Thermal stress and the disruption of redox-sensitive signalling and transcription factor activation: Possible role in radiosensitization

D. Gius*, D. Mattson, C. M. Bradbury, D. K. Smart, D. R. Spitz

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations

Abstract

In spite of ongoing research efforts, the specific mechanism(s) of heat-induced alterations in the cellular response to ionizing radiation (IR) remain ambiguous, in part because they likely involve multiple mechanisms and potential targets. One such group of potential targets includes a class of cytoplasmic signalling and/or nuclear transcription factors known as immediate early response genes, which have been suggested to perform cytotoxic as well as cytoprotective roles during cancer therapy. One established mechanism regulating the activity of these early response elements involves changes in cellular oxidation/reduction (redox) status. After establishing common alterations in early response genes by oxidative stress and heat exposure, one could infer that heat shock may have similarities to other forms of environmental antagonists that induce oxidative stress. In this review, recent evidence supporting a mechanistic link between heat shock and oxidative stress will be summarized. In addition, the hypothesis that one mechanism whereby heat shock alters cellular responses to anticancer agents (including hyperthermic radiosensitization) is through heat-induced disruption of redox-sensitive signalling factors will be discussed.

Original languageEnglish (US)
Pages (from-to)213-223
Number of pages11
JournalInternational Journal of Hyperthermia
Volume20
Issue number2
DOIs
StatePublished - Mar 2004

Keywords

  • AP-1
  • Hyperthermia
  • NF-κB
  • Redox regulation
  • Signalling

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cancer Research

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