ArticleJournal of virology2012
Epstein-Barr virus downregulates microRNA 203 through the oncoprotein latent membrane protein 1: a contribution to increased tumor incidence in epithelial cells.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- MicroRNA changes with macro potential contribute to secondary immunodeficiency in chronic lymphocytic leukemia during epstein barr virus reactivation.Scientific reports · 2025Article
- Integrated analysis of the lncRNA-miRNA-mRNA ceRNA network in nasopharyngeal carcinoma.Translational cancer research · 2024Article
- Proteomic snapshot of saliva samples predicts new pathways implicated in SARS-CoV-2 pathogenesis.Clinical proteomics · 2024Article
- Countenance and implication of Β-sitosterol, Β-amyrin and epiafzelechin in nickel exposed Rat: in-silico and in-vivo approach.Scientific reports · 2023Article
- Helicobacter pylori infection induces abnormal expression of pro-angiogenic gene ANGPT2 and miR-203a in AGS gastric cell line.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023Article
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- Extracellular Vesicles in the Progression and Therapeutic Resistance of Nasopharyngeal Carcinoma.Cancers · 2022Review
- New insights into Epstein‑Barr virus‑associated tumors: Exosomes (Review).Oncology reports · 2022Review
- Epstein-Barr Virus miR-BART1-3p Regulates the miR-17-92 Cluster by Targeting E2F3.International journal of molecular sciences · 2021Article
- Long Noncoding RNA OIP5-AS1 Promotes the Disease Progression in Nasopharyngeal Carcinoma by Targeting miR-203.BioMed research international · 2021Article
- Long noncoding RNAs involvement in Epstein-Barr virus infection and tumorigenesis.Virology journal · 2020Review
- The four‑microRNA signature identified by bioinformatics analysis predicts the prognosis of nasopharyngeal carcinoma patients.Oncology reports · 2019Article
- MicroRNA-18a promotes cancer progression through SMG1 suppression and mTOR pathway activation in nasopharyngeal carcinoma.Cell death & disease · 2019Article
- Targeting Exosomal EBV-LMP1 Transfer and miR-203 Expression via the NF-κB Pathway: The Therapeutic Role of Aspirin in NPC.Molecular therapy. Nucleic acids · 2019Article
- Early Pattern of Epstein-Barr Virus Infection in Gastric Epithelial Cells by "Cell-in-cell".Virologica Sinica · 2019Article
- Exosomal cyclophilin A as a novel noninvasive biomarker for Epstein-Barr virus associated nasopharyngeal carcinoma.Cancer medicine · 2019Article
- The role of exosomal noncoding RNAs in cancer.Molecular cancer · 2019Review
- Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome.Frontiers in microbiology · 2019Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
The Epstein-Barr virus (EBV) is highly associated with nasopharyngeal carcinoma (NPC), and it regulates some microRNAs (miRNAs) that are involved in the development of cancer. The role of EBV in the deregulation of cellular miRNAs and how this affects the progression of NPC remain to be investigated. An analysis of the miRNA profile in an EBV-infected cell line revealed that miRNA 203 (miR-203) was downregulated. miR-203 is expressed specifically in epithelial cells. This downregulation of miR-203 was further verified and functionally analyzed. miR-203 was downregulated substantially in epithelial cells and NPC tissues that were latently infected with EBV. Downregulation of miR-203 also occurred during the early stage of EBV infection. Furthermore, the viral oncoprotein, latent membrane protein 1 (LMP1), was responsible for downregulation of miR-203. Removal of the latent EBV genome or suppression of LMP1 resulted in restoration of miR-203 expression. EBV-LMP1 mediated the downregulation of miR-203 at the primary transcript level. E2F3 and CCNG1 were identified as target genes of miR-203. Ectopic expression of miR-203 inhibited EBV-induced S-phase entry and transformation in vivo. Overexpression of the targets overcame the effects of miR-203 mimics on the cell cycle, and the expression of target genes in tumor models was inhibited by miR-203. Inhibitors of Jun N-terminal protein kinase (JNK) and NF-κB blocked miR-203 downregulation. These results imply that EBV promotes malignancy by downregulating cellular miR-203, which contributes to the etiology of NPC.
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