Deregulation of glucose transporter 1 and glycolytic gene expression by c-Myc

Rebecca C. Osthus, Hyunsuk Shim, Sunkyu Kim, Qing Li, Rahul Reddy, Mita Mukherjee, Yi Xu, Diane Wonsey, Linda A. Lee, Chi V. Dang

Research output: Contribution to journalArticlepeer-review

537 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)21797-21800
Number of pages4
JournalJournal of Biological Chemistry
Issue number29
StatePublished - Jul 21 2000

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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