ArticleProceedings of the National Academy of Sciences of the United States of America2011
Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 126 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.Npj viruses · 2026Article
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.bioRxiv : the preprint server for biology · 2026Article
- Oncoviruses in the Oral Cavity: Recent Advances in Understanding Viral Infections and Tumorigenesis.International journal of molecular sciences · 2025Review
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
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- Human Viral Oncoproteins and Ubiquitin-Proteasome System.Global medical genetics · 2024Review
- How Epstein Barr Virus Causes Lymphomas.Viruses · 2024Review
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- Epstein-Barr virus and host cell 3D genome organization.Journal of medical virology · 2023Review
- E3 Ubiquitin Ligases in Gammaherpesviruses and HIV: A Review of Virus Adaptation and Exploitation.Viruses · 2023Review
- Exploring the link between viruses and cancer in companion animals: a comprehensive and comparative analysis.Infectious agents and cancer · 2023Review
- Epstein-Barr virus: the molecular virology and the associated diseases.Fujita medical journal · 2023Article
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- A DNA tumor virus globally reprograms host 3D genome architecture to achieve immortal growth.Nature communications · 2023Article
- Epstein-Barr Virus and the Pathogenesis of Diffuse Large B-Cell Lymphoma.Life (Basel, Switzerland) · 2023Review
- Genotype characterization of Epstein-Barr virus among adults living with human immunodeficiency virus in Ethiopia.Frontiers in microbiology · 2023Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) and EBNA3A are each essential for EBV conversion of primary human B lymphocytes into continuously proliferating lymphoblast cell lines (LCLs) and for maintaining LCL growth. We now find that EBNA3C and EBNA3A's essential roles are to repress p16(INK4A) and p14(ARF). In the absence of EBNA3C or EBNA3A, p16(INK4A) and p14(ARF) expression increased and cell growth ceased. EBNA3C inactivation did not alter p16(INK4A) promoter CpG methylation, but reduced already low H3K27me3, relative to resting B cells, and increased H3K4me3 and H3-acetylation, linking EBNA3C inactivation to histone modifications associated with increased transcription. Importantly, knockdown of p16(INK4A) or p14(ARF) partially rescued LCLs from EBNA3C or EBNA3A inactivation-induced growth arrest and knockdown of both rescued LCL growth, confirming central roles for p16(INK4A) and p14(ARF) in LCL growth arrest following EBNA3C or EBNA3A inactivation. Moreover, blockade of p16(INK4A) and p14(ARF) effects on pRb and p53 by human papilloma virus type 16 E7 and E6 expression, sustained LCL growth after EBNA3C or EBNA3A inactivation. These data indicate that EBNA3C and EBNA3A joint repression of CDKN2A p16(INK4A) and p14(ARF) is essential for LCL growth.
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