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Under pressure: peroxisomes in cancer therapy resistance

Nicla Lorito1, Francesca Bonechi1, Elisabetta Romano1

  • 1Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale Morgagni 50, Florence, 50134, Italy.

Trends in Molecular Medicine
|June 3, 2026
PubMed

Insights

Therapy resistance in cancer is worsened by metabolic changes. This review explores how peroxisomes, crucial metabolic organelles, contribute to resistance and may offer new therapeutic targets.

Area of Science:

  • Oncology
  • Metabolic pathways
  • Cell biology

Background:

  • Therapy resistance is a major challenge in achieving durable cancer treatment responses.
  • While genetic factors drive resistance, metabolic adaptation is critical for tumor persistence.
  • Peroxisomes are key metabolic organelles involved in lipid metabolism and redox homeostasis.

Purpose of the Study:

  • To review the emerging evidence linking peroxisome biology to cancer therapy resistance.
  • To discuss the role of peroxisomal pathways in supporting metabolic plasticity under therapeutic stress.
  • To explore the potential of peroxisomal pathways as therapeutic targets or biomarkers.

Main Methods:

  • Literature review of studies on peroxisome function in cancer.
  • Synthesis of evidence connecting peroxisomal pathways to various cancer therapies.
  • Analysis of peroxisomal roles in metabolic adaptation and redox buffering.

Main Results:

  • Peroxisomal functions are remodeled under therapeutic pressure to support cancer cells.
  • Peroxisome-associated metabolic pathways are implicated in resistance to chemotherapy, targeted therapy, radiotherapy, and immunotherapy.
  • Metabolic adaptation, involving peroxisomes, enables tumor persistence and contributes to therapy failure.

Conclusions:

  • Peroxisome biology is intricately linked to cancer therapy resistance.
  • Targeting peroxisomal pathways or utilizing them as biomarkers may offer strategies to overcome resistance.
  • Further research into peroxisome function can guide novel therapeutic approaches for resistant cancers.
Keywords:
PPARether phospholipidsfatty acid oxidationpexophagyredox homeostasistherapy resistance

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