Additive roles of XPA and MSH2 genes in UVB-induced skin tumorigenesis in mice

被引：24
作者：
Yoshino, M
Nakatsu, Y
Riele, HT
Hirota, S
Kitamura, Y
Tanaka, K
机构：
[1] Osaka Univ, Grad Sch Frontier Biosci, Labs Organismal Biosyst, Suita, Osaka 5650871, Japan
[2] Japan Sci & Technol Corp, Core Res Evolut Sci & Technol, Suita, Osaka 5650871, Japan
[3] Netherlands Canc Inst, Div Mol Carcinogenesis, NL-1066 CX Amsterdam, Netherlands
[4] Osaka Univ, Grad Sch Med, Dept Pathol, Suita, Osaka 5650871, Japan
来源：
DNA REPAIR | 2002年 / 1卷 / 11期
基金：
日本科学技术振兴机构;
关键词：
MSH2; XPA; double knockout mice; UVB; skin carcinogenesis;
D O I：
10.1016/S1568-7864(02)00144-1
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
We have made xeroderma pigmentosum group A gene (XPA)-knockout mice (XPA(-/-) mice). The XPA(-/-) mice had no detectable activity for nucleotide excision repair (NER) and showed a high incidence of UVB-induced skin tumorigenesis. We have also found that cell lines derived from skin cancers in UVB-irradiated XPA(-/-) mice become tolerant to UV-irradiation and showed abnormal UV-induced cell cycle checkpoints and decreased mismatch repair (MMR) activity. These results suggested that the MMR-downregulation may help cells escape killing by UV-irradiation and thus MMR-deficient clones are selected for during the tumorigenic transformation of XPA(-/-) cells. In this report, we examined whether the incidence of UVB-induced skin tumorigenesis is enhanced in XPA(-/-)MSH2(-/-), XPA(-/-) and MSH2(-/-) mice when compared with that in wild-type mice. Our results indicate that the MSH2-deficiency caused a high incidence of spontaneous and UVB-induced skin tumorigenesis and the XPA and MSH2 genes have additive roles in the UV-induced skin tumorigenesis. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码：935 / 940
页数：6
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