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dc.contributor.authorKont, Kadriye Aktas
dc.contributor.authorPEHLİVANOĞLU, SURAY
dc.contributor.authorŞAHAN, ÖZGE BURCU
dc.contributor.authorPehlivanoglu, Sebnem
dc.date.accessioned2021-12-10T10:04:45Z
dc.date.available2021-12-10T10:04:45Z
dc.identifier.citationPEHLİVANOĞLU S., ŞAHAN Ö. B. , Pehlivanoglu S., Kont K. A. , "Epithelial mesenchymal transition regulator TWIST1 transcription factor stimulates glucose uptake through upregulation of GLUT1, GLUT3, and GLUT12 in vitro", IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, 2021
dc.identifier.issn1071-2690
dc.identifier.othervv_1032021
dc.identifier.otherav_26b019b6-f3b0-42c8-ac88-788a038d7bb4
dc.identifier.urihttp://hdl.handle.net/20.500.12627/169126
dc.identifier.urihttps://doi.org/10.1007/s11626-021-00635-w
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.
dc.language.isoeng
dc.subjectMikrobiyal Genetik
dc.subjectHÜCRE BİYOLOJİSİ
dc.subjectTemel Bilimler
dc.subjectCell Biology
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.subjectEmbryology
dc.subjectLife Sciences
dc.subjectHealth Sciences
dc.subjectSağlık Bilimleri
dc.subjectTemel Tıp Bilimleri
dc.subjectHistoloji-Embriyoloji
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectGELİŞİMSEL BİYOLOJİ
dc.subjectTıp
dc.titleEpithelial mesenchymal transition regulator TWIST1 transcription factor stimulates glucose uptake through upregulation of GLUT1, GLUT3, and GLUT12 in vitro
dc.typeMakale
dc.relation.journalIN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
dc.contributor.departmentNecmettin Erbakan Üniversitesi , Fen Fakültesi , Moleküler Biyoloji Ve Genetik Bölümü
dc.contributor.firstauthorID2770809


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