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Cited 2 time in webofscience Cited 2 time in scopus
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The Role of ZEB2 Expression in Pediatric and Adult Glioblastomas

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dc.contributor.authorMyung, Jae Kyung-
dc.contributor.authorChoi, Seung Ah-
dc.contributor.authorKim, Seung-ki-
dc.contributor.authorKim, Seong Ik-
dc.contributor.authorPark, Jin Woo-
dc.contributor.authorPark, Sung-hye-
dc.date.accessioned2022-07-07T01:45:21Z-
dc.date.available2022-07-07T01:45:21Z-
dc.date.created2021-05-11-
dc.date.issued2021-01-
dc.identifier.issn0250-7005-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/142545-
dc.description.abstractBackground/Aim: Both pediatric glioblastoma (pGB) and adult glioblastoma (aGB) are clinically devastating, and are known to have different molecular pathogenesis. Here, we focused on the role of ZEB2 in pGB and aGB. Materials and Methods: Following transfection with ZEB2 siRNA into pGB cells (KNS42) and aGB cells (U87 and U373), cell proliferation, migration and invasion, and cell cycle progression were evaluated. Results: Targeted inhibition of ZEB2 induced up-regulation of E-cadherin expression and down-regulation of vimentin expression. Furthermore, it reduced invasion and migration of both pGB and aGB cells. Interestingly, in pGB cells, but not in aGB cells, silencing of ZEB2 reduced cell proliferation and viability, and affected the cell cycle progression of tumor cells. Conclusion: Inhibition of ZEB2 altered the mesenchymal features and reduced the migration and invasive ability of both pGB and aGB cells. ZEB2 effects were different in pGB and aGB cells regarding proliferation and cell cycle progression, suggesting that different underlying molecular mechanisms drive progression in these two types of tumors.-
dc.language영어-
dc.language.isoen-
dc.publisherINT INST ANTICANCER RESEARCH-
dc.titleThe Role of ZEB2 Expression in Pediatric and Adult Glioblastomas-
dc.typeArticle-
dc.contributor.affiliatedAuthorMyung, Jae Kyung-
dc.identifier.doi10.21873/anticanres.14763-
dc.identifier.scopusid2-s2.0-85099714564-
dc.identifier.wosid000608568800005-
dc.identifier.bibliographicCitationANTICANCER RESEARCH, v.41, no.1, pp.175 - 185-
dc.relation.isPartOfANTICANCER RESEARCH-
dc.citation.titleANTICANCER RESEARCH-
dc.citation.volume41-
dc.citation.number1-
dc.citation.startPage175-
dc.citation.endPage185-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusEPITHELIAL-MESENCHYMAL TRANSITION-
dc.subject.keywordPlusSMAD-INTERACTING PROTEIN-1-
dc.subject.keywordPlusE-CADHERIN-
dc.subject.keywordPlusGENETIC ALTERATIONS-
dc.subject.keywordPlusSIGNALING PATHWAYS-
dc.subject.keywordPlusSNAIL-
dc.subject.keywordPlusGRADE-
dc.subject.keywordPlusREGULATORS-
dc.subject.keywordPlusINVASION-
dc.subject.keywordPlusOVARIAN-
dc.subject.keywordAuthorAdult glioblastoma (aGB)-
dc.subject.keywordAuthorpediatric glioblastoma (pGB)-
dc.subject.keywordAuthorzinc finger E-box-binding homeobox 2 (ZEB2)-
dc.identifier.urlhttps://ar.iiarjournals.org/content/41/1/175-
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