title: Cancer metabolism as a therapeutic target.
abstract: Cancer is now recognized to be a disease arising from both genetic and metabolic abnormalities. In the mid-1900s, Otto Warburg described the phenomenon of elevated glucose consumption and aerobic glycolysis, and the dependence of cancer cells on this phenomenon for proliferation and growth. The Warburg effect has formed the basis of such diagnostic and prognostic imaging modalities as positron emission tomography (PET); however, we have not yet capitalized on this phenomenon for therapy. Several mechanisms have now been shown to contribute to the Warburg effect.Ongoing studies are attempting to understand the reasons that tumor cells engage in aerobic glycolysis in lieu of oxidative phosphorylation, and the advantages that accrue to them as a result. In this review, we discuss known benefits to tumor cells from this metabolic switch, and we highlight key enzymes that play a role in aerobic glycolysis. We also describe novel therapeutic options targeting glucose metabolism and the importance of continuing to understand the metabolic plasticity of cancer.
authors.forename: Surabhi
authors.initials: S
authors.lastname: Batra
authors.forename: Kehinde U A
authors.initials: KU
authors.lastname: Adekola
authors.forename: Steven T
authors.initials: ST
authors.lastname: Rosen
authors.forename: Mala
authors.initials: M
authors.lastname: Shanmugam
mesh_terms: D005947:Glucose / Q000378:metabolism; D051246:Glucose Transport Proteins, Facilitative / Q000037:antagonists & inhibitors / Q000502:physiology; D006019:Glycolysis / Q000187:drug effects*; D017320:HIV Protease Inhibitors / Q000627:therapeutic use; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008687:Metformin / Q000627:therapeutic use; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism*
chemical_list: D051246:Glucose Transport Proteins, Facilitative; D017320:HIV Protease Inhibitors; D007004:Hypoglycemic Agents; D008687:Metformin; D005947:Glucose