ArticleOncogene1999
Overexpressed BCL6 (LAZ3) oncoprotein triggers apoptosis, delays S phase progression and associates with replication foci.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 72 citations in OpenAlex.
- Investigating Neuron Degeneration in Huntington's Disease Using RNA-Seq Based Transcriptome Study.Genes · 2023Article
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- Novel RGAG1-BCOR gene fusion revealed in a somatic soft tissue sarcoma with a long follow-up.Virchows Archiv : an international journal of pathology · 2022Article
- A Synchronous IRF4-Dependent Gene Regulatory Network in B and Helper T Cells Orchestrating the Antibody Response.Trends in immunology · 2020Review
- Inhibition of the transcriptional repressor complex Bcl-6/BCoR induces endothelial sprouting but does not promote tumor growth.Oncotarget · 2017Article
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- The zinc finger transcription factor ZXDC activates CCL2 gene expression by opposing BCL6-mediated repression.Molecular immunology · 2013Article
- Male-dominant activation of rat renal organic anion transporter 1 (Oat1) and 3 (Oat3) expression by transcription factor BCL6.PloS one · 2012Article
- Inhibition of doxorubicin-induced senescence by PPARδ activation agonists in cardiac muscle cells: cooperation between PPARδ and Bcl6.PloS one · 2012Article
- Transcriptome analysis of monocyte-HIV interactions.Retrovirology · 2010Article
- Functional interaction of HTLV-1 tax protein with the POZ domain of the transcriptional repressor BCL6.Oncogene · 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
- Role of the Transcriptional Repressor BCL6 in Allergic Response and Inflammation.The World Allergy Organization journal · 2008Article
- Bortezomib induces different apoptotic rates in B-CLL cells according to IgVH and BCL-6 mutations.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2006Article
- A novel angiotensin II type 2 receptor signaling pathway: possible role in cardiac hypertrophy.The EMBO journal · 2003Article
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- Ambivalent role of BCL6 in cell survival and transformation.Oncogene · 2003Article
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Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most frequent genetic abnormalities associated with non Hodgkin lymphoma is the structural alteration of the 5' non coding/regulatory region of the BCL6 (LAZ3) protooncogene. BCL6 encodes a POZ/Zn finger protein, a structure similar to that of many Drosophila developmental regulators and to another protein involved in a human hematopoietic malignancy, PLZF. BCL6 is a sequence specific transcriptional repressor controlling germinal center formation and T cell dependent immune response. Although the expression of BCL6 negatively correlates with cellular proliferation in different cell types, the influence of BCL6 on cell growth and survival is currently unknown so that the way its deregulation may contribute to cancer remains elusive. To directly address this issue, we used a tetracycline-regulated system in human U2OS osteosarcoma cells and thus found that BCL6 mediates growth suppression associated with impaired S phase progression and apoptosis. Interestingly, overexpressed BCL6 can colocalize with sites of ongoing DNA synthesis, suggesting that it may directly interfere with S phase initiation and/or progression. In contrast, the isolated Zn finger region of BCL6, which binds BCL6 target sequence but lacks transcriptional repression activity, slows, but does not suppress, U2OS cell growth, is less efficient at delaying S phase progression, and does not trigger apoptosis. Thus, for a large part, the effects of BCL6 overexpression on cell growth and survival depend on its ability to engage protein/protein interactions with itself and/or its transcriptional corepressors. That BCL6 restricts cell growth suggests that its deregulation upon structural alterations may alleviate negative controls on the cell cycle and cell survival.
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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.