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dc.contributor.authorHaldorsson, Skarphedinn
dc.contributor.authorRohatgi, Neha
dc.contributor.authorMagnusdottir, Manuela
dc.contributor.authorChoudhary, Kumari
dc.contributor.authorGudjónsson, Thorarinn
dc.contributor.authorKnutsen, Erik
dc.contributor.authorBarkovskaya, Anna
dc.contributor.authorHilmarsdòttir, Bylgja
dc.contributor.authorPerander, Maria
dc.contributor.authorMælandsmo, Gunhild
dc.contributor.authorGudmundsson, Steinn
dc.contributor.authorRolfsson, Ottar
dc.date.accessioned2018-08-20T09:59:30Z
dc.date.available2018-08-20T09:59:30Z
dc.date.issued2017-03-18
dc.description.abstractEpithelial to mesenchymal transition (EMT) has implications in tumor progression and metastasis. Metabolic alterations have been described in cancer development but studies focused on the metabolic re-wiring that takes place during EMT are still limited. We performed metabolomics profiling of a breast epithelial cell line and its EMT derived mesenchymal phenotype to create genome-scale metabolic models descriptive of both cell lines. Glycolysis and OXPHOS were higher in the epithelial phenotype while amino acid anaplerosis and fatty acid oxidation fueled the mesenchymal phenotype. Through comparative bioinformatics analysis, PPAR-γ1, PPAR- γ2 and AP-1 were found to be the most influential transcription factors associated with metabolic re-wiring. <i>In silico</i> gene essentiality analysis predicts that the LAT1 neutral amino acid transporter is essential for mesenchymal cell survival. Our results define metabolic traits that distinguish an EMT derived mesenchymal cell line from its epithelial progenitor and may have implications in cancer progression and metastasis. Furthermore, the tools presented here can aid in identifying critical metabolic nodes that may serve as therapeutic targets aiming to prevent EMT and inhibit metastatic dissemination.en_US
dc.description.sponsorshipIcelandic Research Councilen_US
dc.descriptionSource at <a href=https://doi.org/10.1016/j.canlet.2017.03.019> https://doi.org/10.1016/j.canlet.2017.03.019</a>. Accepted manuscript version, licensed <a href=http://creativecommons.org/licenses/by-nc-nd/4.0/> CC BY-NC-ND 4.0.</a>en_US
dc.identifier.citationHaldorsson, S., Rohatgi, N., Magnusdottir, M., Choudhary, K.S., Gudjónsson, T., Knutsen, E., ... Rolfsson, Ó. (2017). Metabolic re-wiring of isogenic breast epithelial cell lines following epithelial to mesenchymal transition. Cancer Letters, 396, 117-129. https://doi.org/10.1016/j.canlet.2017.03.019en_US
dc.identifier.cristinIDFRIDAID 1458515
dc.identifier.doi10.1016/j.canlet.2017.03.019
dc.identifier.issn0304-3835
dc.identifier.issn1872-7980
dc.identifier.urihttps://hdl.handle.net/10037/13480
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.relation.journalCancer Letters
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/FRIMEDBIO/239940/Norway/Cancer metabolism: From basic biochemistry to clinical opportunities//en_US
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762en_US
dc.subjectEMTen_US
dc.subjectMetabolismen_US
dc.subjectGenome scale modelsen_US
dc.subjectBreast canceren_US
dc.titleMetabolic re-wiring of isogenic breast epithelial cell lines following epithelial to mesenchymal transitionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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