ArticleJournal of virology1997
Antioxidant-induced changes of the AP-1 transcription complex are paralleled by a selective suppression of human papillomavirus transcription.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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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
30 citing papers in PubMed, 98 citations in OpenAlex.
- Shared and Tissue-Specific Expression Signatures between Bone Marrow from Primary Myelofibrosis and Essential Thrombocythemia.Experimental hematology · 2019Trial
- The Role of Medical Therapies in the Management of Cervical Intraepithelial Neoplasia: A Narrative Review.Medicina (Kaunas, Lithuania) · 2025Review
- Riboflavin for women's health and emerging microbiome strategies.NPJ biofilms and microbiomes · 2024Review
- Viral Venereal Diseases of the Skin.American journal of clinical dermatology · 2021Review
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- Human Papillomavirus and Cellular Pathways: Hits and Targets.Pathogens (Basel, Switzerland) · 2021Review
- Targeting Aberrant Expression of STAT3 and AP-1 Oncogenic Transcription Factors and HPV Oncoproteins in Cervical Cancer byFrontiers in pharmacology · 2021Article
- MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors.PLoS pathogens · 2021Article
- HPV E7-mediated NCAPH ectopic expression regulates the carcinogenesis of cervical carcinoma via PI3K/AKT/SGK pathway.Cell death & disease · 2020Article
- Oxidative stress in female cancers.Oncotarget · 2018Review
- Cervical cancer stem cells manifest radioresistance: Association with upregulated AP-1 activity.Scientific reports · 2017Article
- Selective participation of c-Jun with Fra-2/c-Fos promotes aggressive tumor phenotypes and poor prognosis in tongue cancer.Scientific reports · 2015Article
- Curcumin modulates cellular AP-1, NF-kB, and HPV16 E6 proteins in oral cancer.Ecancermedicalscience · 2015Article
- Oxidative stress and HPV carcinogenesis.Viruses · 2013Review
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- Oncogenic viruses and tumor glucose metabolism: like kids in a candy store.Molecular cancer therapeutics · 2012Review
- Binding site specificity and factor redundancy in activator protein-1-driven human papillomavirus chromatin-dependent transcription.The Journal of biological chemistry · 2011Article
- Berberine modulates AP-1 activity to suppress HPV transcription and downstream signaling to induce growth arrest and apoptosis in cervical cancer cells.Molecular cancer · 2011Article
- Diametrically opposed effects of hypoxia and oxidative stress on two viral transactivators.Virology journal · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Considering the involvement of a redox-regulatory pathway in the expression of human papillomaviruses (HPVs), HPV type 16 (HPV-16)-immortalized human keratinocytes were treated with the antioxidant pyrrolidine-dithiocarbamate (PDTC). PDTC induces elevated binding of the transcription factor AP-1 to its cognate recognition site within the viral regulatory region. Despite of increased AP-1 binding, normally indispensable for efficient HPV-16 transcription, viral gene expression was selectively suppressed at the level of initiation of transcription. Electrophoretic mobility supershift assays showed that the composition of the AP-1 complex, predominantly consisting of Jun homodimers in untreated cells, was altered. Irrespective of enhanced c-fos expression, c-jun was phosphorylated and became primarily heterodimerized with fra-1, which was also induced after PDTC incubation. Additionally, there was also an increased complex formation between c-jun and junB. Because both fra-1 and junB overexpression negatively interferes with c-jun/c-fos trans-activation of AP-1-responsive genes, our results suggest that the observed block in viral transcription is mainly the consequence of an antioxidant-induced reconstitution of the AP-1 transcription complex. Since expression of the c-jun/c-fos gene family is tightly regulated during cellular differentiation, defined reorganization of a central viral transcription factor may represent a novel mechanism controlling the transcription of pathogenic HPVs during keratinocyte differentiation and in the progression to cervical cancer.
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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.