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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 746432, 10 pages
Review Article

The Involvement of NRF2 in Lung Cancer

Department of Environmental and Occupational Health, University of Colorado Anschutz Medical Campus, Mailstop B119-V20, Room. 3125, 12850 East Montview Boulevard, Aurora, CO 80045, USA

Received 8 January 2013; Revised 20 February 2013; Accepted 26 February 2013

Academic Editor: Hye-Youn Cho

Copyright © 2013 Alison K. Bauer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nuclear factor, erythroid-derived 2, like 2 (NRF2) is a key regulator of antioxidants and cellular stress responses. The role of NRF2 in pulmonary neoplasia, a diverse disease for which few biomarkers exist, is complicated and appears to depend on several main factors including the existence of activating mutations in NRF2 and/or loss of function mutations in KEAP1 and the stage of carcinogenesis studied, particularly in the mouse models tested. Therapeutic strategies for lung cancer targeting NRF2 have observed mixed results, both anti- and protumorigenic effects; however, these differences seem to reflect the mutation status of NRF2 or KEAP1. In this paper, we will discuss the studies on human NRF2 and the mechanisms proposed, several mouse models using various mice deficient in NRF2, as well as xenograft models, and the chemotherapeutic strategies using the NRF2 pathway.