Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells
DC Field | Value | Language |
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dc.contributor.author | Kang, Sanghee | - |
dc.contributor.author | Oh, Sang Cheul | - |
dc.contributor.author | Min, Byung Wook | - |
dc.contributor.author | Lee, Dae-Hee | - |
dc.date.available | 2020-11-02T07:47:40Z | - |
dc.date.issued | 2018-02 | - |
dc.identifier.issn | 0250-7005 | - |
dc.identifier.issn | 1791-7530 | - |
dc.identifier.uri | https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3891 | - |
dc.description.abstract | Background/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.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | INT INST ANTICANCER RESEARCH | - |
dc.title | Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells | - |
dc.type | Article | - |
dc.publisher.location | 그리이스 | - |
dc.identifier.doi | 10.21873/anticanres.12285 | - |
dc.identifier.scopusid | 2-s2.0-85042463512 | - |
dc.identifier.wosid | 000423315300023 | - |
dc.identifier.bibliographicCitation | ANTICANCER RESEARCH, v.38, no.2, pp 787 - 794 | - |
dc.citation.title | ANTICANCER RESEARCH | - |
dc.citation.volume | 38 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 787 | - |
dc.citation.endPage | 794 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | EPITHELIAL-MESENCHYMAL TRANSITION | - |
dc.subject.keywordPlus | METASTASIS | - |
dc.subject.keywordPlus | GLIOBLASTOMA | - |
dc.subject.keywordPlus | TARGET | - |
dc.subject.keywordPlus | EMT | - |
dc.subject.keywordAuthor | TGM2 | - |
dc.subject.keywordAuthor | CCSC | - |
dc.subject.keywordAuthor | stemness | - |
dc.subject.keywordAuthor | EMT | - |
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