ArticlePLoS pathogens2017
An essential EBV latent antigen 3C binds Bcl6 for targeted degradation and cell proliferation.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- A tonsil organoid model reveals Epstein-Barr virus-infected germinal center B cell states during primary infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genome-wide mapping of EBV-induced genomic variations identifies the role of MUC19 in EBV latency.mBio · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Human Viral Oncoproteins and Ubiquitin-Proteasome System.Global medical genetics · 2024Review
- Review
- Combination of bortezomib and venetoclax targets the pro-survival function of LMP-1 and EBNA-3C of Epstein-Barr virus in spontaneous lymphoblastoid cell lines.PLoS pathogens · 2024Article
- The F-box E3 ligase protein FBXO11 regulates EBNA3C-associated degradation of BCL6.Journal of virology · 2024Article
- Article
- Epstein-Barr virus evades restrictive host chromatin closure by subverting B cell activation and germinal center regulatory loci.Cell reports · 2023Article
- Transcriptome reprogramming of Epstein-Barr virus infected epithelial and B cells reveals distinct host-virus interaction profiles.Cell death & disease · 2022Article
- Review
- Transcriptional inhibition of miR-486-3p by BCL6 upregulates Snail and induces epithelial-mesenchymal transition during radiation-induced pulmonary fibrosis.Respiratory research · 2022Article
- Review
- The metastasis suppressor protein NM23-H1 modulates the PI3K-AKT axis through interaction with the p110α catalytic subunit.Oncogenesis · 2021Article
- Epstein-Barr Virus Facilitates Expression of KLF14 by Regulating the Cooperative Binding of the E2F-Rb-HDAC Complex in Latent Infection.Journal of virology · 2020Article
- Review
- DNA methylation enzymes and PRC1 restrict B-cell Epstein-Barr virus oncoprotein expression.Nature microbiology · 2020Article
- Quassinoid analogs with enhanced efficacy for treatment of hematologic malignancies target the PI3Kγ isoform.Communications biology · 2020Article
- Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.Frontiers in cellular and infection microbiology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The latent EBV nuclear antigen 3C (EBNA3C) is required for transformation of primary human B lymphocytes. Most mature B-cell malignancies originate from malignant transformation of germinal center (GC) B-cells. The GC reaction appears to have a role in malignant transformation, in which a major player of the GC reaction is Bcl6, a key regulator of this process. We now demonstrate that EBNA3C contributes to B-cell transformation by targeted degradation of Bcl6. We show that EBNA3C can physically associate with Bcl6. Notably, EBNA3C expression leads to reduced Bcl6 protein levels in a ubiquitin-proteasome dependent manner. Further, EBNA3C inhibits the transcriptional activity of the Bcl6 promoter through interaction with the cellular protein IRF4. Bcl6 degradation induced by EBNA3C rescued the functions of the Bcl6-targeted downstream regulatory proteins Bcl2 and CCND1, which resulted in increased proliferation and G1-S transition. These data provide new insights into the function of EBNA3C in B-cell transformation during GC reaction, and raises the possibility of developing new targeted therapies against EBV-associated cancers.
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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.