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5-Aza-2'-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells

Djordje Miljkovic1, Ivana Cvetkovic, Marija Sajic

  • 1Laboratory of Immunology, Institute for Biological Research Sinisa Stankovic, 29. Novembra 142, 11060 Belgrade, Serbia. georgije_zw@yahoo.com

European Journal of Pharmacology
|February 6, 2004
PubMed

Insights

Anti-cancer drugs 5-Aza-2'-deoxycytidine (ADC) and paclitaxel inhibit nitric oxide (NO) production in fibrosarcoma cells by reducing inducible NO synthase (iNOS) expression. This action may enhance their therapeutic efficacy against tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Nitric oxide (NO) plays a critical role in tumor cell biology.
  • Interferon-gamma (IFN-gamma) stimulates NO production via inducible NO synthase (iNOS).

Purpose of the Study:

  • To investigate the effect of anti-cancer drugs 5-Aza-2 -deoxycytidine (ADC) and paclitaxel on NO production in mouse L929 fibrosarcoma cells.
  • To elucidate the mechanism underlying the modulation of NO production by these drugs.

Main Methods:

  • Treatment of L929 fibrosarcoma cells and primary fibroblasts with ADC and paclitaxel.
  • Measurement of NO release and iNOS expression.
  • Analysis of p44/p42 mitogen-activated protein (MAP) kinase activation.

Main Results:

  • Both ADC and paclitaxel significantly reduced IFN-gamma-stimulated NO release in L929 cells and primary fibroblasts.
  • The drugs suppressed IFN-gamma-induced iNOS expression and p44/p42 MAP kinase activation in L929 cells.
  • No significant inhibition of NO release was observed in mouse peritoneal macrophages.

Conclusions:

  • ADC and paclitaxel inhibit NO production in fibrosarcoma cells by downregulating iNOS expression, potentially via the p44/p42 MAP kinase pathway.
  • These findings suggest that the anti-cancer effects of ADC and paclitaxel may be partly mediated by their ability to reduce NO-dependent toxicity in tumors.

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