Epithelial mesenchymal transition regulator TWIST1 transcription factor stimulates glucose uptake through upregulation of GLUT1, GLUT3, and GLUT12 in vitro

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dc.contributor.authorPehlivanoglu, Suray
dc.contributor.authorSahan, Ozge Burcu
dc.contributor.authorPehlivanoglu, Sebnem
dc.contributor.authorKont, Kadriye Aktas
dc.date.accessioned2024-02-23T13:59:40Z
dc.date.available2024-02-23T13:59:40Z
dc.date.issued2021
dc.departmentNEÜen_US
dc.description.abstractTWIST1 is a major regulator of epithelial mesenchymal transition process, essential in cancer metastasis. Cancer cells increase glucose uptake capabilities to meet their high energy requirements. In this study, we explored the potential role of TWIST1 on glucose transport into the 293T cells in an insulin-dependent and insulin-independent manner. For this purpose, the ectopic expression of TWIST1 was successfully performed by electroporation. The altered mRNA expressions of GLUT-1, -3, -4, and -12, insulin receptor (InsR), and insulin receptor substrate (IRS)-1 and -2 were assessed in control and TWIST1-overexpressing cells. Glucose uptake rates of the cells were evaluated by fluorometric glucose uptake assay. Our findings showed that the transcriptional expression levels of GLUT-1, -3, and -12 genes were significantly upregulated by TWIST1. However, TWIST1 did not alter the mRNA and protein expressions of the InsR, its substrates (IRS-1 and -2), and GLUT-4 genes in 293T cells which are main factors for insulin-stimulated glucose uptake pathway. Also, the glucose transport activities were significantly increased in TWIST1-overexpressing cells compared to controls due to fetal bovine serum (FBS) stimulation, but there was a slight non-significant difference in insulin stimulation. Thus, our data suggest that TWIST1 could promote glucose uptake independently of insulin and is possible to be evaluated as a metabolic marker in cancer. Further investigations are needed to clarify the precise molecular mechanisms underlying the cells' glucose uptake and consumption during tumorigenesis.en_US
dc.description.sponsorshipScientific Research Projects Coordination Unit of Necmettin Erbakan University [161315002]en_US
dc.description.sponsorshipThis work was supported by Scientific Research Projects Coordination Unit of Necmettin Erbakan University (Project no: 161315002).en_US
dc.identifier.doi10.1007/s11626-021-00635-w
dc.identifier.endpage943en_US
dc.identifier.issn1071-2690
dc.identifier.issn1543-706X
dc.identifier.issue10en_US
dc.identifier.pmid34791627en_US
dc.identifier.scopus2-s2.0-85119181101en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage933en_US
dc.identifier.urihttps://doi.org/10.1007/s11626-021-00635-w
dc.identifier.urihttps://hdl.handle.net/20.500.12452/11252
dc.identifier.volume57en_US
dc.identifier.wosWOS:000719722800001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofIn Vitro Cellular & Developmental Biology-Animalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGlucose Transportersen_US
dc.subjectGlucose Uptakeen_US
dc.subjectInsulinen_US
dc.subjectTwist1en_US
dc.titleEpithelial mesenchymal transition regulator TWIST1 transcription factor stimulates glucose uptake through upregulation of GLUT1, GLUT3, and GLUT12 in vitroen_US
dc.typeArticleen_US

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