Auhtors: Patra KC, Hay N
PMID: 24196563 PMCID: PMC3875752 DOI: 10.18632/oncotarget.1563
Abstract
It is well established that cancer cells differ from most somatic adult cells by their high rate of aerobic glycolysis despite oxidative phosphorylation. This distinct property of cancer cells is often used for tumor imaging in vivo following the administration of the labeled glucose analog, fluoro deoxy glucose (FDG). The high uptake of the labeled FDG in cancer cells can then be detected by positron emission tomography (PET). The elevated glucose metabolism in cancer cells is not necessarily required for the generation of ATP but rather to provide building blocks for nucleic acid, fatty acid, and protein synthesis in the rapidly dividing cancer cells [1]. Thus, if the high rate of glucose metabolism in cancer cells is being used to distinguish cancer cells from normal cells, it could also be exploited to selectively target cancer cells in cancer therapy. However, a major challenge in targeting glucose metabolism for cancer therapy is to identify a strategy that would selectively target cancer cells while sparing normal cells, and that would not dramatically impair systemic metabolic homeostasis. Another posed question is; which enzymatic activities should be chosen as targets for selective cancer therapy? Although several enzymes in glycolysis and in the pathways branching from the canonical glycolysis pathway were found to be elevated in cancer cells, these enzymes are also expressed in the normal cells.
Keywords: hexokinase 2, oncotarget, cancer cells
