Glutamine-fueled mitochondrial metabolism is decoupled from glycolysis in melanoma

Fabian V. Filipp, Boris Ratnikov, Jessica De Ingeniis, Jeffrey W. Smith, Andrei L. Osterman, David A. Scott

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


In this perspective, we revise the historic notion that cancer is a disease of mitochondria. We summarize recent findings on the function and rewiring of central carbon metabolism in melanoma. Metabolic profiling studies using stable isotope tracers show that glycolysis is decoupled from the tricarboxylic acid (TCA) cycle. This decoupling is not 'dysfunction' but rather an alternate wiring required by tumor cells to remain metabolically versatile. In large part, this requirement is met by glutamine feeding the TCA cycle as an alternative source of carbon. Glutamine is also used in non-conventional ways, like traveling in reverse through the TCA flux to feed fatty acid biosynthesis. Biosynthetic networks linked with non-essential amino acids alanine, serine, arginine, and proline are also significantly impacted by the use of glutamine as an alternate carbon source.

Original languageEnglish
Pages (from-to)732-739
Number of pages8
JournalPigment Cell and Melanoma Research
Issue number6
StatePublished - Nov 2012
Externally publishedYes


  • Glutamine
  • Metabolism
  • Mitochondria
  • NMR
  • Systems biology


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