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Keywords:

  • epigenetics;
  • chromatin;
  • oxidative stress;
  • COPD;
  • NSCLC

Abstract

  • • 
    Oxidative stress, epigenetics, NSCLC and COPD
    • - 
      Cigarette smoke mediated cellular proliferation
    • - 
      Cigarette smoke mediated lung destruction
    • - 
      DNA methylation and lung cancer
    • - 
      Histone post-translational modifications and lung cancer
  • • 
    Linking epigenetics and oxidative stress to the development of COPD and NSCLC
    • - 
      HATs and KATs in the developing lung
    • - 
      HDACs and COPD
    • - 
      Aberrant KAT/HDAC activity in NSCLC
    • - 
      ATP-dependent SWI/SNF chromatin remodelling complexes and NSCLC
    • - 
      KATs/HDACs and oxidative stress pathways
    • - 
      KEAP1-NRF2-ARE signalling pathway
  • • 
    Epigenetics, COPD, NSCLC and oxidative stress pathways/genes
    • - 
      NRF2
    • - 
      Heme oxygenase 1
    • - 
      Hypoxia-inducible factor-1α
    • - 
      PGC-1α
    • - 
      Oxidative stress, epigenetics, glucocorticoids and COPD
    • - 
      Oxidative stress, acetylation and its role in the regulation of NFκB
    • - 
      Targeting epigenetic mechanisms in COPD and NSCLC
  • • 
    Theophylline – a novel agonist of HDACs
    • - 
      Current clinical trials involving epigenetic therapies in COPD and NSCLC
  • • 
    Dietary HDAC inhibitors as therapeutic agents to target -   COPD or NSCLC?
  • • 
    Sulforaphane
  • • 
    Curcumin
  • • 
    Epigallocatechin 3-gallate (EGCG)
  • • 
    Can dietary epigenetic inhibitors work in the clinical setting?
  • • 
    Caveats
  • • 
    Conclusions

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.