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Tumor-generated nitric oxide as an antagonist of photodynamic therapy

Albert W Girotti1

  • 1Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. agirotti@mcw.edu.

Photochemical & Photobiological Sciences : Official Journal of the European Photochemistry Association and the European Society for Photobiology
|February 24, 2015
PubMed

Insights

Tumors use nitric oxide (NO) to resist photodynamic therapy (PDT). Inducible nitric oxide synthase (iNOS) upregulation after PDT enhances cancer cell survival, growth, and invasion, suggesting iNOS inhibitors as a potential therapeutic strategy.

Area of Science:

  • Biochemistry
  • Cancer Biology
  • Medical Science

Background:

  • Nitric oxide (NO) is a molecule produced by nitric oxide synthase (NOS) enzymes.
  • Tumors utilize NO for survival, growth, and to resist therapies like photodynamic therapy (PDT).
  • Mechanisms behind NO's anti-PDT effects are not fully understood, though observed in animal models.

Purpose of the Study:

  • To review current knowledge on NO's negative impact on PDT efficacy.
  • To explore signaling mechanisms involved in NO's anti-PDT effects.
  • To provide insights into attenuating these effects using iNOS inhibitors.

Main Methods:

  • In vitro studies on breast and prostate cancer cells.
  • Analysis of inducible NOS (iNOS) and NO levels after ALA-PDT-like challenge.
  • Assessment of apoptosis, cell growth, migration, and invasion post-photochallenge.

Main Results:

  • iNOS and NO were significantly upregulated in cancer cells post-PDT challenge.
  • Cells exhibited increased resistance to apoptosis.
  • Survivors showed enhanced growth, migration, and invasion, with iNOS/NO playing a key role.

Conclusions:

  • NO, particularly via iNOS, promotes cancer cell survival and progression after PDT.
  • Targeting iNOS may offer a strategy to overcome PDT resistance.
  • Further research into iNOS inhibition could enhance PDT effectiveness.

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