Related Experiment Video

Updated: Jul 5, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

Post-translational modifications induced by nitric oxide (NO): implication in cancer cells apoptosis

Lissbeth Leon1, Jean-François Jeannin, Ali Bettaieb

  • 1EPHE, Laboratoire d'immunologie et immunothérapie des cancers, Inserm U866, Dijon, F-21000, France. leonlissbeth@yahoo.fr

Nitric Oxide : Biology and Chemistry
|May 14, 2008
PubMed

Insights

Nitric oxide (NO) and reactive oxygen species (ROS) modifications impact cell death pathways. This review explores how NO protein modifications influence cancer cell survival and death.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Post-translational modifications (PTMs) are crucial for regulating protein function.
  • Nitric oxide (NO) and reactive oxygen species (ROS) are key signaling molecules involved in cellular processes.
  • PTMs induced by NO and ROS are increasingly implicated in cell death regulation.

Purpose of the Study:

  • To review the current understanding of nitric oxide (NO)-induced protein modifications.
  • To elucidate the dual role of NO modifications in promoting or inhibiting cell death.
  • To focus on the significance of these modifications in cancer cells.

Main Methods:

  • Literature review of existing research on NO, ROS, PTMs, and cell death.
  • Analysis of studies investigating specific NO-protein interactions and their functional outcomes.
  • Synthesis of data focusing on cancer cell models.

Main Results:

  • NO can induce various PTMs, including S-nitrosylation, tyrosine nitration, and S-glutathionylation.
  • These NO-induced PTMs can modulate the activity of proteins involved in apoptosis, autophagy, and necrosis.
  • Evidence suggests NO modifications can both promote and inhibit cancer cell death depending on context.

Conclusions:

  • NO-mediated PTMs represent a critical regulatory mechanism in cell death pathways.
  • Targeting NO-protein interactions offers potential therapeutic strategies for cancer treatment.
  • Further research is needed to fully delineate the complex roles of NO modifications in cancer biology.

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