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Titolo:
BCL-XL MODULATES APOPTOSIS INDUCED BY ANTICANCER DRUGS AND DELAYS DEVDASE AND DNA FRAGMENTATION-PROMOTING ACTIVITIES
Autore:
SCHMITT E; CIMOLI G; STEYAERT A; BERTRAND R;
Indirizzi:
UNIV MONTREAL,INST CANC MONTREAL,HOSP RES CTR,CAMPUS NOTRE DAME MONTREAL PQ H2L 4M1 CANADA UNIV MONTREAL,INST CANC MONTREAL,HOSP RES CTR MONTREAL PQ H2L 4M1 CANADA
Titolo Testata:
Experimental cell research
fascicolo: 1, volume: 240, anno: 1998,
pagine: 107 - 121
SICI:
0014-4827(1998)240:1<107:BMAIBA>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; TOPOISOMERASE-II INHIBITORS; INTERLEUKIN-1-BETA CONVERTING-ENZYME; CHEMOTHERAPY-INDUCED APOPTOSIS; LEUKEMIA HL-60 CELLS; CAENORHABDITIS-ELEGANS; GRANZYME-B; DIFFERENTIAL INDUCTION; SEQUENCE SIMILARITY; PROTEASE INHIBITORS;
Keywords:
APOPTOSIS; BCL-XL; CASPASES; N-TOSYL-L-PHENYLALANYLCHLOROMETHYL KETONE; CANCER CHEMOTHERAPY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
130
Recensione:
Indirizzi per estratti:
Citazione:
E. Schmitt et al., "BCL-XL MODULATES APOPTOSIS INDUCED BY ANTICANCER DRUGS AND DELAYS DEVDASE AND DNA FRAGMENTATION-PROMOTING ACTIVITIES", Experimental cell research, 240(1), 1998, pp. 107-121

Abstract

Using an episomal eucaryotic expression vector, we derived three stable transfected human leukemic U-937 variant lines showing differentialexpression of the Bcl-xL protein. Preventive effect of Bcl-xL on celldeath induced by various concentrations of camptothecin (DNA topoisomerase I inhibitor; CPT) was observed in the three lines with most pronounced effect in cells containing the highest level of Bcl-xL expression. These results show that increased cell death protection by Bcl-xL is correlated with its level of expression. The extent of DNA strand break formation and DNA synthesis inhibition following CPT treatments was similar in control and transfected U-937 cells, suggesting that Bcl-xL acts downstream of CPT-DNA topoisomerase I-mediated DNA strand breaks. Modulation of cell death by Bcl-xL was also observed in cells treated with etoposide, vinblastine, paclitaxel, and cisplatinum(II) diammine dichloride. To define whether Bcl-xL functions downstream or upstream of apoptogenic proteolytic cascade activation, we compared kinetics of DNA fragmentation in treated cells with kinetics of caspase 1-like, caspase 3-like, Bind N-tosyl-L-phenylalanylchloromethyl ketone (TPCK)-sensitive activities. In CPT-treated U-937 cells, caspase 3-like and TPCK-sensitive activities promoting DNA fragmentation in a cell-free system were detected much more rapidly in extracts obtained from CPT-treated U-937 cells compared to those obtained from CPT-treated U-937-Bcl-xL variant cells. These results suggest that Bcl-xL delays their activation that correlates with the occurrence of DNA fragmentation. Addition of:recombinant Bcl-xL in extracts containing DEVDase and TPCK-sensitive activities did not inhibit these activities, suggesting thatBcl-xL acts primarily upstream of their activation in the apoptotic process. Taken together, these results suggest that Bcl-xL is a primarycheckpoint that can block or delay transmission of cell death signalsemerging from DNA damage and prevents activation of an apoptogenic proteolytic cascade. (C) 1998 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 21:36:19