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The small GTPase Rac1 is involved in the maintenance of stemness and malignancies in glioma stem-like cells

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dc.contributor.authorYoon, Chang-Hwan-
dc.contributor.authorHyun, Kyung-Hwan-
dc.contributor.authorKim, Rae-Kwon-
dc.contributor.authorLee, Hyejin-
dc.contributor.authorLim, Eun-Jung-
dc.contributor.authorChung, Hee-Yong-
dc.contributor.authorAn, Sungkwan-
dc.contributor.authorPark, Myung-Jin-
dc.contributor.authorSuh, Yongjoon-
dc.contributor.authorKim, Min-Jung-
dc.contributor.authorLee, Su-Jae-
dc.date.accessioned2021-08-02T19:51:36Z-
dc.date.available2021-08-02T19:51:36Z-
dc.date.issued2011-07-
dc.identifier.issn0014-5793-
dc.identifier.issn1873-3468-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/28120-
dc.description.abstractA subpopulation of cancer cells with stem cell properties is responsible for tumor formation, maintenance, and malignant progression; however, the molecular mechanisms underlying the maintenance of cancer stem-like cell properties have remained unclear. Here, we show that the Rho family GTPase Rac1 is involved in the glioma stem-like cell (GSLC) maintenance and tumorigenicity in human glioma. The Rac1-Pak signaling was markedly activated in GSLCs. Knockdown of Rac1 caused reduction of expression of GSLC markers, self-renewal-related proteins and neurosphere formation. Moreover, down-regulation of Rac1 suppressed the migration, invasion, and malignant transformation in GSLCs. Furthermore, inhibition of Rac1 enhanced radiation sensitivity of GSLCs. These results indicate that the small GTPase Rac1 is involved in the maintenance of stemness and malignancies in GSLCs. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherElsevier BV-
dc.titleThe small GTPase Rac1 is involved in the maintenance of stemness and malignancies in glioma stem-like cells-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1016/j.febslet.2011.05.070-
dc.identifier.scopusid2-s2.0-79960364956-
dc.identifier.wosid000292772800033-
dc.identifier.bibliographicCitationFEBS Letters, v.585, no.14, pp 2331 - 2338-
dc.citation.titleFEBS Letters-
dc.citation.volume585-
dc.citation.number14-
dc.citation.startPage2331-
dc.citation.endPage2338-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusHUMAN BREAST-CANCER-
dc.subject.keywordPlusRHO-GTPASES-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusOVEREXPRESSION-
dc.subject.keywordPlusGLIOBLASTOMA-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusMIGRATION-
dc.subject.keywordPlusINVASION-
dc.subject.keywordAuthorRac1-
dc.subject.keywordAuthorGlioma stem-like cells-
dc.subject.keywordAuthorMigration and invasion-
dc.subject.keywordAuthorRadiation resistance-
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