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Titolo:
Accelerated degradation of cellular FLIP protein through the ubiquitin-proteasome pathway in p53-mediated apoptosis of human cancer cells
Autore:
Fukazawa, T; Fujiwara, T; Uno, F; Teraishi, F; Kadowaki, Y; Itoshima, T; Takata, Y; Kagawa, S; Roth, JA; Tschopp, J; Tanaka, N;
Indirizzi:
Okayama Univ, Grad Sch Med & Dent, Div Surg Oncol, Dept Surg 1, Okayama 7008558, Japan Okayama Univ Okayama Japan 7008558 , Dept Surg 1, Okayama 7008558, Japan Shiga Univ Med Sci, Dept Surg 1, Otsu, Shiga 5202192, Japan Shiga Univ MedSci Otsu Shiga Japan 5202192 1, Otsu, Shiga 5202192, Japan Univ Texas, MD Anderson Canc Ctr, Dept Thorac & Cardiovasc Surg, Sect Thorac Mol Oncol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 t Thorac Mol Oncol, Houston, TX 77030 USA Univ Lausanne, Inst Biochem, CH-1066 Epalinges, Switzerland Univ LausanneEpalinges Switzerland CH-1066 -1066 Epalinges, Switzerland
Titolo Testata:
ONCOGENE
fascicolo: 37, volume: 20, anno: 2001,
pagine: 5225 - 5231
SICI:
0950-9232(20010823)20:37<5225:ADOCFP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; DEATH RECEPTOR; P53; GENE; EXPRESSION; KILLER/DR5; SYSTEM; FADD; MODULATION; FAS;
Keywords:
p53; apoptosis; FLIP; ubiquitin-proteasome; colon cancer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Fujiwara, T Okayama Univ, Grad Sch Med & Dent, Div Surg Oncol, Dept Surg 1, 2-5-1 Shikata Cho, Okayama 7008558, Japan Okayama Univ 2-5-1 Shikata Cho Okayama Japan 7008558 8, Japan
Citazione:
T. Fukazawa et al., "Accelerated degradation of cellular FLIP protein through the ubiquitin-proteasome pathway in p53-mediated apoptosis of human cancer cells", ONCOGENE, 20(37), 2001, pp. 5225-5231

Abstract

Apoptosis is a morphologically distinct form of programmed cell death thatplays a major role in cancer treatments. This cellular suicide program is known to be regulated by many different signals from both intracellular andextracellular stimuli. Here we report that p53 suppressed expression of the cellular FLICE-inhibitory protein (FLIP) that potentially blocks apoptotic signaling in human colon cancer cell lines expressing mutated and wild-type p53. In contrast, the expression of the death receptor KILLER/DR5 (TRAIL-R2) had no effect on FLIP expression, although exogenous p53 is known to induce KILLER/DR5 expression. In line with these observations, FLIP-negativecancer cells were sensitive to both p53- and KILLER/DR5-mediated apoptosis, whereas cells containing high levels of FLIP underwent apoptotic cell death when triggered by ectopic p53 expression but not by KILLER/DR5 expression. Treating the cells with a specific inhibitor of the proteasome inhibitedthe decrease of FLIP by p53, suggesting that p53 enhances the degradation of FLIP via a ubiquitin-proteasome pathway. Thus, the data indicate that p53-mediated downregulation of FLIP may explain the potent sensitization of human cancer cells to the apoptotic suicide program induced by wild-type p53gene transfer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 12:40:39