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Cited 18 time in webofscience Cited 19 time in scopus
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Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells

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dc.contributor.authorKang, Sanghee-
dc.contributor.authorOh, Sang Cheul-
dc.contributor.authorMin, Byung Wook-
dc.contributor.authorLee, Dae-Hee-
dc.date.available2020-11-02T07:47:40Z-
dc.date.issued2018-02-
dc.identifier.issn0250-7005-
dc.identifier.issn1791-7530-
dc.identifier.urihttps://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3891-
dc.description.abstractBackground/Aim: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). Materials and Methods: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (-) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. Results: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and beta-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT-and stemness-related proteins. Conclusion: The metastatic potential of CSCs arises from highly expressed TGM2.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherINT INST ANTICANCER RESEARCH-
dc.titleTransglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells-
dc.typeArticle-
dc.publisher.location그리이스-
dc.identifier.doi10.21873/anticanres.12285-
dc.identifier.scopusid2-s2.0-85042463512-
dc.identifier.wosid000423315300023-
dc.identifier.bibliographicCitationANTICANCER RESEARCH, v.38, no.2, pp 787 - 794-
dc.citation.titleANTICANCER RESEARCH-
dc.citation.volume38-
dc.citation.number2-
dc.citation.startPage787-
dc.citation.endPage794-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusEPITHELIAL-MESENCHYMAL TRANSITION-
dc.subject.keywordPlusMETASTASIS-
dc.subject.keywordPlusGLIOBLASTOMA-
dc.subject.keywordPlusTARGET-
dc.subject.keywordPlusEMT-
dc.subject.keywordAuthorTGM2-
dc.subject.keywordAuthorCCSC-
dc.subject.keywordAuthorstemness-
dc.subject.keywordAuthorEMT-
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