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The aryl hydrocarbon receptor nuclear translocator (Arnt) is required for tumor initiation by benzo[a]pyrene

Title
The aryl hydrocarbon receptor nuclear translocator (Arnt) is required for tumor initiation by benzo[a]pyrene
Authors
Shi S.Yoon D.Y.Hodge-Bell K.C.Bebenek I.G.Whitekus M.J.Zhang R.Cochran A.J.Huerta-Yepez S.Yim S.-H.Gonzalez F.J.Jaiswal A.K.Hankinson O.
Ewha Authors
임선희
Issue Date
2009
Journal Title
Carcinogenesis
ISSN
0143-3334JCR Link
Citation
vol. 30, no. 11, pp. 1957 - 1961
Indexed
SCI; SCIE; SCOPUS scopus
Abstract
Benzo[a]pyrene (B[a]P) is a ligand for the aryl hydrocarbon receptor (Ahr). After binding ligand, Ahr dimerizes with the aryl hydrocarbon receptor nuclear translocator (Arnt) protein, and the dimer upregulates the transcription of Cyp1a1, Cyp1b1 and other enzymes involved in the metabolic activation of B[a]P. Arnt null mice die in utero. Mice in which Arnt deletion occurs constitutively in the epidermis die perinatally. In the current study, mice were developed in which the Arnt gene could be deleted specifically in adult skin epidermis. This deletion had no overt pathological effect. Homozygosity for a null reduced nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase allele was introduced into the above mouse strain to render it more susceptible to tumor initiation by B[a]P. Deletion of Arnt in the epidermis of this strain completely prevented the induction of skin tumors in a tumor initiation-promotion protocol in which a single topical application of B[a]P acted as the tumor-initiating event, and tumor promotion was provided by repeated topical applications of 12-O-tetradecanoyl phorbol-13-acetate (TPA). In contrast, deletion of Arnt did not prevent the induction of skin tumors in a protocol also using TPA as the promoter but using as the initiator N-methyl-N′-nitro-N-nitrosoguanidine, whose activity is unlikely to be affected by the activity of Ahr, Arnt or their target genes. These observations demonstrate that Arnt is required for tumor initiation by B[a]P in this system. © The Author 2009. Published by Oxford University Press. All rights reserved.
DOI
10.1093/carcin/bgp201
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일반대학원 > 생명·약학부 > Journal papers
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