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Titolo:
Caspase-dependent apoptosis induced by telomere cleavage and TRF2 loss
Autore:
Multani, AS; Ozen, M; Narayan, S; Kumar, V; Chandra, J; McConkey, DJ; Newman, RA; Pathak, S;
Indirizzi:
Univ Texas, MD Anderson Canc Ctr, Cellular Genet Lab, Dept Canc Biol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 ab, Dept Canc Biol, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Lab Med, Houston, TX 77030 USA UnivTexas Houston TX USA 77030 Ctr, Dept Lab Med, Houston, TX 77030 USA 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 Univ Florida, Dept Anat & Cell Biol, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 ell Biol, Gainesville, FL 32610 USA Univ Florida, Shands Canc Ctr, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 Canc Ctr, Gainesville, FL 32610 USA
Titolo Testata:
NEOPLASIA
fascicolo: 4, volume: 2, anno: 2000,
pagine: 339 - 345
SICI:
1522-8002(200007/08)2:4<339:CAIBTC>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; CANCER DEVELOPMENT; DNA FRAGMENTATION; EPITHELIAL-CELLS; PROTEIN; LENGTH; BCL-2; ACTIVATION; END; CHROMOSOMES;
Keywords:
telomeric erosion; DNA fragmentation; caspase inhibitors; fluorescence in situ hybridization; telomeric-repeat binding factor (TRF);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Pathak, S Univ Texas, MD Anderson Canc Ctr, Cellular Genet Lab, Dept Canc Biol, 1515Holcombe Blvd,Box 181, Houston, TX 77030 USA Univ Texas 1515 Holcombe Blvd,Box 181 Houston TX USA 77030 0 USA
Citazione:
A.S. Multani et al., "Caspase-dependent apoptosis induced by telomere cleavage and TRF2 loss", NEOPLASIA, 2(4), 2000, pp. 339-345

Abstract

Chromosomal abnormalities involving telomeric associations (TAs) often precede replicative senescence and abnormal chromosome configurations. We report here that telomere cleavage following exposure to pro-apoptotic agents is an early event in apoptosis, Exposure of human and murine cancer cells toa variety of pro-apoptotic stimuli (staurosporine, thapsigargin, anti-fas antibody, and cancer chemotherapeutic agents) resulted in telomere cleavageand aggregation, and finally their extrusion from the nuclei. Telomere loss was associated with arrest of cells in G(2)/M phase and preceded DNA fragmentation. Telomere erosion and subsequent large-scale chromatin cleavage were inhibited by overexpression of the anti-apoptotic protein, bcl-2, and two peptide caspase inhibitors (BACMK and zVADfmk), indicating that both events are regulated by caspase activation. The results demonstrate that telomere cleavage is an early chromatin alteration detected in various cancer cell lines leading to drug-induced apoptosis, and suggest that this event contributes to mitotic catastrophe and induction of cell death. Results also suggest that the decrease of telomeric-repeat binding factor 2 (TRF2) may bethe earliest event in the ara-C-induced telomere shortening, induction of endoreduplication and chromosomal fragmentation leading to cell death.

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Documento generato il 04/04/20 alle ore 08:33:28