ArticleCell death & disease2018
Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Changes in gene expression levels caused by H3K9me3/H3K9ac modifications are associated with BmCPV infection inVirulence · 2025Article
- Death-associated protein kinase 1: a double-edged sword in health and disease.Frontiers in immunology · 2025Review
- Exploring the interplay between EBV and autophagy-related gene expression patterns in nasopharyngeal carcinoma.Frontiers in oncology · 2025Article
- Acetylation modification in the regulation of macroautophagy.Advanced biotechnology · 2024Review
- Differential carbonic anhydrase activities control EBV-induced B-cell transformation and lytic cycle reactivation.PLoS pathogens · 2024Article
- Histone methylation in Epstein-Barr virus-associated diseases.Epigenomics · 2024Review
- The roles of autophagy and mitophagy in corneal pathology: current knowledge and future perspectives.Frontiers in medicine · 2023Review
- CD4+ Cytotoxic T Cells Involved in the Development of EBV-Associated Diseases.Pathogens (Basel, Switzerland) · 2022Review
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- The regulatory effect of acetylation of HMGN2 and H3K27 on pyocyanin-induced autophagy in macrophages by affecting Ulk1 transcription.Journal of cellular and molecular medicine · 2021Article
- Review
- Modulation of Endosome Function, Vesicle Trafficking and Autophagy by Human Herpesviruses.Cells · 2021Review
- An immune epigenetic insight to COVID-19 infection.Epigenomics · 2021Review
- Therapeutic Potential of Exploiting Autophagy Cascade Against Coronavirus Infection.Frontiers in microbiology · 2021Review
- As Evidence-Based Tumorigenic Role of Epstein-Barr Virus miR-BART1-3p in Neurological Tumors.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Autophagy in Viral Development and Progression of Cancer.Frontiers in oncology · 2021Review
- Epigenetic Regulation of Autophagy Beyond the Cytoplasm: A Review.Frontiers in cell and developmental biology · 2021Review
- MHC class I antigen cross-presentation mediated by PapMV nanoparticles in human antigen-presenting cells is dependent on autophagy.PloS one · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) oncoprotein EBNA3C is indispensable for primary B-cell transformation and maintenance of lymphoblastoid cells outgrowth. EBNA3C usurps two putative cellular pathways-cell-cycle and apoptosis, essentially through modulating ubiquitin-mediated protein-degradation or gene transcription. In cancer cells, these two pathways are interconnected with autophagy,-a survival-promoting catabolic network in which cytoplasmic material including mis/un-folded protein aggregates and damaged organelles along with intracellular pathogens are degraded and recycled in lysosomal compartments. Studies have shown that tumor viruses including EBV can manipulate autophagy as a survival strategy. Here, we demonstrate that EBNA3C elevates autophagy, which serves as a prerequisite for apoptotic inhibition and maintenance of cell growth. Using PCR based micro-array we show that EBNA3C globally accelerates autophagy gene transcription under growth limiting conditions. Reanalyzing the ENCODE ChIP-sequencing data (GSE52632 and GSE26386) followed by ChIP-PCR demonstrate that EBNA3C recruits several histone activation epigenetic marks (H3K4me1, H3K4me3, H3K9ac, and H3K27ac) for transcriptional activation of autophagy genes, notably ATG3, ATG5, and ATG7 responsible for autophagosome formation. Moreover, under growth limiting conditions EBNA3C further stimulates the autophagic response through upregulation of a number of tumor suppressor genes, notably cyclin-dependent kinase inhibitors-CDKN1B (p27
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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.