ArticleScientific reports2019
Comparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- High-risk HPV E6 induces an aneuploidy-prone chromosome congression defect through destabilization of CENP-E.Journal of virology · 2026Article
- Cholesterol Metabolism: An Ally in the Development and Progression of Cervical Cancer.International journal of molecular sciences · 2026Review
- Splicing of HPV16 E6 promotes aggressive invasion in oropharyngeal cancer via endocytosis of E-cadherin.bioRxiv : the preprint server for biology · 2025Article
- 'Nelfinavir sensitizes a clinically relevant chemo-radioresistant cervical cancerBiochemistry and biophysics reports · 2025Article
- Analysis of Expression and Regulation of AKR1C2 in HPV-Positive and -Negative Oropharyngeal Squamous Cell Carcinoma.Cancers · 2024Article
- Structure and transcription of integrated HPV DNA in vulvar carcinomas.NPJ genomic medicine · 2024Article
- Article
- HPV E6/E7: insights into their regulatory role and mechanism in signaling pathways in HPV-associated tumor.Cancer gene therapy · 2024Review
- Upregulation of HPV16E1 and E7 expression and FOXO3a mRNA downregulation in high-grade cervical neoplasia.PeerJ · 2024Article
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Human papillomavirus E6/E7 oncoproteins promote radiotherapy-mediated tumor suppression by globally hijacking host DNA damage repair.Theranostics · 2023Article
- Article
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Repurposing the Hybrid Capture 2 (HC2) screening test for whole-genome sequencing of human papillomaviruses.Archives of virology · 2021Article
- EGFR Protein Expression Relates with Tumor Histology, Methylation Status of EGFR and HPV16 E6 Viral Load in Oropharyngeal Carcinoma.Head and neck pathology · 2021Article
- Causes and Consequences of HPV Integration in Head and Neck Squamous Cell Carcinomas: State of the Art.Cancers · 2021Review
- The exon junction complex core factor eIF4A3 is a key regulator of HPV16 gene expression.Bioscience reports · 2021Article
- The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk Human Papillomavirus infections are responsible for anogenital and oropharyngeal cancers. Alternative splicing is an important mechanism controlling HPV16 gene expression. Modulation in the splice pattern leads to polycistronic HPV16 early transcripts encoding a full length E6 oncoprotein or truncated E6 proteins, commonly named E6*. Spliced E6*I transcripts are the most abundant RNAs produced in HPV-related cancers. To date, the biological function of the E6*I isoform remains controversial. In this study, we identified, by RNA sequencing, cellular targets deregulated by E6*I, among which genes related to ROS metabolism. Concomitantly, E6*I-overexpressing cells display high levels of ROS. However, co-overexpression of both E6 and E6*I has no effect on ROS production. In HPV16-infected cells expressing different E6/E6*I levels, we show that the newly identified targets CCL2 and RAC2 are increased by E6*I but decreased by E6 expression, suggesting that E6 abrogates the effect of E6*I. Taken together, these data support the idea that E6*I acts independently of E6 to increase ROS production and that E6 has the ability to counteract the effects of E6*I. This asks the question of how E6*I can be considered separately of E6 in the natural history of HPV16 infection.
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