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Metallothionein deficiency enhances skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate in metallothionein-null mice
Suzuki, JS; Nishimura, N; Zhang, BX; Nakatsuru, Y; Kobayashi, S; Satoh, M; Tohyama, C
刊名CARCINOGENESIS
2003-06-01
DOI10.1093/carcin/bgg052
24期:6页:1123-1132
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]POLYCYCLIC AROMATIC-HYDROCARBONS ; GTPASE ACTIVATING PROTEIN ; EPOXIDE-DNA-BINDING ; TREATED MOUSE SKIN ; H-RAS GENE ; METABOLIC-ACTIVATION ; OXIDATIVE STRESS ; RADICAL CATIONS ; PROTECTIVE ROLE ; EXPRESSION
英文摘要

To clarify the physiological role(s) of metallothionein (MT) in carcinogenesis, we studied the susceptibility of MT-null mice to chemically mediated carcinogenesis in the 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced two-stage carcinogenesis model. The MT-null mice were subjected to a single topical application of DMBA (50 or 100 mug/mouse) and, 1 week later, to promotion with TPA (10 mug/mouse) twice a week for 20 weeks. At week 21, nearly all of the MT-null mice developed tumors in the skin, in contrast to only 10-40% of wild-type mice. No tumors were observed in MT-null or wild-type mice that were administered TPA alone. By using the PCR-restriction fragment length polymorphism and PCR-single strand conformation polymorphism methods, we found a transversion of A(182) to T in codon 61 of c-Ha-ras in the papilloma tissue of MT-null mice and wild-type mice but failed to find any mutations in the c-Ki-ras and c-N-ras genes. In two-stage skin carcinogenesis induction by DMBA/TPA, p53 and p21(WAF1/Cip1) expression levels were found to be increased in MT-null mice compared with wild-type mice. As to an earlier change at the promotion stage triggered by TPA application, MT-null mice were found to have both hyperplasia of the epithelium and a marked degree of inflammation in the basal layer, indicating that the induced as well as endogenous MT acted as a protective factor against tumorigenesis. In conclusion, the present study has demonstrated that MT has antitumorigenic potential in both the initiation and promotion stages of the two-stage chemical skin carcinogenesis model.

语种英语
WOS记录号WOS:000183836800015
引用统计
被引频次:39[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67361
专题北京大学公共卫生学院_毒理学系
作者单位1.Natl Inst Environm Studies, Environm Hlth Sci Div, Tsukuba, Ibaraki 3058506, Japan
2.Beijing Univ, Sch Publ Hlth, Dept Toxicol, Beijing 100083, Peoples R China
3.Univ Tokyo, Grad Sch Med, Dept Mol Pathol, Tokyo 1130033, Japan
4.Kyoritsu Coll Pharmaceut Sci, Dept Biol, Tokyo 1058512, Japan
5.Gifu Pharmaceut Univ, Dept Hyg, Gifu 5028585, Japan
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GB/T 7714
Suzuki, JS,Nishimura, N,Zhang, BX,et al. Metallothionein deficiency enhances skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate in metallothionein-null mice[J]. CARCINOGENESIS,2003,24(6):1123-1132.
APA Suzuki, JS.,Nishimura, N.,Zhang, BX.,Nakatsuru, Y.,Kobayashi, S.,...&Tohyama, C.(2003).Metallothionein deficiency enhances skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate in metallothionein-null mice.CARCINOGENESIS,24(6),1123-1132.
MLA Suzuki, JS,et al."Metallothionein deficiency enhances skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate in metallothionein-null mice".CARCINOGENESIS 24.6(2003):1123-1132.
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