Unlike normal mammalian cells, which use oxygen to generate energy, cancer cells 
rely on glycolysis for energy and are therefore less dependent on oxygen. We 
previously observed that the c-Myc oncogenic transcription factor regulates 
lactate dehydrogenase A and induces lactate overproduction. We, therefore, 
sought to determine whether c-Myc controls other genes regulating glucose 
metabolism. In Rat1a fibroblasts and murine livers overexpressing c-Myc, the 
mRNA levels of the glucose transporter GLUT1, phosphoglucose isomerase, 
phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate 
kinase, and enolase were elevated. c-Myc directly transactivates genes encoding 
GLUT1, phosphofructokinase, and enolase and increases glucose uptake in Rat1 
fibroblasts. Nuclear run-on studies confirmed that the GLUT1 transcriptional 
rate is elevated by c-Myc. Our findings suggest that overexpression of the c-Myc 
oncoprotein deregulates glycolysis through the activation of several components 
of the glucose metabolic pathway.