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

Authors
Park, Ga BinSong, HyunkeunKim, Yeong-SeokSung, MinjungRyu, Jeoung W.Lee, Hyun-KyungCho, Dae-HoKim, DaejinLee, Wang J.Hur, Dae Y.
Issue Date
Nov-2009
Publisher
WILEY
Keywords
apoptosis; B cells; B7-H4; cancer; cell cycle; costimulation; Epstein-Barr virus
Citation
IMMUNOLOGY, v.128, no.3, pp.360 - 368
Journal Title
IMMUNOLOGY
Volume
128
Number
3
Start Page
360
End Page
368
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13657
DOI
10.1111/j.1365-2567.2009.03111.x
ISSN
0019-2805
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.
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