Abstract
Cancer cells feature altered glucose metabolism that allows their rapid growth. They consume large amounts of glucose to produce lactate, even in the presence of ample oxygen, which is known as the Warburg effect. Pyruvate kinase M2 (PKM2) contributes to the Warburg effect by previously unknown mechanisms. Hypoxia-inducible factor 1 (HIF-1) mediates PKM2 gene transcription and glucose reprogramming in cancer cells. The recent discovery of novel physical and functional interactions between PKM2 and HIF-1 in cancer cells has provided insight into molecular mechanisms underlying the Warburg effect.
Highlights
Altered glucose metabolism is a key feature that distinguishes cancer cells from normal cells
Hypoxia-inducible factor 1 (HIF-1) activation shifts the balance of metabolism from oxidative phosphorylation toward glycolysis and mediates the Warburg effect in von HippelLindau (VHL)-null renal carcinoma cells [30]
We recently identified a hypoxia response element (HRE) within the first intron of the human Pyruvate kinase M2 (PKM2) gene [9]
Summary
Altered glucose metabolism is a key feature that distinguishes cancer cells from normal cells. HIF-1 activates the transcription of genes encoding proteins that mediate angiogenesis, invasion, metastasis, and the shift from oxidative to glycolytic metabolism [12, 18, 19, 22, 23]. By activating the transcription of genes encoding glucose transporters and glycolytic enzymes, HIF-1 enhances glucose uptake and glycolysis in cells [23,24,25,26,27].
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