HDAC inhibitors in models of inflammation-related tumorigenesis

Cancer Lett. 2009 Aug 8;280(2):154-9. doi: 10.1016/j.canlet.2008.11.019. Epub 2008 Dec 19.

Abstract

Histone deacetylase (HDAC) inhibitors have been described in detail for their anti-proliferative potency. Recently, an anti-inflammatory property was characterized in vitro and in vivo. This dual efficacy of HDAC inhibitors is highly attractive, since chronic inflammations such as ulcerative colitis are associated with an increased risk of developing carcinomas. Additionally, in models of colitis and inflammation-induced tumorigenesis inflammation as well as tumor development was significantly inhibited by HDAC inhibitor treatment. The mechanisms involved reach beyond the simple regulation of histone acetylation and deacetylation. The currently known key target structures and mechanisms mediating this dual effect will be discussed in this review.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acetylation
  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Anticarcinogenic Agents / therapeutic use*
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / physiology
  • Cell Transformation, Neoplastic / drug effects*
  • Cell Transformation, Neoplastic / immunology
  • Colitis / drug therapy
  • Colitis / immunology
  • Colitis / pathology
  • Colonic Neoplasms / immunology
  • Colonic Neoplasms / pathology
  • Colonic Neoplasms / prevention & control
  • Histone Deacetylase Inhibitors
  • Histone Deacetylases / metabolism*
  • Humans
  • Inflammation / drug therapy
  • Inflammation / immunology
  • NF-kappa B / metabolism
  • Neoplasms / drug therapy*
  • Neoplasms / immunology

Substances

  • Anti-Inflammatory Agents
  • Anticarcinogenic Agents
  • Histone Deacetylase Inhibitors
  • NF-kappa B
  • Histone Deacetylases