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Metabolic Reprogramming Into a Glycolysis Phenotype Induced by Extracellular Vesicles Derived From Prostate Cancer

Yoon-Jin Lee1, Chul Won Seo1, Shinwon Chae1

  • 1Department of Biochemistry, Soonchunhyang University, College of Medicine, Cheonan, Republic of Korea.

Molecular & Cellular Proteomics : MCP
|March 15, 2025
PubMed
Summary

Prostate cancer cells release extracellular vesicles (EVs) that reprogram recipient cells to adopt the Warburg effect, enhancing survival in acidic tumor environments. This metabolic shift increases glucose consumption and proliferation.

Keywords:
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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Cancer cells often exhibit aerobic glycolysis (Warburg effect) for survival and proliferation in low-oxygen tumor microenvironments.
  • The acidic tumor microenvironment can impair immune responses, aiding cancer cell immune evasion.
  • Tumor-derived extracellular vesicles (EVs) are known to transfer materials and influence recipient cells, but their role in metabolic reprogramming is less understood.

Purpose of the Study:

  • To investigate the role of EVs from prostate cancer cells in metabolic reprogramming.
  • To identify specific EV components that mediate metabolic changes in recipient cells.
  • To understand how EV-mediated metabolic reprogramming contributes to cancer cell survival in acidic conditions.

Main Methods:

  • Established prostate cancer cell lines (PC-3 and PC-3AcT) adapted to acidic, lactic acid-rich conditions.
  • Quantitative proteomics analysis of EVs isolated from PC-3 and PC-3AcT cells.
  • Assessed the impact of PC-3AcT EVs on recipient PC-3 cell metabolism, proliferation, and survival.

Main Results:

  • Identified 935 EV proteins, with 159 regulated proteins related to energy metabolism, cellular shape, and extracellular matrix in adapted cells.
  • EVs from adapted cells were enriched in glycolytic enzymes and apolipoproteins, notably apolipoprotein B-100 (APOB).
  • APOB on EVs facilitated uptake by recipient cells, increasing hexokinase and phosphofructokinase activity, promoting the Warburg phenotype and enhancing survival.

Conclusions:

  • Prostate cancer cell-derived EVs contribute to metabolic reprogramming of recipient cells.
  • EVs mediate the acquisition of the Warburg phenotype, enhancing cancer cell survival and proliferation.
  • This study highlights a novel mechanism by which cancer cells adapt to and thrive within the tumor microenvironment through EV-mediated metabolic reprogramming.