ArticleCancers2022
HPV16 E7 Nucleotide Variants Found in Cancer-Free Subjects Affect E7 Protein Expression and Transformation.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Longitudinal analysis of high-risk HPV infections reveals within-host viral genome changes over time.PLoS pathogens · 2026Article
- Characterization of patient-derived HPV16 E6 and E7 variant alleles.Journal of virology · 2026Article
- Genetic Diversity of Selected High-Risk HPV Types Prevalent in Africa and Not Covered by Current Vaccines: A Pooled Sequence Data Analysis.International journal of molecular sciences · 2025Article
- Designing a Multi-Epitope Vaccine Against HPV 16, 18, 33, and 45 Targeting L1 and E7 Proteins: An Immunoinformatics Approach for Cervical Cancer Prevention and Therapy.Bioinformatics and biology insights · 2025Article
- Emerging trends and hotspots in cervical intraepithelial neoplasia research from 2013 to 2023: A bibliometric analysis.Heliyon · 2024Article
- Recombinant adenoviruses expressing HPV16/18 E7 upregulate the HDAC6 and DNMT3B genes in C33A cells.Frontiers in cellular and infection microbiology · 2024Article
- Editorial: The association between viral infection and human cancers.Frontiers in microbiology · 2024Article
- Human papillomaviruses: Knowns, mysteries, and unchartered territories.Journal of medical virology · 2023Review
- E7 Oncogene HPV58 Variants Detected in Northeast Brazil: Genetic and Functional Analysis.Microorganisms · 2023Article
- A replicative recombinant HPV16 E7 expression virus upregulates CD36 in C33A cells.Frontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The human papillomavirus (HPV) type 16 E7 oncogene is critical to carcinogenesis and highly conserved. Previous studies identified a preponderance of non-synonymous E7 variants amongst HPV16-positive cancer-free controls compared to those with cervical cancer. To investigate the function of E7 variants, we constructed full-length HPV16 E7 genes and tested variants at positions H9R, D21N, N29S, E33K, T56I, D62N, S63F, S63P, T64M, E80K, D81N, P92L, and P92S (found only in controls); D14E, N29H cervical intraepithelial neoplasia (CIN2), and P6L, H51N, R77S (CIN3). We determined the steady-state level of cytoplasmic and nuclear HPV16 E7 protein. All variants from controls showed a reduced level of E7 protein, with 7/13 variants having lower protein levels. In contrast, 2/3 variants from the CIN3 precancer group had near-wild type E7 levels. We assayed the activity of representative variants in stably transfected NIH3T3 cells. The H9R, E33K, P92L, and P92S variants found in control subjects had lower transforming activity than D14E and N29H variants (CIN2), and the R77S (CIN3) had activity only slightly reduced from wild-type E7. In addition, R77S and WT E7 caused increased migration of NIH3T3 cells in a wound-healing assay compared with H9R, E33K, P92L, and P92S (controls) and D14E (CIN2). These data provide evidence that the E7 variants found in HPV16-positive cancer-free women are partially defective for transformation and cell migration, further demonstrating the importance of fully active E7 in cancer development.
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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.