ArticleJournal of virology2000
Mechanisms of human papillomavirus E2-mediated repression of viral oncogene expression and cervical cancer cell growth inhibition.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed.
- Role of Oncoviruses in Cancer Progression and Emerging Phytochemical-Based Therapies from Medicinal Plants.Molecular biotechnology · 2026Review
- HPV Integration in Head and Neck Cancer: Downstream Splicing Events and Expression Ratios Linked with Poor Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- The Natural History of Cervical Cancer and the Case for MicroRNAs: Is Human Papillomavirus Infection the Whole Story?International journal of molecular sciences · 2024Review
- Senataxin mediates R-loop resolution on HPV episomes.Journal of virology · 2024Article
- The role of HR-HPV integration in the progression of premalignant lesions into different cancer types.Heliyon · 2024Review
- Review
- Unraveling the Complex Nexus of Human Papillomavirus (HPV) in Extragenital Keratinocyte Skin Tumors: A Comprehensive Analysis of Bowen's Disease and In Situ Squamous-Cell Carcinoma.Journal of clinical medicine · 2024Article
- Focal Adhesion Kinase Binds to the HPV E2 Protein to Regulate Initial Replication after Infection.Pathogens (Basel, Switzerland) · 2023Article
- Protein-DNA Interactions Regulate Human Papillomavirus DNA Replication, Transcription, and Oncogenesis.International journal of molecular sciences · 2023Review
- The complexity of human papilloma virus in cancers: a narrative review.Infectious agents and cancer · 2023Review
- SETD6 Regulates E2-Dependent Human Papillomavirus Transcription.Journal of virology · 2022Article
- Review
- Potential role of human papillomavirus proteins associated with the development of cancer.Virusdisease · 2022Review
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs.Nucleic acids research · 2022Article
- Article
- Integration sites of human papillomavirus 18 in esophageal cancer samples.Oncology letters · 2018Article
- Genotype-specific methylation of HPV in cervical intraepithelial neoplasia.Journal of gynecologic oncology · 2017Article
- Article
- Mate-Pair Sequencing as a Powerful Clinical Tool for the Characterization of Cancers with a DNA Viral Etiology.Viruses · 2015Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The papillomavirus E2 gene product plays a pivotal role in viral replication. E2 has multiple functions, including (i) transcriptional activation and repression of viral promoters and (ii) the enhancement of viral DNA replication. It was previously reported that E2 suppressed the growth of papillomavirus-positive cervical carcinoma cell lines. In the present study, we investigated the mechanisms of E2 growth inhibition. We found that the transcriptional activation function of E2 is required for inhibition of the growth of HeLa cells as well as for transcriptional repression of the viral E6/E7 promoter. It had been previously postulated that transcriptional repression of the E6/E7 promoter results from E2 binding its cognate sites proximal to the E6/E7 promoter and displacing other cellular transcriptional factors. In this study, we report a requirement for the transcription activation function for the binding of E2 to transcriptionally active templates.
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Registered trials
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