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PMID: 15476858 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Contribution of NAD(P)H:quinone oxidoreductase 1 to protection against carcinogenesis, and regulation of its gene by the Nrf2 basic-region leucine zipper and the arylhydrocarbon receptor basic helix-loop-helix transcription factors.

Mutation research ·Vol. 555 ·No. 1-2 ·2004-11-02 ·Pages 149-71

Nioi P, Hayes JD

Abstract

NAD(P)H:quinone oxidoreductase 1 (NQO1) is a key enzyme involved in defence against reactive forms of oxygen and inhibition of neoplasia. Under conditions of oxidative stress, expression of NQO1 is induced, and the resulting increase in oxidoreductase protein provides the cell with multiple layers of protection against environmental insults. Firstly, the catalytic activity of NQO1 is directed towards the complete reduction and detoxication of highly reactive quinones. Secondly, the oxidoreductase maintains the endogenous lipid-soluble antioxidants, alpha-tocopherol-hydroquinone and ubiquinol in their reduced and active forms. Thirdly, NQO1 is required for the stabilisation of p53 protein in response to DNA-damaging stimuli, and it thereby influences cell fate decisions. In view of the anticarcinogenic actions of NQO1, an understanding of the mechanisms that govern its expression is desirable. The redox sensitivity of NQO1 transcription occurs through a cis-acting antioxidant response element (ARE) located within the regulatory region of the mouse, rat and human genes. This element recruits the positively acting basic leucine zipper (bZip) transcription factor NF-E2 p45-related factor 2 (Nrf2). Under normal constitutive conditions, Nrf2 associates with the cytoskeletal-binding protein Keap1, which regulates the subcellular distribution of the bZip factor and also targets it for proteasome-dependent degradation. Oxidative stress inhibits the Nrf2-Keap1 interaction, thus promoting nuclear accumulation of the transcription factor and transactivation of NQO1 and other ARE-driven genes. Mouse, rat and human NQO1 can also be induced by planar aromatic hydrocarbons through a cis-acting xenobiotic response element (XRE) located in their gene promoters. The XRE recruits the arylhydrocarbon receptor (AhR) and AhR nuclear translocator. Cross-talk may occur between Nrf2 and AhR, but the details of this process remain to be elucidated.

MeSH Terms
Animals Antioxidants/pharmacology Base Sequence DNA-Binding Proteins/metabolism Gene Expression Regulation, Enzymologic Helix-Loop-Helix Motifs/physiology Humans Leucine Zippers/physiology Molecular Sequence Data NAD(P)H Dehydrogenase (Quinone)/physiology NF-E2-Related Factor 2 Neoplasms/prevention & control Oxidation-Reduction Quinones/metabolism Receptors, Aryl Hydrocarbon/metabolism Response Elements/genetics Signal Transduction Trans-Activators/metabolism,physiology Transcription Factors/physiology
Chemicals
Antioxidants DNA-Binding Proteins NF-E2-Related Factor 2 NFE2L2 protein, human Quinones Receptors, Aryl Hydrocarbon Trans-Activators Transcription Factors NAD(P)H Dehydrogenase (Quinone) NQO1 protein, human
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Nioi Paul
Biomedical Research Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland, United Kingdom.
Hayes John D
Article Info
Journal
Mutation research
Abbr.
Mutat Res
ISSN
0027-5107
Published
2004-11-02
Pages
149-71
Language
English
Region
Netherlands
NLM ID
0400763
Subset
IM
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