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Distinct effects of etoposide on glutamine-addicted neuroblastoma

Kadri Valter1, Polina Maximchik2, Alibek Abdrakhmanov2

  • 1Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden.

Cellular and Molecular Life Sciences : CMLS
|August 9, 2019
PubMed

Insights

Anticancer drugs like etoposide can destabilize mitochondria and, when combined with glutamine withdrawal, induce cancer cell death. Depleting antioxidants enhances this mitochondrial-targeted cancer therapy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Most anticancer drugs damage DNA; their direct impact on mitochondria is unclear.
  • Tumors like neuroblastoma often depend on glutamine, a nonessential amino acid.

Purpose of the Study:

  • To investigate the direct effects of common anticancer drugs on mitochondrial activity.
  • To assess the impact of combining these drugs with glutamine withdrawal on cancer cell apoptosis.

Main Methods:

  • Treatment of cancer cells with etoposide.
  • Glutamine withdrawal experiments.
  • Assessment of mitochondrial activity, reactive oxygen species (ROS) production, and apoptosis.

Main Results:

  • Etoposide inhibits mitochondrial Complex I, increasing superoxide radical formation.
  • Etoposide alone did not induce apoptosis.
  • Apoptosis was observed only when glutamine withdrawal depleted glutathione (an antioxidant).
  • Combined etoposide and glutamine withdrawal destabilized mitochondria, releasing cytochrome c and activating apoptosis.

Conclusions:

  • Simultaneous glutathione depletion and mitochondrial destabilization by ROS trigger the mitochondrial apoptotic pathway.
  • Inhibiting cellular antioxidant responses can enhance mitochondrial targeting for stronger antitumor therapy.
Keywords:
ApoptosisMitochondriaNeuroblastomaOxidative stressRespiratory chain

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