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dc.contributor.author Xue X
dc.contributor.author Ramakrishnan SK
dc.contributor.author Weisz K
dc.contributor.author Triner D
dc.contributor.author Xie L
dc.contributor.author Pant A
dc.contributor.author Attili D
dc.contributor.author Győrffy, Balázs
dc.contributor.author Zhan M
dc.contributor.author Carter-Su C
dc.contributor.author Hardiman KM
dc.contributor.author Wang TD
dc.contributor.author Dame MK
dc.contributor.author Varani J
dc.contributor.author Brenner D
dc.contributor.author Fearon ER
dc.contributor.author Shah YM
dc.date.accessioned 2018-10-16T06:48:13Z
dc.date.available 2018-10-16T06:48:13Z
dc.date.issued 2016
dc.identifier 84990848528
dc.identifier.citation pagination=447-461; journalVolume=24; journalIssueNumber=3; journalTitle=CELL METABOLISM;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/5679
dc.identifier.uri doi:10.1016/j.cmet.2016.07.015
dc.description.abstract Dietary iron intake and systemic iron balance are implicated in colorectal cancer (CRC) development, but the means by which iron contributes to CRC are unclear. Gene expression and functional studies demonstrated that the cellular iron importer, divalent metal transporter 1 (DMT1), is highly expressed in CRC through hypoxia-inducible factor 2alpha-dependent transcription. Colon-specific Dmt1 disruption resulted in a tumor-selective inhibitory effect of proliferation in mouse colon tumor models. Proteomic and genomic analyses identified an iron-regulated signaling axis mediated by cyclin-dependent kinase 1 (CDK1), JAK1, and STAT3 in CRC progression. A pharmacological inhibitor of DMT1 antagonized the ability of iron to promote tumor growth in a CRC mouse model and a patient-derived CRC enteroid orthotopic model. Our studies implicate a growth-promoting signaling network instigated by elevated intracellular iron levels in tumorigenesis, offering molecular insights into how a key dietary component may contribute to CRC.
dc.relation.ispartof urn:issn:1550-4131
dc.title Iron Uptake via DMT1 Integrates Cell Cycle with JAK-STAT3 Signaling to Promote Colorectal Tumorigenesis
dc.type Journal Article
dc.date.updated 2018-06-26T07:21:04Z
dc.language.rfc3066 en
dc.identifier.mtmt 3115040
dc.identifier.wos 000384016500016
dc.identifier.pubmed 27546461
dc.contributor.department SE/AOK/K/II. Sz. Gyermekgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem


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