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Targeting Mitochondria in Melanoma.

Sepideh Aminzadeh-Gohari1, Daniela D Weber1, Luca Catalano1

  • 1Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, University Hospital of the Paracelsus Medical University, 5020 Salzburg, Austria.

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|October 3, 2020
PubMed
Summary

Cancer cells often exhibit high glycolysis and functional oxidative phosphorylation (OXPHOS), but possess dysfunctional mitochondria. The novel agent ONC212 shows promise in targeting mitochondrial respiration for cancer therapy.

Keywords:
BRAFNRASONC212Warburg effectanti-parasitic drugantibioticmelanomamitochondrial respiration

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Area of Science:

  • Biochemistry
  • Cancer Biology
  • Mitochondrial Metabolism

Background:

  • Cancer cells exhibit altered metabolism, notably increased glycolysis.
  • While previously thought to be exclusive, many cancer cells retain functional oxidative phosphorylation (OXPHOS) alongside elevated glycolysis.
  • Targeting mitochondrial metabolism is an emerging strategy in cancer treatment.

Purpose of the Study:

  • To investigate mitochondrial respiration and OXPHOS complex activity in melanoma cell lines.
  • To evaluate the anti-cancer effects of approved antibiotics, an anti-parasitic drug, and a novel agent (ONC212) on melanoma cells and normal fibroblasts.
  • To identify potential therapeutic targets within cancer cell mitochondrial pathways.

Main Methods:

  • Seahorse real-time cell metabolic analysis to measure mitochondrial respiration.
  • Immunoblotting and spectrophotometry to assess OXPHOS complex amount and activity.
  • In vitro testing of antibiotics, pyrvinium pamoate, and ONC212 on melanoma cells and human dermal fibroblasts (HDFs).

Main Results:

  • Three of four melanoma cell lines showed elevated glycolysis and OXPHOS but had dysfunctional mitochondria.
  • The anti-parasitic drug pyrvinium pamoate significantly inhibited respiration and proliferation in both melanoma cells and HDFs.
  • ONC212 reduced respiration in melanoma cells and HDFs and inhibited melanoma cell proliferation.

Conclusions:

  • Melanoma cells can possess both high glycolysis and OXPHOS with mitochondrial dysfunction.
  • ONC212 demonstrates potential as a therapeutic agent for targeting mitochondrial respiration in cancer.
  • Further research into ONC212's mechanism and efficacy is warranted for cancer treatment development.