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Radiation therapy generates platelet-activating factor agonists.

Ravi P Sahu1, Kathleen A Harrison2, Jonathan Weyerbacher3

  • 1Department of Pharmacology and Toxicology, Boonshoft School of Medicine at Wright State University, Dayton, OH, USA.

Oncotarget
|March 10, 2016
PubMed
Summary
This summary is machine-generated.

Ionizing radiation generates platelet-activating factor-receptor (PAF-R) agonists, which can suppress immunity and promote tumor growth. This discovery offers new strategies to enhance radiation therapy effectiveness.

Keywords:
antioxidantscyclooxygenase type 2 enzymeoxidized glycerophosphocholinesplatelet-activating factorradiation therapy

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Area of Science:

  • Oncology
  • Immunology
  • Biochemistry

Background:

  • Pro-oxidative stressors, including radiation therapy, generate reactive oxygen species.
  • These stressors can produce oxidized lipid agonists that activate the platelet-activating factor-receptor (PAF-R).
  • PAF-R activation can suppress host immunity, potentially impacting cancer treatment outcomes.

Purpose of the Study:

  • To determine if ionizing radiation generates PAF-R agonists.
  • To investigate if these radiation-induced lipids can subvert host immunity.
  • To explore the role of PAF-R agonists in tumor growth during radiation therapy.

Main Methods:

  • In-vitro irradiation of tumor cell lines.
  • In-vivo irradiation of tumors in a murine melanoma model.
  • Analysis of human subjects undergoing radiation therapy for skin tumors.
  • Structural characterization of radiation-induced PAF-R agonistic lipids.
  • Pharmacological blockade using a cyclooxygenase-2 inhibitor.

Main Results:

  • Radiation exposure consistently generated PAF-R agonists across cell lines, tumors, and human subjects.
  • Identified PAF and oxidized glycerophosphocholines as non-enzymatically produced PAF-R agonists.
  • Irradiation of one tumor enhanced the growth of a non-treated tumor in a PAF-R-dependent manner.
  • This tumor growth augmentation was inhibited by a cyclooxygenase-2 inhibitor.

Conclusions:

  • Ionizing radiation produces PAF-R agonists, including PAF and oxidized lipids.
  • These agonists can suppress host immunity and promote tumor growth, potentially leading to treatment failure.
  • Targeting PAF-R pathways presents a novel therapeutic strategy to improve radiation therapy efficacy.