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dc.contributor.authorLiu, Hen_US
dc.contributor.authorErtay, Aen_US
dc.contributor.authorPeng, Pen_US
dc.contributor.authorLi, Jen_US
dc.contributor.authorLiu, Den_US
dc.contributor.authorXiong, Hen_US
dc.contributor.authorZou, Yen_US
dc.contributor.authorQiu, Hen_US
dc.contributor.authorHancock, Den_US
dc.contributor.authorYuan, Xen_US
dc.contributor.authorHuang, W-Cen_US
dc.contributor.authorEwing, RMen_US
dc.contributor.authorDownward, Jen_US
dc.contributor.authorWang, Yen_US
dc.date.accessioned2020-06-03T10:13:06Z
dc.date.issued2019-09
dc.identifier.citationMolecular oncology, 2019, 13 (9), pp. 1874 - 1886
dc.identifier.issn1574-7891
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3678
dc.identifier.eissn1878-0261
dc.identifier.doi10.1002/1878-0261.12530
dc.description.abstractSodium/glucose cotransporter 1 (SGLT1), an essential active glucose transport protein that helps maintain high intracellular glucose levels, was previously shown to interact with epidermal growth factor receptor (EGFR); the SGLT1-EGFR interaction maintains intracellular glucose levels to promote survival of cancer cells. Here, we explore the role of SGLT1 in triple-negative breast cancer (TNBC), which is the most aggressive type of breast cancer. We performed TCGA analysis coupled to in vitro experiments in TNBC cell lines as well as in vivo xenografts established in the mammary fat pad of female nude mice. Tissue microarrays of TNBC patients with information of clinical-pathological parameters were also used to investigate the expression and function of SGLT1 in TNBC. We show that high levels of SGLT1 are associated with greater tumour size in TNBC. Knockdown of SGLT1 compromises cell growth in vitro and in vivo. We further demonstrate that SGLT1 depletion results in decreased levels of phospho-EGFR, and as a result, the activity of downstream signalling pathways (such as AKT and ERK) is inhibited. Hence, targeting SGLT1 itself or the EGFR-SGLT1 interaction may provide novel therapeutics against TNBC.en_US
dc.formatPrint-Electronic
dc.format.extent1874 - 1886
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectCell Line, Tumoren_US
dc.subjectHumansen_US
dc.subjectNeoplasm Proteinsen_US
dc.subjectCell Survivalen_US
dc.subjectMAP Kinase Signaling Systemen_US
dc.subjectFemaleen_US
dc.subjectSodium-Glucose Transporter 1en_US
dc.subjectTriple Negative Breast Neoplasmsen_US
dc.subjectErbB Receptorsen_US
dc.titleSGLT1 is required for the survival of triple-negative breast cancer cells via potentiation of EGFR activity.
dc.typeJournal Article
dcterms.dateAccepted2019-06-10
rioxxterms.versionofrecord10.1002/1878-0261.12530
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2019-09
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfMolecular oncologyen_US
pubs.issue9
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Lung Cancer Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Lung Cancer Group
pubs.publication-statusPublished
pubs.volume13en_US
pubs.embargo.termsNot known
icr.researchteamLung Cancer Groupen_US
dc.contributor.icrauthorDownward, Julian David Harryen


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