Publication:
PFKFB2 regulates glycolysis and proliferation in pancreatic cancer cells

dc.contributor.coauthorSarioglu, Aybike
dc.contributor.coauthorAltunok, Tugba H.
dc.contributor.coauthorAkkoc, Ahmet
dc.contributor.coauthorGuzel, Saime
dc.contributor.coauthorGuler, Sabire
dc.contributor.coauthorImbert-Fernandez, Yoannis
dc.contributor.coauthorMuchut, Robertino J.
dc.contributor.coauthorIglesias, Alberto A.
dc.contributor.coauthorGurpinar, Yunus
dc.contributor.coauthorClem, Amy L.
dc.contributor.coauthorChesney, Jason A.
dc.contributor.coauthorYalçın, Abdullah
dc.contributor.departmentKUTTAM (Koç University Research Center for Translational Medicine)
dc.contributor.kuauthorÖzcan, Selahattin Can
dc.contributor.schoolcollegeinstituteResearch Center
dc.date.accessioned2024-11-09T22:58:52Z
dc.date.issued2020
dc.description.abstractTumor cells increase glucose metabolism through glycolysis and pentose phosphate pathways to meet the bioenergetic and biosynthetic demands of rapid cell proliferation. The family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1-4) are key regulators of glucose metabolism via their synthesis of fructose-2,6-bisphosphate (F2,6BP), a potent activator of glycolysis. Previous studies have reported the co-expression of PFKFB isozymes, as well as the mRNA splice variants of particular PFKFB isozymes, suggesting non-redundant functions. Majority of the evidence demonstrating a requirement for PFKFB activity in increased glycolysis and oncogenic properties in tumor cells comes from studies on PFKFB3 and PFKFB4 isozymes. In this study, we show that the PFKFB2 isozyme is expressed in tumor cell lines of various origin, overexpressed and localizes to the nucleus in pancreatic adenocarcinoma, relative to normal pancreatic tissue. We then demonstrate the differential intracellular localization of two PFKFB2 mRNA splice variants and that, when ectopically expressed, cytoplasmically localized mRNA splice variant causes a greater increase in F2,6BP which coincides with an increased glucose uptake, as compared with the mRNA splice variant localizing to the nucleus. We then show that PFKFB2 expression is required for steady-state F2,6BP levels, glycolytic activity, and proliferation of pancreatic adenocarcinoma cells. In conclusion, this study may provide a rationale for detailed investigation of PFKFB2's requirement for the glycolytic and oncogenic phenotype of pancreatic adenocarcinoma cells.
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue44958
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK) [114Z496]
dc.description.sponsorshipTUBITAK[2214] This study was supported by the Scientific and Technological Research Council of Turkey (TUBITAK#114Z496). SCO was the recipient of a predoctoral training grant from TUBITAK(#2214).
dc.description.volume470
dc.identifier.doi10.1007/s11010-020-03751-5
dc.identifier.eissn1573-4919
dc.identifier.issn0300-8177
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85084666115
dc.identifier.urihttps://doi.org/10.1007/s11010-020-03751-5
dc.identifier.urihttps://hdl.handle.net/20.500.14288/7775
dc.identifier.wos533059300001
dc.keywordsPancreatic adenocarcinoma
dc.keywordsGlycolysis
dc.keywordsPfkfb2
dc.keywordsFructose-2
dc.keywords6-Bisphosphate
dc.keywords6-Phosphofructo-2-Kinase Pfkfb3
dc.keywords6-Phosphofructo-2-Kinase/fructose-2,6-Bisphosphatase
dc.keywordsExpression
dc.keywordsMetabolism
dc.keywordsGlucose
dc.keywordsMigration
dc.keywordsInvasion
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofMolecular and Cellular Biochemistry
dc.subjectCell biology
dc.titlePFKFB2 regulates glycolysis and proliferation in pancreatic cancer cells
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorÖzcan, Selahattin Can
local.publication.orgunit1Research Center
local.publication.orgunit2KUTTAM (Koç University Research Center for Translational Medicine)
relation.isOrgUnitOfPublication91bbe15d-017f-446b-b102-ce755523d939
relation.isOrgUnitOfPublication.latestForDiscovery91bbe15d-017f-446b-b102-ce755523d939
relation.isParentOrgUnitOfPublicationd437580f-9309-4ecb-864a-4af58309d287
relation.isParentOrgUnitOfPublication.latestForDiscoveryd437580f-9309-4ecb-864a-4af58309d287

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