ArticlemSphere2020
Human Papillomavirus 16 E6 and E7 Synergistically Repress Innate Immune Gene Transcription.
Article in mSphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Article
- Silencing HPV: the rise of RNA therapeutics in cervical cancer.Infectious agents and cancer · 2026Review
- Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026Review
- Innate immune recognition and microenvironmental reprogramming in HPV-induced cervical cancer: from pattern recognition receptor activation to immune tolerance disruption.Frontiers in cellular and infection microbiology · 2026Review
- New mouse model based on adenocarcinoma 4T1 cells expressing HPV16 E6 and E7 applied to assess the efficacy of therapeutic and prophylactic E6/E7-based HPV16 vaccines.Infectious agents and cancer · 2025Article
- HPV16 E7 inhibits HBD2 expression by down-regulation of ASK1-p38 MAPK pathway in cervical cancer.Virology journal · 2025Article
- Variable Expression of Oncogene-Induced Senescence/SASP Surrogates in HPV-Associated Precancerous Cervical Tissue.Current issues in molecular biology · 2024Article
- Fibroblast stromal support model for predicting human papillomavirus-associated cancer drug responses.Journal of virology · 2024Article
- Fibroblasts Regulate the Transformation Potential of Human Papillomavirus-positive Keratinocytes.bioRxiv : the preprint server for biology · 2024Article
- Human papillomavirus 16 replication converts SAMHD1 into a homologous recombination factor and promotes its recruitment to replicating viral DNA.Journal of virology · 2024Article
- HPV E6/E7: insights into their regulatory role and mechanism in signaling pathways in HPV-associated tumor.Cancer gene therapy · 2024Review
- Global transcriptomic network analysis of the crosstalk between microbiota and cancer-related cells in the oral-gut-lung axis.Frontiers in cellular and infection microbiology · 2024Article
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- Human Papillomavirus Genome Copy Number Is Maintained by S-Phase Amplification, Genome Loss to the Cytosol during Mitosis, and Degradation in GJournal of virology · 2023Article
- Exploring the Bioactive Mycocompounds (Fungal Compounds) of Selected Medicinal Mushrooms and Their Potentials against HPV Infection and Associated Cancer in Humans.Life (Basel, Switzerland) · 2023Review
- Human papillomavirus 16 E2 blocks cellular senescence in response to activation of the DNA damage response.Virology · 2022Article
- HPV E6 regulates therapy responses in oropharyngeal cancer by repressing the PGC-1α/ERRα axis.JCI insight · 2022Article
- LOXL2 small molecule inhibitor restrains malignant transformation of cervical cancer cells by repressingCell cycle (Georgetown, Tex.) · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Human papillomaviruses (HPV) are causative agents in 5% of all cancers, including the majority of anogenital and oropharyngeal cancers. Downregulation of innate immune genes (IIGs) by HPV to promote the viral life cycle is well documented; E6 and E7 are known repressors of these genes. More recently, we demonstrated that E2 could also repress IIGs. These studies have been carried out in cells overexpressing the viral proteins, and to further investigate the role of individual viral proteins in this repression, we introduced stop codons into E6 and/or E7 in the entire HPV16 genome and generated N/Tert-1 cells stably maintaining the HPV16 genomes. We demonstrate that E6 or E7 individually is not sufficient to repress IIG expression in the context of the entire HPV16 genome; both are required for a synergistic repression. The DNA damage response (DDR) is activated by HPV16 irrespective of E6 and E7 expression, presumably due to viral replication; E1 is a known activator of the DDR. In addition, replication stress was apparent in HPV16-positive cells lacking E6 and E7, manifested by attenuated cellular growth and activation of replication stress genes. These studies led us to the following model. Viral replication
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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.