Nucleophosmin redistribution following heat shock: a role in heat-induced radiosensitization

Cancer Res. 2009 Aug 15;69(16):6454-62. doi: 10.1158/0008-5472.CAN-08-4896. Epub 2009 Jul 28.

Abstract

Cellular survival from radiation-induced DNA damage requires access to sites of damage for the assembly of repair complexes and the subsequent repair, particularly the repair of DNA double strand breaks (DSB). Hyperthermia causes changes in protein-protein/DNA interactions in the nucleus that block access to sites of DNA damage. Studies presented here indicate that the nucleolar protein, nucleophosmin (NPM), redistributes from the nucleolus following hyperthermia, increases its association with DNA, and blocks access to DNA DSBs. Reduction of NPM significantly reduces heat-induced radiosensitization, but reduced NPM level does not alter radiation sensitivity per se. NPM knockdown reduces heat-induced inhibition of DNA DSB repair. Also, these results suggest that NPM associates with nuclear matrix attachment region DNA in heat-shocked cells.

Publication types

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

MeSH terms

  • DNA Breaks, Double-Stranded / drug effects
  • DNA Breaks, Double-Stranded / radiation effects
  • DNA Repair / drug effects
  • DNA Repair / genetics
  • HeLa Cells
  • Heat-Shock Response / drug effects
  • Heat-Shock Response / genetics
  • Heat-Shock Response / physiology*
  • Hot Temperature*
  • Humans
  • Models, Biological
  • Nuclear Proteins / antagonists & inhibitors
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Nucleophosmin
  • RNA, Small Interfering / pharmacology
  • Radiation Dosage
  • Radiation Tolerance / drug effects
  • Radiation Tolerance / genetics
  • Radiation Tolerance / physiology*
  • Tissue Distribution / drug effects
  • Tumor Cells, Cultured

Substances

  • NPM1 protein, human
  • Nuclear Proteins
  • RNA, Small Interfering
  • Nucleophosmin