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Titolo:
Activator protein 1 (AP-1)- and nuclear factor kappa B (NF-kappa B)-dependent transcriptional events in carcinogenesis
Autore:
Hsu, TC; Young, MR; Cmarik, J; Colburn, NH;
Indirizzi:
NCI, Gene Regulat Sect, FCRDC, Basic Res Lab, Frederick, MD 21702 USA NCIFrederick MD USA 21702 FCRDC, Basic Res Lab, Frederick, MD 21702 USA SAIC Frederick, IRSP, Frederick, MD USA SAIC Frederick Frederick MD USASAIC Frederick, IRSP, Frederick, MD USA
Titolo Testata:
FREE RADICAL BIOLOGY AND MEDICINE
fascicolo: 9, volume: 28, anno: 2000,
pagine: 1338 - 1348
SICI:
0891-5849(20000501)28:9<1338:AP1(AN>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; MOUSE EPIDERMAL-CELLS; MANGANESE-SUPEROXIDE-DISMUTASE; DNA-BINDING ACTIVITY; INDUCED NEOPLASTIC TRANSFORMATION; PROMOTER-INDUCED TRANSFORMATION; SIGNAL-TRANSDUCTION PATHWAYS; SENSITIVE JB6 CELLS; BREAST-CANCER CELLS; KINASE-C SUBSTRATE;
Keywords:
AP-1; NF-kappa B; JB6 cells; tumor promotion; free radical;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
168
Recensione:
Indirizzi per estratti:
Indirizzo: Colburn, NH NCI, Gene Regulat Sect, FCRDC, Basic Res Lab, Bldg 560,Room 21-89, Frederick, MD 21702 USA NCI Bldg 560,Room 21-89 Frederick MD USA 21702k, MD 21702 USA
Citazione:
T.C. Hsu et al., "Activator protein 1 (AP-1)- and nuclear factor kappa B (NF-kappa B)-dependent transcriptional events in carcinogenesis", FREE RAD B, 28(9), 2000, pp. 1338-1348

Abstract

Generation of reactive oxygen species (ROS) during metabolic conversion ofmolecular oxygen imposes a constant threat to aerobic organisms. Other than the cytotoxic effects, many ROS and oxidants are also potent tumor promoters linking oxidative stress to carcinogenesis. Clonal variants of mouse epidermal JB6 cells originally identified for their differential susceptibility to tumor promoters also show differential reduction-oxidation (redox) responses providing a unique model to study oxidative events in tumor promotion. AP-1 and NF-kappa B, inducible by tumor promoters or oxidative stimuli,show differential protein levels or activation in response to tumor promoters in JB6 cells. We further demonstrated that AP-1 and NF-kappa B are bothrequired for maintaining the transformed phenotypes where inhibition of either activity suppresses transformation response in JB6 cells as well as human keratinocytes and transgenic mouse. NF-kappa B proteins or extracellular signal-regulated kinase (ERK) but not AP-1 proteins are shown to be sufficient for conversion from transformation-resistant to transformation-susceptible phenotype. Insofar as oxidative events regulate AP-1 and NF-kappa B transactivation, these oxidative events can be important molecular targets for cancer prevention. (C) 2000 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 00:56:57