ArticleProceedings of the National Academy of Sciences of the United States of America2012
Cyclin D1 overexpression supports stable EBV infection in nasopharyngeal epithelial cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 158 citations in OpenAlex.
- Efficient immortalization of primary nasopharyngeal epithelial cells for EBV infection study.PloS one · 2013Trial
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- ebv-sisRNA-3 contributes to the formation of G4-associated R-loop upstream of EBV lytic replication origin in latently infected cells.Cell & bioscience · 2025Article
- Oncogene-Induced Senescence Transcriptomes Signify Premalignant Colorectal Adenomas.Current issues in molecular biology · 2025Article
- Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression.Frontiers in oncology · 2025Review
- Epstein-Barr virus replication within differentiated epithelia requires pRb sequestration of activator E2F transcription factors.Journal of virology · 2024Article
- Nasopharyngeal Carcinoma Cell Lines: Reliable Alternatives to Primary Nasopharyngeal Cells?Cells · 2024Article
- Establishment and Characterization of an Epstein-Barr Virus-positive Cell Line from a Non-keratinizing Differentiated Primary Nasopharyngeal Carcinoma.Cancer research communications · 2024Article
- USP2 inhibition prevents infection with ACE2-dependent coronaviruses in vitro and is protective against SARS-CoV-2 in mice.Science translational medicine · 2023Article
- Retinoblastoma Protein Is Required for Epstein-Barr Virus Replication in Differentiated Epithelia.Journal of virology · 2023Article
- Pathogenesis and therapeutic implications of EBV-associated epithelial cancers.Frontiers in oncology · 2023Review
- The role of Epstein-Barr virus in nasopharyngeal carcinoma.Frontiers in microbiology · 2023Review
- Updates on Epstein-Barr Virus (EBV)-Associated Nasopharyngeal Carcinoma: Emphasis on the Latent Gene Products of EBV.Medicina (Kaunas, Lithuania) · 2022Review
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells.International journal of molecular sciences · 2022Review
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- Nasopharyngeal Carcinoma Progression: Accumulating Genomic Instability and Persistent Epstein-Barr Virus Infection.Current oncology (Toronto, Ont.) · 2022Review
- It Takes Two to Tango: A Review of Oncogenic Virus and Host Microbiome Associated Inflammation in Head and Neck Cancer.Cancers · 2022Review
- CDK4/6 inhibitors sensitize gammaherpesvirus-infected tumor cells to T-cell killing by enhancing expression of immune surface molecules.Journal of translational medicine · 2022Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Undifferentiated nasopharyngeal carcinomas (NPCs) are commonly present with latent EBV infection. However, events regulating EBV infection at early stages of the disease and the role of EBV in disease pathogenesis are largely undefined. Genetic alterations leading to activation of cyclin D1 signaling in premalignant nasopharyngeal epithelial (NPE) cells have been postulated to predispose cells to EBV infection. We previously reported that loss of p16, a negative regulator of cyclin D1 signaling, is a frequent feature of NPC tumors. Here, we report that early premalignant lesions of nasopharyngeal epithelium overexpress cyclin D1. Furthermore, overexpression of cyclin D1 is closely associated with EBV infection. Therefore we investigated the potential role of cyclin D1 overexpression in dysplastic NPE cells in vitro. In human telomerase reverse transcriptase-immortalized NPE cells, overexpression of cyclin D1 or a p16-resistant form of CDK4 (CDK4(R24C)) suppressed differentiation. This suppression may have implications for the close association of EBV infection with undifferentiated NPC. In these in vitro models, we found that cellular growth arrest and senescence occurred in EBV-infected cell populations immediately after infection. Nevertheless, overexpression of cyclin D1 or a p16-resistant form of CDK4 or knockdown of p16 in the human telomerase reverse transcriptase-immortalized NPE cell lines could counteract the EBV-induced growth arrest and senescence. We conclude that dysregulated expression of cyclin D1 in NPE cells may contribute to NPC pathogenesis by enabling persistent infection of EBV.
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