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dc.contributor.author이영복-
dc.date.accessioned2019-12-02T00:44:31Z-
dc.date.available2019-12-02T00:44:31Z-
dc.date.issued2017-11-
dc.identifier.citationSCIENTIFIC REPORTS, v. 7, Article no. 16159en_US
dc.identifier.issn2045-2322-
dc.identifier.urihttps://www.nature.com/articles/s41598-017-16327-z-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/116141-
dc.description.abstractThe new oncologic paradigm of precision medicine is focused on identifying metabolic, proteomic, transcriptomic and genomic variabilities in tumors that can be exploited to tailor treatments and improve patient outcomes. Metabolic changes are a hallmark of cancer, and inhibition of metabolic pathways is now a major strategy in medicinal chemistry for targeting cancers. However, non-invasive biomarkers to categorize metabolic subtypes are in short supply. The purpose of this study was to characterize the intracellular and extracellular metabolic profiles of four prostate cancer cell lines with varying degrees of aggressiveness. We observed metabolic differences between the aggressive prostate cancer cell line PC3 and the even more aggressive, metastatic subline PC3M assessed by hyperpolarized in vivo pyruvate studies, nuclear magnetic resonance spectroscopy, and carbon-13 feeding studies. On further examination of the differences between these two cell lines, we found increased glutamine utilization in the metastatic PC3M subline that led directly to sensitivity to glutaminase inhibitor CB839. Our study supports the theory that metastatic progression increases glutamine utilization and the inhibition of glutaminolysis could have clinical implications.en_US
dc.description.sponsorshipWe want to thank Dr. Mark Titus at MD Anderson Cancer Center and the Department of Scientific Publications at MD Anderson Cancer Center for reading and editing the manuscript. In addition, we thank Calithera Biosciences for the CB-839. The research was funded in part by a grant from the U.S. Department of Defense (CDMRP PC110065, NMZ, SS, YL); by Institutional Research Grants (NMZ, PB) and a Startup grant (PB) from MD Anderson Cancer Center; by grants from the U.S. National Cancer Institute (5 P50 CA 094056-14, PB; U54 CA151668, PB; R21CA185536), and by a grant from the Gulf Coast Consortium (JM, PB). YL was funded partially by the Odyssey Postdoctoral Fellowship. This work also was supported by the National Institutes of Health/NCI Cancer Center Support Grant under award number P30CA016672 and used the characterized cell line core facility, the small animal imaging facility, and the NMR core facility at MD Anderson.en_US
dc.language.isoen_USen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectGLYCOLYTIC METABOLISMen_US
dc.subjectABIRATERONE ACETATEen_US
dc.subjectCELL-PROLIFERATIONen_US
dc.subjectCITRATEen_US
dc.subjectLACTATEen_US
dc.subjectPROTEINen_US
dc.subjectEXPRESSIONen_US
dc.subjectLEUKEMIAen_US
dc.subjectPYRUVATEen_US
dc.subjectSURVIVALen_US
dc.titleMetabolic Differences in Glutamine Utilization Lead to Metabolic Vulnerabilities in Prostate Canceren_US
dc.typeArticleen_US
dc.relation.volume7-
dc.identifier.doi10.1038/s41598-017-16327-z-
dc.relation.page16159-16159-
dc.relation.journalSCIENTIFIC REPORTS-
dc.contributor.googleauthorZacharias, Niki Marie i-
dc.contributor.googleauthorMcCullough, Christopher-
dc.contributor.googleauthorShanmugavelandy, Sriram-
dc.contributor.googleauthorLee, Jaehyuk-
dc.contributor.googleauthorLee, Youngbok-
dc.contributor.googleauthorDutta, Prasanta-
dc.contributor.googleauthorMcHenry, James-
dc.contributor.googleauthorNguyen, Linda-
dc.contributor.googleauthorNorton, William-
dc.contributor.googleauthorJones, Lawrence W.-
dc.relation.code2017012089-
dc.sector.campusS-
dc.sector.daehakGRADUATE SCHOOL[S]-
dc.sector.departmentDEPARTMENT OF BIONANOTECHNOLOGY-
dc.identifier.pidyblee-


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