ArticleFrontiers in immunology2019
E6/E7 and E6
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- Role of soluble human leukocyte antigen-G in virus-associated cancers: A focused minireview.World journal of virology · 2026Review
- A Dusty Affair: SIRT1-S682 Modulation Orchestrates ERK-FN1-p38-NF-κB Signaling and Composite-Dependent IL-8 Responses in Gingival Keratinocytes Exposed to Dental Dust and Eluates.Journal of functional biomaterials · 2026Article
- Article
- The impact of gut microbiota on cervical cancer and precancerous lesions: neglected status, mechanisms, challenges, and a call to action.Frontiers in immunology · 2026Review
- Anthracycline Treatments and the Presence of Tumor Cells Synergistically Modify the Composition of Macrophage Subpopulations in the Co-Culture System.International journal of molecular sciences · 2025Article
- Predictive and prognostic value of inflammatory factors (IL-6, IL-8, and TNF-α) in saliva for radiotherapy response in patients with HPV-associated oropharyngeal squamous cell carcinoma.Discover oncology · 2025Article
- Article
- Human papillomavirus infection and vaccination with thyroid diseases: mechanistic links and immunological insights.Frontiers in immunology · 2025Review
- ELF3 Overexpression Contributes to the Malignant Transformation of HPV16 E6/E7-Immortalized Keratinocytes by Promoting CCNE2 Expression.Journal of microbiology and biotechnology · 2024Article
- The prevalence of HPV in Chongqing, China from 2017 to 2022: a retrospective cohort study.Scientific reports · 2024Article
- Transcriptomic profiling of peripheral blood cells in HPV-associated carcinoma patients receiving combined valproic acid and avelumab.Molecular oncology · 2024Article
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Cervical HPV infection and related diseases among 149,559 women in Fujian: an epidemiological study from 2018 to 2023.Frontiers in microbiology · 2024Article
- Interplay between reactive oxygen species and ERK activation in cervical cancer cells.Frontiers in cell and developmental biology · 2024Article
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- The Value of CXCL1, CXCL2, CXCL3, and CXCL8 as Potential Prognosis Markers in Cervical Cancer: Evidence of E6/E7 from HPV16 and 18 in Chemokines Regulation.Biomedicines · 2023Article
- Advancing Immunotherapies for HPV-Related Cancers: Exploring Novel Vaccine Strategies and the Influence of Tumor Microenvironment.Vaccines · 2023Review
- Herpes Simplex Virus, Human Papillomavirus, and Cervical Cancer: Overview, Relationship, and Treatment Implications.Cancers · 2023Review
- Splicing Characterization and Isoform Switch Events in Human Keratinocytes Carrying Oncogenes from High-Risk HPV-16 and Low-Risk HPV-84.International journal of molecular sciences · 2023Article
- Network Pharmacology Combined with an Experimental Validation Study to Reveal the Effect and Mechanism ofFoods (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keratinocyte infection with high-risk human papillomavirus genotypes has been linked to cancer development. In cervix, the alpha HPV16 and HPV18 have been reported as the mayor causative agents of cervical cancer. Oncogenic progression and chronic inflammation are closely related processes, with IL-6 as one of the main pro-inflammatory cytokines involved. However, there are limited studies about the regulation of IL-6 by low and high risk HPVs and the HPV proteins implicated in this modulation. In this work, we report the overexpression of IL-6 in HPV infected cervical cancer derived cell lines (HeLa and SiHa) compared to non-tumorigenic keratinocytes (HaCaT), and in Cervical Intraepithelial Neoplasia grade 1 HPV16 and HPV18 positive cervical samples compared to HPV negative samples without lesions. Moreover, we generated HaCaT keratinocytes that express E5, E6, and E7 from high risk (16 or 18) or low risk (62 and 84) HPVs. E5 proteins do not modify IL-6 expression, while E7 modestly increase it. Interestingly, E6 proteins in HaCaT cells upregulate IL-6 mRNA expression and protein secretion. Indeed, in HaCaT cells that express high risk HPV16E6 or HPV18E6 proteins, only the truncated E6
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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.