Oct1 loss of function induces a coordinate metabolic shift that opposes tumorigenicity

Nat Cell Biol. 2009 Mar;11(3):320-7. doi: 10.1038/ncb1840. Epub 2009 Feb 15.


Cancer cells frequently undergo a shift from oxidative to glycolytic metabolism. Although there is interest in targeting metabolism as a form of cancer therapy, this area still remains in its infancy. Using cells, embryos and adult animals, we show here that loss of the widely expressed transcription factor Oct1 induces a coordinated metabolic shift: mitochondrial activity and amino acid oxidation are increased, while glucose metabolism is reduced. Altered expression of direct Oct1 targets encoding metabolic regulators provides a mechanistic underpinning to these results. We show that these metabolic changes directly oppose tumorigenicity. Collectively, our findings show that Oct1, the genes it regulates and the pathways these genes affect could be used as targets for new modes of cancer therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids / metabolism
  • Animals
  • Embryo, Mammalian / cytology
  • Embryo, Mammalian / metabolism
  • Embryo, Mammalian / ultrastructure
  • Fibroblasts / metabolism
  • Fibroblasts / ultrastructure
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Glucose / metabolism
  • Glycolysis
  • Humans
  • Metabolome
  • Mice
  • Mitochondria / metabolism
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Octamer Transcription Factor-1 / deficiency*
  • Octamer Transcription Factor-1 / metabolism
  • Oxidation-Reduction


  • Amino Acids
  • Octamer Transcription Factor-1
  • Glucose