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.