Cell cycle arrest induced by engagement of B7-H4 on Epstein-Barr virus-positive B-cell lymphoma cell lines
DC Field | Value | Language |
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dc.contributor.author | Park, Ga Bin | - |
dc.contributor.author | Song, Hyunkeun | - |
dc.contributor.author | Kim, Yeong-Seok | - |
dc.contributor.author | Sung, Minjung | - |
dc.contributor.author | Ryu, Jeoung W. | - |
dc.contributor.author | Lee, Hyun-Kyung | - |
dc.contributor.author | Cho, Dae-Ho | - |
dc.contributor.author | Kim, Daejin | - |
dc.contributor.author | Lee, Wang J. | - |
dc.contributor.author | Hur, Dae Y. | - |
dc.date.available | 2021-02-22T14:16:04Z | - |
dc.date.issued | 2009-11 | - |
dc.identifier.issn | 0019-2805 | - |
dc.identifier.issn | 1365-2567 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13657 | - |
dc.description.abstract | P>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.format.extent | 9 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | Cell cycle arrest induced by engagement of B7-H4 on Epstein-Barr virus-positive B-cell lymphoma cell lines | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/j.1365-2567.2009.03111.x | - |
dc.identifier.scopusid | 2-s2.0-70349662155 | - |
dc.identifier.wosid | 000270588300006 | - |
dc.identifier.bibliographicCitation | IMMUNOLOGY, v.128, no.3, pp 360 - 368 | - |
dc.citation.title | IMMUNOLOGY | - |
dc.citation.volume | 128 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 360 | - |
dc.citation.endPage | 368 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | PHOSPHATIDYLINOSITOL 3-KINASE/AKT | - |
dc.subject.keywordPlus | MULTIPLE-MYELOMA | - |
dc.subject.keywordPlus | CDK INHIBITORS | - |
dc.subject.keywordPlus | OVARIAN-CANCER | - |
dc.subject.keywordPlus | CLASS-I | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | EBV | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | B cells | - |
dc.subject.keywordAuthor | B7-H4 | - |
dc.subject.keywordAuthor | cancer | - |
dc.subject.keywordAuthor | cell cycle | - |
dc.subject.keywordAuthor | costimulation | - |
dc.subject.keywordAuthor | Epstein-Barr virus | - |
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