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Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy
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 o...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4498937/ https://www.ncbi.nlm.nih.gov/pubmed/19602054 http://dx.doi.org/10.1111/j.1582-4934.2009.00845.x |
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author | Lawless, Matthew W O’Byrne, Kenneth J Gray, Steven G |
author_facet | Lawless, Matthew W O’Byrne, Kenneth J Gray, Steven G |
author_sort | Lawless, Matthew W |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4498937 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | John Wiley & Sons, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-44989372015-07-16 Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy Lawless, Matthew W O’Byrne, Kenneth J Gray, Steven G J Cell Mol Med Reviews 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. John Wiley & Sons, Ltd 2009-09 2009-07-07 /pmc/articles/PMC4498937/ /pubmed/19602054 http://dx.doi.org/10.1111/j.1582-4934.2009.00845.x Text en © 2009 The Authors Journal compilation © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd |
spellingShingle | Reviews Lawless, Matthew W O’Byrne, Kenneth J Gray, Steven G Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title | Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title_full | Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title_fullStr | Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title_full_unstemmed | Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title_short | Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy |
title_sort | oxidative stress induced lung cancer and copd: opportunities for epigenetic therapy |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4498937/ https://www.ncbi.nlm.nih.gov/pubmed/19602054 http://dx.doi.org/10.1111/j.1582-4934.2009.00845.x |
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