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Vnn1 pantetheinase limits the Warburg effect and sarcoma growth by rescuing mitochondrial activity

Caroline Giessner1, Virginie Millet1, Konrad J Mostert2

  • 1Aix Marseille Univ, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Centre d'Immunologie de Marseille Luminy, Marseille, France.

Life Science Alliance
|November 21, 2018
PubMed

Insights

Vnn1 pantetheinase enzyme activity limits aggressive soft tissue sarcoma (STS) growth by restoring oxidative phosphorylation (OXPHOS) and limiting glycolysis. Higher VNN1 expression in STS patients correlates with improved prognosis, suggesting therapeutic potential.

Area of Science:

  • Biochemistry
  • Oncology
  • Metabolic pathways

Background:

  • Aggressive soft tissue sarcomas (STS) exhibit altered energy metabolism, relying on glycolysis (Warburg effect) over mitochondrial oxidative phosphorylation (OXPHOS).
  • Coenzyme A (CoA) is crucial for energy metabolism, and its availability can influence tumor growth.
  • Vnn1 pantetheinase degrades pantetheine into pantothenate (vitamin B5) and cysteamine, impacting CoA biosynthesis and potentially cellular metabolism.

Purpose of the Study:

  • To investigate the role of Vnn1 pantetheinase in the growth and metabolism of soft tissue sarcomas (STS).
  • To determine the impact of Vnn1 activity on tumor differentiation, growth rate, and patient prognosis.
  • To elucidate the mechanisms by which Vnn1 influences cellular energy metabolism in STS.

Main Methods:

  • Utilized two STS models to study Vnn1 function.
  • Analyzed VNN1 expression levels in patient STS samples.
  • Employed combined biochemical and cellular approaches to assess metabolic changes.
  • Measured CoA pools, OXPHOS, glycolysis, and lactate production.

Main Results:

  • Vnn1-positive (Vnn1+) STS exhibited slower growth and remained differentiated.
  • Detectable VNN1 expression in patient STS was associated with an improved prognosis.
  • Vnn1 activity restored CoA pools, supporting OXPHOS.
  • Cysteamine production by Vnn1 limited glycolysis and lactate release, inhibiting STS growth in vitro and in vivo.

Conclusions:

  • Vnn1 pantetheinase can limit aggressive STS growth by reversing the Warburg effect.
  • Restoration of CoA pools and maintenance of OXPHOS are key mechanisms.
  • Vnn1-induced metabolic rewiring, including cysteamine production, contributes to tumor growth inhibition.
  • Vnn1 represents a potential therapeutic target for soft tissue sarcomas.

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