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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Targeting PGE2 mediated senescent neuron improves tumor therapy.

Jianyi Zhao1,2, Linshi Wu3, Gang Cai1,2

  • 1Shanghai Key Laboratory of Proton-Therapy, Shanghai, China.

Neuro-Oncology
|February 18, 2025
PubMed
Summary

Tumor cells create prostaglandin E2 (PGE2) to induce neuronal senescence after therapy. Targeting this AEP/PGE2 feedback loop may improve glioblastoma treatment outcomes.

Keywords:
PGE2neuronradio-/chemotherapysenescencetumor

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Area of Science:

  • Neuro-oncology
  • Cancer biology
  • Molecular mechanisms of therapy resistance

Background:

  • Tumor-neuron signaling is crucial but poorly understood in the context of radio-/chemotherapy.
  • Obscure tumor-neuron interactions hinder effective glioblastoma treatment strategies.

Purpose of the Study:

  • To elucidate the mechanisms of neuron-tumor interactions during radio-/chemotherapy.
  • To identify therapeutic targets for improving glioblastoma treatment.

Main Methods:

  • Glioblastoma organoids (GBOs) and primary neuron co-cultures were used.
  • Techniques included metabonomics, RNA sequencing, mass spectrometry, and in vivo mouse models.
  • Diagnostic and prognostic values were assessed in patient data (serum, tissue microarrays, TCGA).

Main Results:

  • Tumor-derived prostaglandin E2 (PGE2) induced neuronal senescence post-therapy.
  • Asparagine endopeptidase (AEP) cleaved eIF4A1, stabilizing PTGES3 mRNA and increasing PGE2.
  • Inhibiting PGE2 or AEP reduced senescence and delayed tumor progression; high PTGES3 correlated with poor prognosis.

Conclusions:

  • A feedback loop involving AEP and PGE2 drives tumor-induced neuronal senescence during radio-/chemotherapy.
  • This pathway represents a potential therapeutic target to enhance glioblastoma treatment.