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Progesterone Modulates Mitochondrial Functions in Human Glioblastoma Cells.

Fahim Atif1, Seema Yousuf2, Claudia Espinosa-Garcia2

  • 1Brain Research Laboratory, Department of Emergency Medicine, Emory University School of Medicine, Whitehead Biomedical Research Building, Room 655A, Atlanta, GA, 30322, USA. fatif@emory.edu.

Molecular Neurobiology
|April 13, 2021
PubMed
Summary

High-dose progesterone (P4) inhibits mitochondrial respiration and glycolysis in glioblastoma multiforme (GBM) cells. This suggests P4 could be a potential treatment to slow GBM tumor growth.

Keywords:
Glioblastoma multiformeGlycolysisMitochondriaOxidative phosphorylationProgesterone treatment

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Area of Science:

  • Oncology
  • Mitochondrial Biology
  • Metabolic Disease

Background:

  • Cancer is increasingly recognized as a metabolic disease.
  • Mitochondria play crucial roles in cellular metabolism and are sexually dimorphic.
  • Progesterone (P4) is a key regulator of mitochondrial functions.

Purpose of the Study:

  • To investigate the effects of P4 on mitochondrial functions in human glioblastoma multiforme (GBM) cell lines.
  • To determine how P4 influences mitochondrial respiration and glycolysis in GBM cells.

Main Methods:

  • Human GBM cell lines were treated with varying concentrations of P4.
  • Mitochondrial function was assessed using Seahorse XF analysis, measuring oxygen consumption rate (OCR) and extracellular acidification rate (ECAR).
  • Mitochondrial superoxide radical generation was examined via confocal microscopy.

Main Results:

  • P4 demonstrated a dose-dependent inhibitory effect on OCR, ECAR, and spare respiratory capacity (SRC) in GBM cells.
  • P4 altered basal respiration, maximum respiration, ATP production, and proton leak.
  • High-dose P4 (80 μM) significantly inhibited GBM cell mitochondrial respiration and glycolysis, with a concurrent 11-22% increase in superoxide radical generation.

Conclusions:

  • High-dose P4 inhibits both mitochondrial respiration and glycolysis in human GBM cells.
  • These inhibitory effects on cellular metabolism suggest a potential therapeutic strategy for controlling GBM progression.
  • P4 may represent a novel treatment to reduce tumor size and growth rate in glioblastoma.