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dc.contributor.author신인철-
dc.date.accessioned2019-02-27T08:05:30Z-
dc.date.available2019-02-27T08:05:30Z-
dc.date.issued2016-10-
dc.identifier.citationBIOCHEMICAL JOURNAL, v. 473, no. 19, Page. 3013-3030en_US
dc.identifier.issn0264-6021-
dc.identifier.issn1470-8728-
dc.identifier.urihttp://www.biochemj.org/content/473/19/3013-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/99302-
dc.description.abstractCluster of differentiation 44 (CD44) is a transmembrane glycoprotein that has been identified as a cancer stem cell marker in various cancer cells. Although many studies have focused on CD44 as a cancer stem cell marker, its effect on cancer cell metabolism remains unclear. To investigate the role of CD44 on cancer cell metabolism, we established CD44 knock-down cells via retroviral delivery of shRNA against CD44 in human breast cancer cells. Silencing of CD44 decreased the glycolytic phenotype of cancer cells, affecting glucose uptake, ATP production, and lactate production. We also found that ablation of the CD44-induced lactate dehydrogenase (LDH) isoenzyme results in a shift to LDH1 due to LDHA down-regulation and LDHB up-regulation, implying the importance of LDH isoenzyme modulation on cancer metabolism. The expression of glycolysis- related proteins including hypoxia inducible factor-1 alpha (HIF-1 alpha) and LDHA was decreased by CD44 silencing. These effects were due to the up-regulation of liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) a activity by reduction in c-Src and Akt activity in CD44 knock-down cells. Finally, induction of LKB1/AMPK alpha activity blocked the expression of HIF-1 alpha and its target gene, LDHA. Inversely, LDHB expression was repressed by HIF-1 alpha. Collectively, these results indicate that the CD44 silencing-induced metabolic shift is mediated by the regulation of c-Src/Akt/LKB1/AMPK alpha/HIF-1 alpha signaling in human breast cancer cells.en_US
dc.description.sponsorshipThis work was supported by an NRF grant [2013R1A1A2059143] from the Korea Research Foundation; the Converging Research Center Program funded by the Ministry of Science, ICT & Future Planning [Project No. 2015054348]; and the Civil research projects for solving social problems through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (grant no. [2015M3C8A6A06012226]).en_US
dc.language.isoenen_US
dc.publisherPORTLAND PRESS LTDen_US
dc.subjectACTIVATED PROTEIN-KINASEen_US
dc.subjectINDUCIBLE FACTOR-Ien_US
dc.subjectLACTATE-DEHYDROGENASE-Aen_US
dc.subjectCANCER-CELLSen_US
dc.subjectCYTOSKELETON ACTIVATIONen_US
dc.subjectMETABOLIC CHECKPOINTen_US
dc.subjectAEROBIC GLYCOLYSISen_US
dc.subjectRESPONSE ELEMENTSen_US
dc.subjectUPSTREAM KINASEen_US
dc.subjectPYRUVATE-KINASEen_US
dc.titleAblation of CD44 induces glycolysis-to-oxidative phosphorylation transition via modulation of the c-Src-Akt-LKB1-AMPK alpha pathwayen_US
dc.typeArticleen_US
dc.relation.volume473-
dc.identifier.doi10.1042/BCJ20160613-
dc.relation.page3013-3030-
dc.relation.journalBIOCHEMICAL JOURNAL-
dc.contributor.googleauthorNam, KeeSoo-
dc.contributor.googleauthorOh, Sunhwa-
dc.contributor.googleauthorShin, Incheol-
dc.relation.code2016002949-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF NATURAL SCIENCES[S]-
dc.sector.departmentDEPARTMENT OF LIFE SCIENCE-
dc.identifier.pidincheol-
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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