ArticleJournal of virology2001
Papillomavirus type 16 oncogenes downregulate expression of interferon-responsive genes and upregulate proliferation-associated and NF-kappaB-responsive genes in cervical keratinocytes.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.
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Who cites it
169 citing papers in PubMed, 1 synthesis or guideline pooled it, 387 citations in OpenAlex.
- Impact of Human Papillomavirus on microRNA-21 Expression in Oral and Oropharyngeal Cancer-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Post-translational control of IL-1β via the human papillomavirus type 16 E6 oncoprotein: a novel mechanism of innate immune escape mediated by the E3-ubiquitin ligase E6-AP and p53.PLoS pathogens · 2013Trial
- The interplay between HPV, vaginal microbiota and host immunity in cervical carcinogenesis.Discover oncology · 2026Review
- The Exploration of Therapeutic Antivirals for Human Papillomavirus in the Last 40 Years: Bibliometric Research.Pathogens (Basel, Switzerland) · 2026Article
- An Overview of the Mechanisms of HPV-Induced Cervical Cancer: The Role of Kinase Targets in Pathogenesis and Drug Resistance.Cancers · 2026Review
- Role of hypoxia-inducible factor - 1 alpha on the progression of cervical intraepithelial neoplasia and cervical cancer: a narrative review.Frontiers in oncology · 2026Review
- Regulation of Energy Metabolism and Lipid Metabolites by IMP3 in Cervical Cancer.Current issues in molecular biology · 2025Article
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- New evidence for miRNA testing in head and neck squamous cell cancer patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Observational
- NF-κB Activation Is Essential for Cervical Cell Proliferation and Malignant Transformation.International journal of molecular sciences · 2025Article
- Uncoupling protein 2 and signal transducer and activator of transcription 1 are targets of human papillomavirus oncoproteins and may be prognostic markers for cervical cancer development.Frontiers in oncology · 2025Article
- Repression of CADM1 transcription by HPV type 18 is mediated by three-dimensional rearrangement of promoter-enhancer interactions.PLoS pathogens · 2025Article
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- Human papillomavirus E2 proteins suppress innate antiviral signaling pathways.Frontiers in immunology · 2025Article
- The roles of DNA damage repair and innate immune surveillance pathways in HPV pathogenesis.Virology · 2024Review
- Repurposing of sericin combined with dactolisib or vitamin D to combat non-small lung cancer cells through computational and biological investigations.Scientific reports · 2024Article
- The immune microenvironment of cancer of the uterine cervix.Histology and histopathology · 2024Review
- Transcriptome and microbiome-immune changes across preinvasive and invasive anal cancer lesions.JCI insight · 2024Article
- Identification and Functional Implications of the E5 Oncogene Polymorphisms of Human Papillomavirus Type 16.Tropical medicine and infectious disease · 2024Article
109 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with high-risk human papillomaviruses (HPV) is a major risk factor for development of cervical cancer. Expression of the HPV E6 and E7 oncoproteins increases in differentiating keratinocytes, resulting in inactivation of the p53 and retinoblastoma proteins, two important transcriptional regulators. We used cDNA microarrays to examine global alterations in gene expression in differentiating cervical keratinocytes after infection with retroviruses encoding HPV type 16 (HPV-16) E6 and E7. Expression of 80 cellular genes (approximately 4% of the genes on the array) was altered reproducibly by E6 and/or E7. Cluster analysis classified these genes into three functional groups: (i) interferon (IFN)-responsive genes, (ii) genes stimulated by NF-kappaB, and (iii) genes regulated in cell cycle progression and DNA synthesis. HPV-16 E6 or a dominant negative p53 protein downregulated multiple IFN-responsive genes. E6 decreased expression of IFN-alpha and -beta, downregulated nuclear STAT-1 protein, and decreased binding of STAT-1 to the IFN-stimulated response element. E7 alone was less effective; however, coexpression of E6 and E7 downregulated IFN-responsive genes more efficiently than E6. The HPV-16 E6 protein also stimulated expression of multiple genes known to be inducible by NF-kappaB and AP-1. E6 enhanced expression of functional components of the NF-kappaB signal pathway, including p50, NIK, and TRAF-interacting protein, and increased binding to NF-kappaB and AP-1 DNA consensus binding sites. Secretion of interleukin-8, RANTES, macrophage inflammatory protein 1alpha, and 10-kappaDa IFN-gamma-inducible protein were increased in differentiating keratinocytes by E6. Thus, high-level expression of the HPV-16 E6 protein in differentiating keratinocytes directly alters expression of genes that influence host resistance to infection and immune function.
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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.