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Cell cycle arrest induced by engagement of B7-H4 on Epstein-Barr virus-positive B-cell lymphoma cell lines

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dc.contributor.authorPark, Ga Bin-
dc.contributor.authorSong, Hyunkeun-
dc.contributor.authorKim, Yeong-Seok-
dc.contributor.authorSung, Minjung-
dc.contributor.authorRyu, Jeoung W.-
dc.contributor.authorLee, Hyun-Kyung-
dc.contributor.authorCho, Dae-Ho-
dc.contributor.authorKim, Daejin-
dc.contributor.authorLee, Wang J.-
dc.contributor.authorHur, Dae Y.-
dc.date.available2021-02-22T14:16:04Z-
dc.date.created2020-09-03-
dc.date.issued2009-11-
dc.identifier.issn0019-2805-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13657-
dc.description.abstractP>B7-H4 is a recently discovered B7 family member that has inhibitory effects on T-cell immunity. However, the reverse signalling mechanism of the B7-H4-expressing cells remains unclear. Previous work has shown that B7-H4 expression was enhanced on B cells following Epstein-Barr virus (EBV) infection, and engagement of cell-surface-expressed B7-H4 induces cell death of EBV-transformed B cells. Here we found that B7-H4 was constitutively expressed on EBV-positive lymphoma cells, Raji and IM-9 cells, but was not expressed on EBV-negative lymphoma cells (Ramos). Engagement of B7-H4 significantly reduced cell growth of Raji and IM-9 cells and resulted in cell cycle arrest at G0-G1 phase in a dose- and time-dependent manner. To clarify the mechanism of cell cycle arrest via activation of B7-H4, cell cycle regulatory factors were examined by reverse transcription-polymerase chain reaction and immunoblotting. We found that B7-H4 triggered down-regulation of CDK4/6 and up-regulation of p21 expression at both protein and RNA levels. Furthermore, CDK2 and cyclin E/D expression was down-regulated by B7-H4 triggering. Additionally, the down-regulation of phospho-AKT and phospho-cyclin E were clearly detected in B7-H4-activated Raji cells, but the phosphorylation of p53 was constitutively maintained. These results indicate that B7-H4-mediated signalling on EBV-positive B-cell lymphoma cells modulates the cell cycle through down-regulation of the AKT pathway. Consequently, B7-H4 may be a new potential target for use in EBV-positive lymphoma therapy.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.subjectPHOSPHATIDYLINOSITOL 3-KINASE/AKT-
dc.subjectMULTIPLE-MYELOMA-
dc.subjectCDK INHIBITORS-
dc.subjectOVARIAN-CANCER-
dc.subjectCLASS-I-
dc.subjectPATHWAY-
dc.subjectPROGRESSION-
dc.subjectEXPRESSION-
dc.subjectAPOPTOSIS-
dc.subjectEBV-
dc.titleCell cycle arrest induced by engagement of B7-H4 on Epstein-Barr virus-positive B-cell lymphoma cell lines-
dc.typeArticle-
dc.contributor.affiliatedAuthorCho, Dae-Ho-
dc.identifier.doi10.1111/j.1365-2567.2009.03111.x-
dc.identifier.scopusid2-s2.0-70349662155-
dc.identifier.wosid000270588300006-
dc.identifier.bibliographicCitationIMMUNOLOGY, v.128, no.3, pp.360 - 368-
dc.relation.isPartOfIMMUNOLOGY-
dc.citation.titleIMMUNOLOGY-
dc.citation.volume128-
dc.citation.number3-
dc.citation.startPage360-
dc.citation.endPage368-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusPHOSPHATIDYLINOSITOL 3-KINASE/AKT-
dc.subject.keywordPlusMULTIPLE-MYELOMA-
dc.subject.keywordPlusCDK INHIBITORS-
dc.subject.keywordPlusOVARIAN-CANCER-
dc.subject.keywordPlusCLASS-I-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusEBV-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorB cells-
dc.subject.keywordAuthorB7-H4-
dc.subject.keywordAuthorcancer-
dc.subject.keywordAuthorcell cycle-
dc.subject.keywordAuthorcostimulation-
dc.subject.keywordAuthorEpstein-Barr virus-
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