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O-GlcNAcylation in cellular senescence: From molecular insights to anti-cancer therapeutic opportunities

Adrien Pioger1, Nathalie Martin1, Corinne Abbadie1

  • 1Univ. Lille, CNRS, Inserm, Institut Pasteur de Lille, CHU Lille, UMR9020-U1366 - CRCLille - Cancer Research Center of Lille, F-59000 Lille, France.

Biochimica Et Biophysica Acta. Reviews on Cancer
|July 20, 2026
PubMed

Insights

Cellular senescence, a key stress response, is modulated by O-GlcNAcylation. Targeting O-GlcNAc cycling enzymes may improve anti-cancer therapies by controlling senescence.

Area of Science:

  • Cellular biology
  • Cancer research
  • Metabolism

Background:

  • Cellular senescence is a crucial stress response in aging and disease, acting as a double-edged sword in cancer therapy.
  • Senescent cells undergo significant metabolic reprogramming, but the role of O-GlcNAcylation in this process remains under investigation.
  • O-GlcNAcylation, a nutrient-sensitive post-translational modification, is implicated in cancer progression and therapy resistance.

Purpose of the Study:

  • To review the current understanding of O-GlcNAcylation's role in cellular senescence.
  • To explore how O-GlcNAcylation influences key hallmarks of senescence.
  • To discuss the therapeutic potential of targeting O-GlcNAc cycling enzymes in cancer treatment.

Main Methods:

  • Literature review of studies on O-GlcNAcylation and cellular senescence.
  • Analysis of evidence linking O-GlcNAcylation to senescence hallmarks.
  • Discussion of therapeutic strategies targeting O-GlcNAc cycling enzymes.

Main Results:

  • O-GlcNAcylation levels change during senescence, and its cycling enzymes impact senescence onset, maintenance, and escape.
  • O-GlcNAcylation influences cell cycle arrest, DNA damage response, apoptosis resistance, metabolic rewiring, and mitochondrial signaling in senescent cells.
  • Modulating O-GlcNAc cycling enzymes shows potential for controlling cancer cell senescence.

Conclusions:

  • O-GlcNAcylation is a significant regulator of cellular senescence and its associated hallmarks.
  • Targeting O-GlcNAc cycling enzymes offers a promising therapeutic avenue to enhance anti-cancer treatments by modulating senescence.
  • Further research into O-GlcNAcylation in senescence could lead to improved strategies for limiting tumor relapse and minimal residual disease.
Keywords:
CancerO-GlcNAcylationRelapseSenescenceTolerant persister cells

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