc Inst Room 724 HWCRC,4100 John R Detroit MI USA 48201
Citazione:
N.R. Wall et al., "Treatment-induced expression of anti-apoptotic proteins in WSU-CLL, a human chronic lymphocytic leukemia cell line", J DRUG TAR, 9(5), 2001, pp. 329-339

Abstract

Bryostatin 1 (bryo 1) has been shown to potentiate the anti-tumor activityof 2-chloro-2-deoxyadenosine (2-CdA) in chronic lymphocytic leukemia (CLL)and in the WSU-CLL cell line. However, like resistant CLL, WSU-CLL cells lose their sensitivity to bryo 1/2-CdA treatment. We report that 2-CdA-induced IAP expression may be a possible mechanism whereby resistance to apoptosis is acquired in these cells. In WSU-CLL cells, three members of the Inhibitors of Apoptosis (IAP) family were identified. Bryo I treatment of WSU-CLL cells leads to initiation of the apoptotic cascade and induced a marginalincrease in XIAP protein expression. In contrast, 2-CdA treatment, alone or in combination with bryo 1, induced a substantial increase in survivin and XIAP proteins and phosphorylation of BAD. Bryo I alone induced caspase-7 and -9 dependent [poly ADP-ribose] polymerase (PARP) cleavage, while sequential treatment with bryo 1(72 h) followed by 2-CdA (24 h) induced caspase-3,-7, and -9 dependent PARP cleavage and increased apoptosis. Although exposure to bryo I initiated apoptotic events, apoptosis was first enhanced by 2-CdA, and then reversed in a time-dependent manner by 2-CdA-induced expression of survival proteins. Taken together, resistance to bryo 1/2-CdA treatment may be the result of 2-CdA-induced LAY inhibition of the intrinsic apoptotic pathway caspases.

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Documento generato il 01/04/20 alle ore 09:17:37