Regulation of glucose metabolism by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases in cancer

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dc.contributor.authorTelang, Sucheta
dc.contributor.authorClem, Brian F.
dc.contributor.authorChesney, Jason
dc.contributor.buuauthorYalçın, Abdullah
dc.contributor.departmentUludağ Üniversitesi/ Veterinerlik Fakültesi/ Biyokimya Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0001-8519-8375tr_TR
dc.contributor.researcheridABI-4164-2020tr_TR
dc.contributor.researcheridA-5261-2016tr_TR
dc.contributor.scopusid36857831000tr_TR
dc.date.accessioned2021-10-21T08:59:35Z
dc.date.available2021-10-21T08:59:35Z
dc.date.issued2009-06
dc.description.abstractA high rate of glycolytic flux, even in the presence of oxygen, is a central metabolic hallmark of neoplastic tumors. Cancer cells preferentially utilize glycolysis in order to satisfy their increased energetic and biosynthetic requirements. This metabolic phenotype has been confirmed in human studies using positron emission tomography (PET) with F-18-2-fluoro-deoxy-glucose which have demonstrated that tumors take up 10-fold more glucose than adjacent normal tissues in vivo. The high glucose metabolism of cancer cells is caused by a combination of hypoxia-responsive transcription factors, activation of oncogenic proteins and the loss of tumor suppressor function. Over-expression of HIF-1 alpha and myc, activation of ras and loss of p53 function each have been found to stimulate glycolysis in part by activating a family of regulatory bifunctional 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB). The PFKFB enzymes synthesize fructose-2,6-bisphosphate (F2,6BP) which allosterically activates 6-phosphofructo-1-kinase (PFK-1), a rate-limiting enzyme and essential control point in the glycolytic pathway. PFK-1 is inhibited by ATP when energy stores are abundant and F2,6BP can override this inhibition and enhance glucose uptake and glycolytic flux. It is therefore not surprising that F2,6BP synthesis is stimulated by several oncogenic alterations which simultaneously cause both enhanced consumption of glucose and growth. Importantly, these studies suggest that selective depletion of intracellular F2,6BP in cancer cells may suppress glycolytic flux and decrease their survival, growth and invasiveness. This review will summarize the requirement of the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases for the regulation of glycolysis in tumor cells and their potential utility as targets for the development of antineoplastic agents.en_US
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA (1P20RR018733)en_US
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA (1R01CA116428)en_US
dc.description.sponsorshipLeukemia and Lymphoma Societyen_US
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Cancer Institute (NCI) ( R01CA116428)en_US
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Center for Research Resources (NCRR) ( P20RR018733)en_US
dc.identifier.citationYalçın, A. vd. (2009). "Regulation of glucose metabolism by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases in cancer". Experimental And Molecular Pathology, 86(3), 174-179.tr_TR
dc.identifier.endpage179tr_TR
dc.identifier.issn0014-4800
dc.identifier.issue3tr_TR
dc.identifier.pubmed19454274tr_TR
dc.identifier.scopus2-s2.0-67349131613tr_TR
dc.identifier.startpage174tr_TR
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0014480009000082
dc.identifier.urihttps://doi.org/10.1016/j.yexmp.2009.01.003
dc.identifier.urihttp://hdl.handle.net/11452/22423
dc.identifier.volume86tr_TR
dc.identifier.wos000266280100005tr_TR
dc.indexed.pubmedPubmeden_US
dc.indexed.scopusScopusen_US
dc.indexed.wosSCIEen_US
dc.language.isoenen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.relation.collaborationYurt dışıtr_TR
dc.relation.journalExperimental and Molecular Pathologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGlycolysisen_US
dc.subjectFructose-2,6-bisphosphateen_US
dc.subjectRasen_US
dc.subjectNeoplastic transformationen_US
dc.subjectChemotherapyen_US
dc.subjectPFKFB3en_US
dc.subjecthypoxia-inducible factoren_US
dc.subjectFructose 2,6-bisphosphateen_US
dc.subjectC-mycen_US
dc.subjectTumor-cellsen_US
dc.subjectPfkfb3 geneen_US
dc.subjectadenocarcinoma cellsen_US
dc.subjectGlycolytic-enzymesen_US
dc.subjectAerobic glycolysisen_US
dc.subjectBreast-canceren_US
dc.subjectNucleic-aciden_US
dc.subject.emtree6 phosphofructo 2 kinaseen_US
dc.subject.emtreeAntineoplastic agenten_US
dc.subject.emtreeFructose 2,6 bisphosphateen_US
dc.subject.emtreeHypoxia inducible factoren_US
dc.subject.emtree1alphaen_US
dc.subject.emtreeImatiniben_US
dc.subject.emtreeMyc proteinen_US
dc.subject.emtreeProtein farnesyltransferase inhibitoren_US
dc.subject.emtreeProtein p53en_US
dc.subject.emtreeRas proteinen_US
dc.subject.emtreeCancer cellen_US
dc.subject.emtreeEnzyme activityen_US
dc.subject.emtreeGene overexpressionen_US
dc.subject.emtreeGucose metabolismen_US
dc.subject.emtreeGlycolysisen_US
dc.subject.emtreeHumanen_US
dc.subject.emtreeNonhumanen_US
dc.subject.emtreeReviewen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntineoplastic agentsen_US
dc.subject.meshEnzyme inhibitorsen_US
dc.subject.meshGenes, rasen_US
dc.subject.meshGlucoseen_US
dc.subject.meshGlycolysisen_US
dc.subject.meshHumansen_US
dc.subject.meshNeoplasmsen_US
dc.subject.meshPhosphofructokinase-2en_US
dc.subject.meshTransformation, geneticen_US
dc.subject.scopusPhosphofructokinase-2; Fructose 2,6-Diphosphate; Glycolysisen_US
dc.subject.wosPathologyen_US
dc.titleRegulation of glucose metabolism by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases in canceren_US
dc.typeReview
dc.wos.quartileQ2en_US

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