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Titolo:
The von Hippel-Lindau tumor suppressor gene protects cells from UV-mediated apoptosis
Autore:
Schoenfeld, AR; Parris, T; Eisenberger, A; Davidowitz, EJ; De Leon, M; Talasazan, F; Devarajan, P; Burk, RD;
Indirizzi:
Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Microbiol & Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med, Albert Einstein Comprehens Canc Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Canc Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Pediat, Bronx,NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 pt Pediat, Bronx,NY 10461 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Epidemiol & Social Med, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 cial Med, Bronx, NY 10461 USA
Titolo Testata:
ONCOGENE
fascicolo: 51, volume: 19, anno: 2000,
pagine: 5851 - 5857
SICI:
0950-9232(20001130)19:51<5851:TVHTSG>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
BIOLOGICALLY-ACTIVE PRODUCT; CARCINOMA-CELLS; VHL GENE; P53; PHOSPHORYLATION; IDENTIFICATION; INITIATION; INHIBITION; COMPLEX; PATHWAY;
Keywords:
VHL; von Hippel-Lindau; renal cell carcinoma; apoptosis; UV;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Burk, RD Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Microbiol & Immunol, Ullmann Bldg,Rm 515,1300 Morris Pk Ave, Bronx, NY 10461 USAAlbert Einstein Coll Med Ullmann Bldg,Rm 515,1300 Morris Pk Ave Bronx NY USA 10461
Citazione:
A.R. Schoenfeld et al., "The von Hippel-Lindau tumor suppressor gene protects cells from UV-mediated apoptosis", ONCOGENE, 19(51), 2000, pp. 5851-5857

Abstract

The familial cancer syndrome, von Hlippel-Lindau (VHL) disease, characterized by a predisposition to renal cell carcinoma and certain other tumor types, is caused by mutational inactivation of the VHL tumor suppressor gene. Loss of VHL gene function is detected also in the vast majority of sporadicrenal cell carcinomas. Previous reports have determined a protective role for VHL in response to serum withdrawal and glucose deprivation, In this study, the effect of UV irradiation on VHL-negative and VHL-positive renal carcinoma cells was examined, VHL-negative 786-O renal carcinoma cells underwent apoptosis following UV irradiation, In contrast, reintroduction of wild-type VHL expression protected 786-O cells from UV-mediated cell death, p53and Bax levels were equivalent in VHL-negative and VHL-positive 786-O cells. Strikingly, cyclin-dependent kinase? inhibitors p21 and p27 underwent proteasome-dependent degradation in VHL-negative 786-O cells following UV treatment. However, p21 and p27 protein levels were stable in VHL-positive cells. Also, levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xL were elevated in VH L-positive cells, consistent with the protection from apoptotic stimuli, UV treatment led to increased S phase in VHL-negative, but not VHL-positive cells, Thus, following UV irradiation, diminution of p21 and p27 levels resulted in a hyperproliferative state in VHL-negative cells, leading to apoptosis, These results suggest that loss of VHL function promotes apoptosis and may provide selective pressure toward cells that are able to escape apoptosis, leading to tumorigenesis.

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Documento generato il 28/01/21 alle ore 07:47:43