ArticleOncogene2004
Transcriptional repressor BCL-6 immortalizes germinal center-like B cells in the absence of p53 function.
Article in Oncogene, 2004. 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, 41 citations in OpenAlex.
- The F-box E3 ligase protein FBXO11 regulates EBNA3C-associated degradation of BCL6.Journal of virology · 2024Article
- Immortalized B Cells Transfected with mRNA of Antigen Fused to MITD (IBMAM): An Effective Tool for Antigen-Specific T-Cell Expansion and TCR Validation.Biomedicines · 2023Article
- Combinatorial analyses reveal cellular composition changes have different impacts on transcriptomic changes of cell type specific genes in Alzheimer's Disease.Scientific reports · 2021Article
- Reciprocal negative regulation between the tumor suppressor protein p53 and B cell CLL/lymphoma 6 (BCL6) via control of caspase-1 expression.The Journal of biological chemistry · 2019Article
- Correlation Between C-MYC, BCL-2, and BCL-6 Protein Expression and Gene Translocation as Biomarkers in Diagnosis and Prognosis of Diffuse Large B-cell Lymphoma.Frontiers in pharmacology · 2018Article
- An essential EBV latent antigen 3C binds Bcl6 for targeted degradation and cell proliferation.PLoS pathogens · 2017Article
- Loss of PRDM1/BLIMP-1 function contributes to poor prognosis of activated B-cell-like diffuse large B-cell lymphoma.Leukemia · 2017Article
- The Expanding Role of the BCL6 Oncoprotein as a Cancer Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- Inhibition of the transcriptional repressor complex Bcl-6/BCoR induces endothelial sprouting but does not promote tumor growth.Oncotarget · 2017Article
- The feedback loop of LITAF and BCL6 is involved in regulating apoptosis in B cell non-Hodgkin's-lymphoma.Oncotarget · 2016Article
- Nanodiamonds coupled with 5,7-dimethoxycoumarin, a plant bioactive metabolite, interfere with the mitotic process in B16F10 cells altering the actin organization.International journal of nanomedicine · 2016Article
- Article
- Control systems and decision making for antibody production.Nature immunology · 2010Review
- BCL6 cooperates with CD40 stimulation and loss of p53 function to rapidly transform primary B cells.International journal of cancer · 2009Article
- BCL6-mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a p53-dependent pathway in a cell context-dependent manner.The Journal of biological chemistry · 2008Article
- Article
- Repression of BCL-6 is required for the formation of human memory B cells in vitro.The Journal of experimental medicine · 2007Article
- Conserved alternative and antisense transcripts at the programmed cell death 2 locus.BMC genomics · 2007Article
- Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6.Immunologic research · 2007Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal rearrangements in non-Hodgkin's B-cell lymphoma implicate BCL-6 as an oncogene, yet direct evidence for BCL-6 acting as an oncogene in B cells has been lacking. Here, we show that BCL-6 can immortalize primary B cells, but only in the absence of p53 tumor suppressor function. The expression of BCL-6 led to greatly increased B-cell proliferation, particularly in response to CD40 stimulation. Furthermore, BCL-6-infected p53-deficient B cells gave rise to immortalized cell lines that could be maintained by CD40 stimulation. We found that in primary mouse B cells, BCL-6 repressed expression of the Blimp-1, p27kip1, and cyclin D2 target genes. BCL-6 did not markedly repress the PDCD2 and BCL-XL target genes. The BCL-6 immortalized cell lines had a phenotype consistent with germinal center B cells, they expressed the germinal center-specific M17 gene, and a significant fraction of the cells stained positive with PNA. Our data indicate that BCL-6 may act to maintain B cells in a germinal center-like state, and repression of Blimp-1 by BCL-6 may be particularly crucial for stabilization of the germinal center phenotype. Our data also suggest that disruption of the p53 pathway may be crucial for the development of BCL-6-expressing B-cell lymphomas.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.