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dc.contributor.authorLibby, Catherine J
dc.contributor.authorGc, Sajina
dc.contributor.authorBenavides, Gloria A
dc.contributor.authorFisher, Jennifer L
dc.contributor.authorWilliford, Sarah E
dc.contributor.authorZhang, Sixue
dc.contributor.authorTran, Anh Nhat
dc.contributor.authorGordon, Emily R
dc.contributor.authorJones, Amber B
dc.contributor.authorTuy, Kaysaw
dc.contributor.authorFlavahan, William
dc.contributor.authorGordillo, Juan
dc.contributor.authorLong, Ashlee
dc.contributor.authorCooper, Sara J
dc.contributor.authorLasseigne, Brittany N
dc.contributor.authorAugelli-Szafran, Corinne E
dc.contributor.authorDarley-Usmar, Victor
dc.contributor.authorHjelmeland, Anita B
dc.date.accessioned2023-04-07T20:03:24Z
dc.date.available2023-04-07T20:03:24Z
dc.date.issued2021-04-12
dc.identifier.citationLibby CJ, Gc S, Benavides GA, Fisher JL, Williford SE, Zhang S, Tran AN, Gordon ER, Jones AB, Tuy K, Flavahan W, Gordillo J, Long A, Cooper SJ, Lasseigne BN, Augelli-Szafran CE, Darley-Usmar V, Hjelmeland AB. A role for GLUT3 in glioblastoma cell invasion that is not recapitulated by GLUT1. Cell Adh Migr. 2021 Dec;15(1):101-115. doi: 10.1080/19336918.2021.1903684. PMID: 33843470; PMCID: PMC8043167.en_US
dc.identifier.eissn1933-6926
dc.identifier.doi10.1080/19336918.2021.1903684en_US
dc.identifier.pmid33843470
dc.identifier.urihttp://hdl.handle.net/20.500.14038/51927
dc.description.abstractThe multifaceted roles of metabolism in invasion have been investigated across many cancers. The brain tumor glioblastoma (GBM) is a highly invasive and metabolically plastic tumor with an inevitable recurrence. The neuronal glucose transporter 3 (GLUT3) was previously reported to correlate with poor glioma patient survival and be upregulated in GBM cells to promote therapeutic resistance and survival under restricted glucose conditions. It has been suggested that the increased glucose uptake mediated by GLUT3 elevation promotes survival of circulating tumor cells to facilitate metastasis. Here we suggest a more direct role for GLUT3 in promoting invasion that is not dependent upon changes in cell survival or metabolism. Analysis of glioma datasets demonstrated that GLUT3, but not GLUT1, expression was elevated in invasive disease. In human xenograft derived GBM cells, GLUT3, but not GLUT1, elevation significantly increased invasion in transwell assays, but not growth or migration. Further, there were no changes in glycolytic metabolism that correlated with invasive phenotypes. We identified the GLUT3 C-terminus as mediating invasion: substituting the C-terminus of GLUT1 for that of GLUT3 reduced invasion. RNA-seq analysis indicated changes in extracellular matrix organization in GLUT3 overexpressing cells, including upregulation of osteopontin. Together, our data suggest a role for GLUT3 in increasing tumor cell invasion that is not recapitulated by GLUT1, is separate from its role in metabolism and survival as a glucose transporter, and is likely broadly applicable since GLUT3 expression correlates with metastasis in many solid tumors.en_US
dc.language.isoenen_US
dc.relation.ispartofCell Adhesion & Migrationen_US
dc.relation.urlhttps://doi.org/10.1080/19336918.2021.1903684en_US
dc.rights© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectGlucose transporteren_US
dc.subjectglioblastomaen_US
dc.subjectinvasionen_US
dc.subjectmetabolismen_US
dc.titleA role for GLUT3 in glioblastoma cell invasion that is not recapitulated by GLUT1en_US
dc.typeJournal Articleen_US
dc.source.journaltitleCell adhesion & migration
dc.source.volume15
dc.source.issue1
dc.source.beginpage101
dc.source.endpage115
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.identifier.journalCell adhesion & migration
refterms.dateFOA2023-04-07T20:03:25Z
dc.contributor.departmentMolecular, Cell and Cancer Biologyen_US


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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.