ArticleJournal of virology2003
Human papillomavirus type 16 E2 protein has no effect on transcription from episomal viral DNA.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 118 citations in OpenAlex.
- Investigation of molecular mechanisms underlying JAK/STAT signaling pathway in HPV-induced cervical carcinogenesis using 'omics' approach.Medical oncology (Northwood, London, England) · 2022Article
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Co-Delivery ofFrontiers in pharmacology · 2022Article
- The Involvement of Natural Polyphenols in the Chemoprevention of Cervical Cancer.International journal of molecular sciences · 2021Review
- MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors.PLoS pathogens · 2021Article
- E7-Targeted Nanotherapeutics for Key HPV Afflicted Cervical Lesions by Employing CRISPR/Cas9 and Poly (Beta-Amino Ester).International journal of nanomedicine · 2021Article
- Molecular pathways in the development of HPV-induced cervical cancer.EXCLI journal · 2021Review
- Differences in Stability of Viral and Viral-Cellular Fusion Transcripts in HPV-Induced Cervical Cancers.International journal of molecular sciences · 2019Article
- Carbon-ion irradiation overcomes HPV-integration/E2 gene-disruption induced radioresistance of cervical keratinocytes.Journal of radiation research · 2019Article
- Serum bradykinin levels as a diagnostic marker in cervical cancer with a potential mechanism to promote VEGF expression via BDKRB2.International journal of oncology · 2019Article
- The function of histone acetylation in cervical cancer development.Bioscience reports · 2019Review
- HPV16 viral characteristics in primary, recurrent and metastatic vulvar carcinoma.Papillomavirus research (Amsterdam, Netherlands) · 2018Article
- Nanoparticles Based on Poly (β-Amino Ester) and HPV16-Targeting CRISPR/shRNA as Potential Drugs for HPV16-Related Cervical Malignancy.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Targeting Head and Neck Cancer by Vaccination.Frontiers in immunology · 2018Review
- Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift?Viruses · 2017Review
- Article
- Extrachromosomal HPV-16 LCR transcriptional activation by HDACi opposed by cellular differentiation and DNA integration.Oncotarget · 2016Article
- Article
- Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human papillomavirus (HPV) E2 protein plays an important role in viral DNA replication. Many studies with high-risk HPVs have demonstrated that the E2 protein can also repress transcription of the E6 and E7 oncogenes. This conclusion, based on experiments carried out with cervical cancer cells bearing integrated HPV genomes, is currently assumed to be applicable to the normal HPV life cycle, in which the viral genomes are episomal. Here, we have tested experimentally whether this assumption is correct. We made use of a pair of isogenic cell lines, W12 and S12. W12 cells contain episomal HPV16 genomes, whereas S12 cells, which are derived from the W12 line, contain HPV DNA as integrated copies. When we expressed E2 in S12 cells, we observed strong repression of E6 and E7 transcription. In contrast, no effect of E2 on the transcription of these genes was detected in W12 cells. While integration of the viral genome into the host DNA contributes to the difference between W12 and S12 cells, integration by itself is not sufficient to explain this difference. Instead, the chromatin structure in the region of the E6 and E7 promoter (p97), which we show to be very different in these two cell lines, is likely to be the cause of the different responsiveness of p97 to the E2 protein. Experiments with the histone deacetylase inhibitor trichostatin A (TSA) indicated that the episomal HPV16 DNA is in a relatively inaccessible state prior to TSA treatment. Our results, together with those of others, suggest that any effect of the E2 protein on the expression of the E6 and E7 genes during the normal viral life cycle is of secondary importance compared to the function of E2 in 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.