Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation

FEBS Lett. 2006 Aug 7;580(18):4353-6. doi: 10.1016/j.febslet.2006.06.092. Epub 2006 Jul 10.

Abstract

Histone acetyltransferases (HATs) regulate transcription, chromatin structure and DNA repair. Here, we utilized a novel HAT inhibitor, anacardic acid, to examine the role of HATs in the DNA damage response. Anacardic acid inhibits the Tip60 HAT in vitro, and blocks the Tip60-dependent activation of the ATM and DNA-PKcs protein kinases by DNA damage in vivo. Further, anacardic acid sensitizes human tumor cells to the cytotoxic effects of ionizing radiation. These results demonstrate a central role for HATs such as Tip60 in regulating the DNA damage response. HAT inhibitors provide a novel therapeutic approach for increasing the sensitivity of tumors to radiation therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anacardic Acids / pharmacology
  • Anacardic Acids / therapeutic use*
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / antagonists & inhibitors
  • Cell Line, Tumor
  • DNA-Activated Protein Kinase / antagonists & inhibitors
  • DNA-Binding Proteins / antagonists & inhibitors
  • Enzyme Inhibitors / pharmacology
  • Enzyme Inhibitors / therapeutic use
  • HeLa Cells
  • Histone Acetyltransferases / antagonists & inhibitors*
  • Humans
  • Lysine Acetyltransferase 5
  • Neoplasms / radiotherapy*
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Radiation, Ionizing*
  • Radiation-Sensitizing Agents*
  • Tumor Suppressor Proteins / antagonists & inhibitors

Substances

  • Anacardic Acids
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Enzyme Inhibitors
  • Radiation-Sensitizing Agents
  • Tumor Suppressor Proteins
  • anacardic acid
  • Histone Acetyltransferases
  • KAT5 protein, human
  • Lysine Acetyltransferase 5
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • DNA-Activated Protein Kinase
  • Protein Serine-Threonine Kinases