The double-edged sword of Nrf2: subversion of redox homeostasis during the evolution of cancer

John D Hayes; Michael McMahon

doi:10.1016/j.molcel.2006.03.004

The double-edged sword of Nrf2: subversion of redox homeostasis during the evolution of cancer

Mol Cell. 2006 Mar 17;21(6):732-4. doi: 10.1016/j.molcel.2006.03.004.

Authors

John D Hayes¹, Michael McMahon

Affiliation

¹ Biomedical Research Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland, United Kingdom.

PMID: 16543142
DOI: 10.1016/j.molcel.2006.03.004

Abstract

Low levels of Nrf2 activity predispose cells to chemical carcinogenesis. Surprisingly, Padmanabhan et al. (2006) provide evidence in a recent issue of Molecular Cell to support the notion that elevated Nrf2 activity may also play a role in the evolution of cancer.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Adaptor Proteins, Signal Transducing / genetics
Animals
Carcinogens / pharmacology
Cytoskeletal Proteins / genetics
Evolution, Molecular
Gene Expression Regulation, Neoplastic / physiology
Genetic Predisposition to Disease*
Humans
Intracellular Signaling Peptides and Proteins
Kelch-Like ECH-Associated Protein 1
Mice
Models, Biological
NF-E2-Related Factor 2 / chemistry
NF-E2-Related Factor 2 / metabolism*
Neoplasms / genetics*
Oxidation-Reduction
Proteins / genetics*
Reactive Oxygen Species / metabolism

Substances

Adaptor Proteins, Signal Transducing
Carcinogens
Cytoskeletal Proteins
Intracellular Signaling Peptides and Proteins
KEAP1 protein, human
Keap1 protein, mouse
Kelch-Like ECH-Associated Protein 1
NF-E2-Related Factor 2
Proteins
Reactive Oxygen Species