ArticleOncogene2003
Disruption of the B-cell specific transcriptional program in HHV-8 associated primary effusion lymphoma cell lines.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 53 citations in OpenAlex.
- IRF-4-mediated CIITA transcription is blocked by KSHV encoded LANA to inhibit MHC II presentation.PLoS pathogens · 2013Trial
- PAX5 functions as a tumor suppressor by RB-E2F-mediated cell cycle arrest in Kaposi sarcoma-associated herpesvirus-infected primary effusion lymphoma.Neoplasia (New York, N.Y.) · 2024Article
- Mechanism and therapeutic implications of pomalidomide-induced immune surface marker upregulation in EBV-positive lymphomas.Scientific reports · 2023Article
- Primary effusion lymphoma enhancer connectome links super-enhancers to dependency factors.Nature communications · 2020Article
- Article
- Kinome profiling of non-Hodgkin lymphoma identifies Tyro3 as a therapeutic target in primary effusion lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human herpesvirus-encoded kinase induces B cell lymphomas in vivo.The Journal of clinical investigation · 2018Article
- Expression and Subcellular Localization of the Kaposi's Sarcoma-Associated Herpesvirus K15P Protein during Latency and Lytic Reactivation in Primary Effusion Lymphoma Cells.Journal of virology · 2017Article
- Restoring PU.1 induces apoptosis and modulates viral transactivation via interferon-stimulated genes in primary effusion lymphoma.Oncogene · 2017Article
- K1 and K15 of Kaposi's Sarcoma-Associated Herpesvirus Are Partial Functional Homologues of Latent Membrane Protein 2A of Epstein-Barr Virus.Journal of virology · 2015Article
- IRF4 and IRF8: Governing the virtues of B Lymphocytes.Frontiers in biology · 2014Article
- Downregulation of IRF4 induces lytic reactivation of KSHV in primary effusion lymphoma cells.Virology · 2014Article
- Host genetic variants and gene expression patterns associated with Epstein-Barr virus copy number in lymphoblastoid cell lines.PloS one · 2014Article
- Role of IRF4 in IFN-stimulated gene induction and maintenance of Kaposi sarcoma-associated herpesvirus latency in primary effusion lymphoma cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Review
- Transcription factor Spi-B binds unique sequences present in the tandem repeat promoter/enhancer of JC virus and supports viral activity.The Journal of general virology · 2010Article
- Role of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi's sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma.Journal of virology · 2009Article
- Interferon regulatory factor family of transcription factors and regulation of oncogenesis.Cancer science · 2008Review
- Article
- A requirement for NF-kappaB induction in the production of replication-competent HHV-8 virions.Oncogene · 2004Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary effusion lymphoma (PEL) is a lymphoproliferative disease of B-cell origin that is associated with HHV-8 infection. PEL cells harbor a non-B, non-T phenotype and lack significant surface immunoglobulin (Ig) expression, a characteristic that has not been fully explained. In the present study, we demonstrate that PEL cells constitutively express interferon regulatory factor (IRF)-4, a transcription factor that regulates the activity of the immunoglobulin light-chain enhancer elements lambdaB and kappaE3' through binding to a composite Ets-IRF site. IRF-4 activity requires its physical interaction with PU.1, an Ets family member involved in the activation of genes essential for B-cell development. However, in PEL-derived B-cell lines, PU.1 expression was completely abrogated; expression of the B cell specific transcription factor Oct-2, which is known to regulate PU.1 expression, was also abolished. Moreover, the B-cell-specific coactivator of octamer factors, BOB-1/OcaB, was expressed at very decreased levels in PEL cells. Ectopic expression of Oct-2 was able to fully restore PU.1 promoter activity in the PEL cell line BCBL-1, while PU.1 expression also reconstituted the activity of the lambdaB Ets-IRF site. In addition, protein levels of BSAP/Pax-5 and IRF-8/ICSBP were undetectable in PEL cells. The pattern of transcription factor ablation observed in PEL was found to be comparable to that observed in classical Hodgkin's disease-derived cell lines, which also lack B-cell-specific surface markers. These observations indicate that disruption of the B-cell-specific transcriptional program is likely to contribute to the incomplete B-cell phenotype characteristic of PEL cells.
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Registered trials
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