ArticleThe Journal of biological chemistry2008
BCL6-mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a p53-dependent pathway in a cell context-dependent manner.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Key Functions of the Transcription Factor BCL6 During T-Cell Differentiation.Advances in experimental medicine and biology · 2024Review
- Mouse models of diffuse large B cell lymphoma.Frontiers in immunology · 2023Review
- BCL6 BTB-specific inhibitor reversely represses T-cell activation, Tfh cells differentiation, and germinal center reaction in vivo.European journal of immunology · 2021Article
- The effect of caffeic acid phenethyl ester on cell cycle control gene expressions in breast cancer cells.Molecular biology research communications · 2021Article
- Article
- Article
- Article
- Histone deacetylase 3 controls a transcriptional network required for B cell maturation.Nucleic acids research · 2019Article
- 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
- Hair follicle dermal condensation forms via Fgf20 primed cell cycle exit, cell motility, and aggregation.eLife · 2018Article
- Apoptosis in inner ear sensory hair cells.Journal of otology · 2017Review
- Article
- IFI16 Expression Is Related to Selected Transcription Factors during B-Cell Differentiation.Journal of immunology research · 2015Article
- Histone deacetylases 1 and 2 regulate DNA replication and DNA repair: potential targets for genome stability-mechanism-based therapeutics for a subset of cancers.Cell cycle (Georgetown, Tex.) · 2015Review
- LITAF, a BCL6 target gene, regulates autophagy in mature B-cell lymphomas.British journal of haematology · 2013Article
- Integrative epigenomic analysis identifies biomarkers and therapeutic targets in adult B-acute lymphoblastic leukemia.Cancer discovery · 2012Article
- Pathogenesis of human B cell lymphomas.Annual review of immunology · 2012Review
- The BTB-ZF family of transcription factors: key regulators of lineage commitment and effector function development in the immune system.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- A kinase shRNA screen links LATS2 and the pRB tumor suppressor.Genes & development · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The BCL6 oncogenic transcriptional repressor is required for development of germinal center centroblasts, which undergo simultaneous genetic recombination and massive clonal expansion. Although BCL6 is required for survival of centroblasts, its expression in earlier B-cells is toxic. Understanding these opposing effects could provide critical insight into normal B-cell biology and lymphomagenesis. We examined the transcriptional and biological effects of BCL6 in various primary cells. BCL6 repression of ATR was previously shown to play a critical role in the centroblast phenotype. Likewise, we found that BCL6 could impose an ATR-dependent phenotype of attenuated DNA damage sensing and repair in primary fibroblasts and B-cells. BCL6 induced true genomic instability because DNA repair was delayed and was qualitatively impaired, which could be critical for BCL6-induced lymphomagenesis. Although BCL6 can directly repress TP53 in centroblasts, BCL6 induced TP53 expression in primary fibroblasts and B-cells, and these cells underwent p53-dependent growth arrest and senescence in the presence of physiological levels of BCL6. This differential ability to trigger a functional p53 response explains at least in part the different biological response to BCL6 expression in centroblasts versus other cells. The data suggest that targeted re-activation of TP53 could be of therapeutic value in centroblast-derived lymphomas.
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Registered trials
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.