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Cited 29 time in webofscience Cited 29 time in scopus
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YB-1 overexpression promotes a TGF-beta 1-induced epithelial-mesenchymal transition via Akt activation

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dc.contributor.authorHa, Bin-
dc.contributor.authorLee, Eun Byul-
dc.contributor.authorCu, Jun-
dc.contributor.authorKim, Yosup-
dc.contributor.authorJang, Ho Hee-
dc.date.available2020-02-28T09:46:16Z-
dc.date.created2020-02-06-
dc.date.issued2015-03-06-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/10684-
dc.description.abstractThe Y-box binding protein-1 (YB-1) is a transcription/translation regulatory protein, and the expression thereof is associated with cancer aggressiveness. In the present study, we explored the regulatory effects of YB-1 during the transforming growth factor-beta 1 (TGF-beta 1)-induced epithelial-to-mesenchymal transition (EMT) in lung adenocarcinoma cells. Downregulation of YB-1 increased E-cadherin promoter activity, and upregulation of YB-1 decreased promoter activity, suggesting that the YB-1 level may be correlated with the EMT. TGF-beta 1 induced YB-1 expression, and TGF-beta 1 translocated cytosolic YB-1 into the nucleus. YB-1 overexpression promoted TGF-beta 1-induced downregulation of epithelial markers, upregulation of mesenchymal markers, and cell migration. Moreover, YB-1 overexpression enhanced the expression of E-cadherin transcriptional repressors via TGF-beta 1-induced Akt activation. Our findings afford new insights into the role played by YB-1 in the TGF-beta 1 signaling pathway. (C) 2015 Elsevier Inc. All rights reserved.-
dc.language영어-
dc.language.isoen-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.subjectBOX-BINDING-PROTEIN-
dc.subjectTRANSCRIPTION FACTOR YB-1-
dc.subjectBREAST-CANCER-
dc.subjectTGF-BETA-
dc.subjectGENE-EXPRESSION-
dc.subjectNUCLEAR EXPRESSION-
dc.subjectMESSENGER-RNA-
dc.subjectE-CADHERIN-
dc.subjectPROGRESSION-
dc.subjectRESISTANCE-
dc.titleYB-1 overexpression promotes a TGF-beta 1-induced epithelial-mesenchymal transition via Akt activation-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000351482200021-
dc.identifier.doi10.1016/j.bbrc.2015.01.114-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.458, no.2, pp.347 - 351-
dc.identifier.scopusid2-s2.0-84923268973-
dc.citation.endPage351-
dc.citation.startPage347-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume458-
dc.citation.number2-
dc.contributor.affiliatedAuthorHa, Bin-
dc.contributor.affiliatedAuthorLee, Eun Byul-
dc.contributor.affiliatedAuthorCu, Jun-
dc.contributor.affiliatedAuthorKim, Yosup-
dc.contributor.affiliatedAuthorJang, Ho Hee-
dc.type.docTypeArticle-
dc.subject.keywordAuthorYB-1-
dc.subject.keywordAuthorTGF-beta 1-
dc.subject.keywordAuthorEpithelial-mesenchymal transition-
dc.subject.keywordAuthorE-cadherin-
dc.subject.keywordAuthorAkt-
dc.subject.keywordPlusBOX-BINDING-PROTEIN-
dc.subject.keywordPlusTRANSCRIPTION FACTOR YB-1-
dc.subject.keywordPlusBREAST-CANCER-
dc.subject.keywordPlusTGF-BETA-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusNUCLEAR EXPRESSION-
dc.subject.keywordPlusMESSENGER-RNA-
dc.subject.keywordPlusE-CADHERIN-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusRESISTANCE-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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