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Titolo:
Decreased UV sensitivity, mismatch repair activity and abnormal cell cyclecheckpoints in skin cancer cell lines derived from UVB-irradiated XPA-deficient mice
Autore:
Ichikawa, M; Nakane, H; Marra, G; Corti, C; Jiricny, J; Fitch, M; Ford, JM; Ikejima, M; Shimada, T; Yoshino, M; Takeuchi, S; Nakatsu, Y; Tanaka, K;
Indirizzi:
Osaka Univ, Inst Mol & Cellular Biol, Div Cellular Genet, Osaka 5650871, Japan Osaka Univ Osaka Japan 5650871 Div Cellular Genet, Osaka 5650871, Japan Univ Zurich, Inst Med Radiobiol, CH-8008 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8008 biol, CH-8008 Zurich, Switzerland Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Med, Dept Med, Stanford, CA 94305 USA Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 d, Dept Genet, Stanford, CA 94305 USA Nippon Med Sch, Dept Biochem & Mol Biol, Bunkyo Ku, Tokyo 1138602, Japan Nippon Med Sch Tokyo Japan 1138602 Biol, Bunkyo Ku, Tokyo 1138602, Japan
Titolo Testata:
MUTATION RESEARCH-DNA REPAIR
fascicolo: 4, volume: 459, anno: 2000,
pagine: 285 - 298
SICI:
0921-8777(20000531)459:4<285:DUSMRA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEOTIDE EXCISION-REPAIR; ULTRAVIOLET-B; DNA ADDUCTS; P53; APOPTOSIS; MUTATIONS; TUMORS; GENE; EXPRESSION; CISPLATIN;
Keywords:
xeroderma pigmentosum; nucleotide excision repair; mismatch repair; cell cycle checkpoint; skin cancer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Tanaka, K Osaka Univ, Inst Mol & Cellular Biol, Div Cellular Genet, 1-3 Yamadaoka, Osaka 5650871, Japan Osaka Univ 1-3 Yamadaoka Osaka Japan 5650871aka 5650871, Japan
Citazione:
M. Ichikawa et al., "Decreased UV sensitivity, mismatch repair activity and abnormal cell cyclecheckpoints in skin cancer cell lines derived from UVB-irradiated XPA-deficient mice", MUT R-DNA R, 459(4), 2000, pp. 285-298

Abstract

Xeroderma pigmentosum group A gene (XPA)-deficient mice are defective in nucleotide excision repair (NER) and are therefore highly sensitive to ultraviolet (UV)-induced skin carcinogenesis. We established cell lines from skin cancers of WE-irradiated XPA-deficient mice to investigate the phenotypicchanges occurring during skin carcinogenesis. As anticipated, the skin cancer cell lines were devoid of NER activity but were less sensitive to killing by UV-irradiation than the XPA(- / -) fibroblast cell line. The lines were also more resistant to B-thioguanine (6-TG) than XPA(- / -) and XPA( + /+) fibroblasts, which was suggestive of a mismatch repair (MMR) defect. Indeed, in vitro mismatch binding and MMR activity were impaired in several of these cell lines. Moreover, these cell lines displayed cell cycle checkpoint derangements following UV-irradiation and 6-TG exposure. The above findings suggest that MMR downregulation may help cells escape killing by UVB, as was seen previously for methylating agents and cisplatin, and thus that MMR deficient clones are selected for during the tumorigenic transformationof XPA(- / -) cells. (C) 2000 Elsevier Science B.V, All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 08:30:42