S-Nitrosylation in TNF superfamily signaling pathway: Implication in cancer

Stéphanie Plenchette1, Sabrina Romagny1, Véronique Laurens1

  • 1Univ. Bourgogne Franche-Comté, LIIC EA7269, F-21000 Dijon, France; Ecole Pratique des Hautes Etudes, LIIC EA7269, F-21000 Dijon, France.

Redox Biology
|October 9, 2015
PubMed

Insights

Tumor cells resist apoptosis, necessitating new therapies. S-nitrosylation, a nitric oxide modification, shows promise in activating death receptor pathways for tumor elimination.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Tumor cells often develop resistance to apoptosis, hindering cancer treatment.
  • Activating death receptor signaling pathways is a potential strategy to induce tumor cell apoptosis.
  • Nitric oxide (NO) plays a complex role in cancer, with S-nitrosylation emerging as a key regulator of cell death.

Purpose of the Study:

  • To review the role of S-nitrosylation in regulating death receptor signaling pathways.
  • To explore how S-nitrosylation influences cell fate decisions in the context of tumor elimination.
  • To highlight novel therapeutic strategies targeting apoptotic resistance in cancer.

Main Methods:

  • Literature review of studies on S-nitrosylation and death receptor signaling.
  • Analysis of protein post-translational modifications by S-nitrosylation.
  • Examination of signaling pathways regulated by TNF superfamily members.

Main Results:

  • S-nitrosylation modifies proteins involved in Fas, DR4, and TNFR1 signaling.
  • This modification influences signaling pathways initiated by Fas ligand (FasL), TRAIL, and TNFα.
  • S-nitrosylation can promote cell death in tumor cells by modulating these pathways.

Conclusions:

  • S-nitrosylation is a critical post-translational modification impacting cancer cell apoptosis.
  • Targeting S-nitrosylation offers a promising avenue for developing novel cancer therapeutics.
  • Understanding S-nitrosylation's role in death receptor signaling is key to overcoming apoptotic resistance.

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