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Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor

Viral D Oza1,2, Kenan A Flores1, Yelena Chernyavskaya1

  • 1Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky, USA.

Journal of Extracellular Vesicles
|October 30, 2025
PubMed
Summary

Pediatric brain tumors called H3K27M-pDMG resist radiation. Resistant tumor cells release vesicles that protect sensitive cells, suggesting new therapeutic targets.

Keywords:
DIPGDNA repairdiffuse midline gliomaextracellular vesiclesglioma stem cellsmiRNAoxidative phosphorylationradiation therapy

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Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Cellular Communication

Background:

  • Pediatric diffuse midline gliomas with the H3K27M mutation (H3K27M-pDMG) are aggressive brain tumors.
  • These tumors inherently resist radiation therapy, the standard treatment.
  • Intratumoral heterogeneity and cell-to-cell communication via extracellular vesicles may drive resistance.

Purpose of the Study:

  • To investigate the role of small extracellular vesicles (sEVs) in radiation resistance of H3K27M-pDMG.
  • To characterize sEV uptake, surface proteins, and cargo.
  • To determine if sEVs from radioresistant cells can protect radiosensitive cells.

Main Methods:

  • Characterized sEV uptake in H3K27M-pDMG cells.
  • Identified key sEV surface proteins.
  • Performed molecular profiling of sEVs (proteins, miRNAs, metabolites).
  • Assessed the impact of RR-sEVs on recipient cell gene expression, metabolism, DNA repair, and survival post-radiation.

Main Results:

  • sEVs from radioresistant (RR) H3K27M-pDMG cells conferred radioprotective effects on radiosensitive cells.
  • RR-sEVs were enriched with molecules involved in glycolysis, oxidative phosphorylation, and DNA repair.
  • Uptake of RR-sEVs reprogrammed recipient cells, enhancing their survival after radiation exposure.

Conclusions:

  • sEV-mediated communication contributes to radiation resistance in H3K27M-pDMG.
  • RR-sEVs promote survival by altering recipient cell metabolism and DNA repair.
  • Targeting sEV pathways could be a strategy to overcome radiation resistance in these pediatric brain tumors.