Oxidative stress induced lung cancer and COPD : opportunities for epigenetic therapy

Lawless, M. W., O'Byrne, Kenneth J., & Gray, S. G. (2009) Oxidative stress induced lung cancer and COPD : opportunities for epigenetic therapy. Journal of Cellular and Molecular Medicine, 13(9 A), pp. 2800-2821.

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Reactive oxygen species (ROS) form as a natural by-product of the normal metabolism of oxygen and play important roles within the cell. Under normal circumstances the cell is able to maintain an adequate homeostasis between the formation of ROS and its removal through particular enzymatic pathways or via antioxidants. If however, this balance is disturbed a situation called oxidative stress occurs. Critically, oxidative stress plays important roles in the pathogenesis of many diseases, including cancer. Epigenetics is a process where gene expression is regulated by heritable mechanisms that do not cause any direct changes to the DNA sequence itself, and disruption of epigenetic mechanisms has important implications in disease. Evidence is emerging that histone deacetylases (HDACs) play decisive roles in regulating important cellular oxidative stress pathways including those involved with sensing oxidative stress and those involved with regulating the cellular response to oxidative stress. In particular aberrant regulation of these pathways by HDACs may play critical roles in cancer progression. In this review we discuss the current evidence linking epigenetics and oxidative stress and cancer, using chronic obstructive pulmonary disease and non-small cell lung cancer to illustrate the importance of epigenetics on these pathways within these disease settings. © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

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ID Code: 65181
Item Type: Journal Article
Refereed: Yes
Keywords: Chromatin, COPD, Epigenetics, NSCLC, Oxidative stress, histone deacetylase inhibitor, animal, chronic obstructive lung disease, drug effect, genetic epigenesis, genetics, human, lung tumor, pathology, review, signal transduction, Animals, Epigenesis, Genetic, Histone Deacetylase Inhibitors, Humans, Lung Neoplasms, Pulmonary Disease, Chronic Obstructive
DOI: 10.1111/j.1582-4934.2009.00845.x
ISSN: 1582-1838
Divisions: Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
Copyright Owner: Copyright 2009 Wiley-Blackwell Publishing Ltd.
Deposited On: 06 Dec 2013 03:47
Last Modified: 12 Mar 2014 05:49

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