ArticleThe Journal of pathology2009
RNA splicing factors regulated by HPV16 during cervical tumour progression.
Article in The Journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 76 citations in OpenAlex.
- Review
- HPV-driven transcriptome and splicing rewiring under SRPK1 inhibition in cervical cancer.Frontiers in oncology · 2025Article
- PRMT1 Modulates Alternative Splicing to Enhance HPV18 mRNA Stability and Promote the Establishment of Infection.bioRxiv : the preprint server for biology · 2024Article
- Long noncoding RNA MALAT-1: A versatile regulator in cancer progression, metastasis, immunity, and therapeutic resistance.Non-coding RNA research · 2024Review
- Review
- Multidimensional outlook on the pathophysiology of cervical cancer invasion and metastasis.Molecular and cellular biochemistry · 2023Review
- Network modeling suggests HIV infection phenocopies PI3K-AKT pathway mutations to enhance HPV-associated cervical cancer.Molecular omics · 2023Article
- Characterization of 3D organotypic epithelial tissues reveals tonsil-specific differences in tonic interferon signaling.bioRxiv : the preprint server for biology · 2023Article
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- Characterization of 3D organotypic epithelial tissues reveals tonsil-specific differences in tonic interferon signaling.PloS one · 2023Article
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention.Nucleic acids research · 2022Article
- Identification of heterogenous nuclear ribonucleoproteins (hnRNPs) and serine- and arginine-rich (SR) proteins that induce human papillomavirus type 16 late gene expression and alter L1 mRNA splicing.Archives of virology · 2022Article
- Association of Long Non-Coding RNAs (lncRNAs)Pharmacogenomics and personalized medicine · 2022Article
- The chromatin insulator CTCF regulates HPV18 transcript splicing and differentiation-dependent late gene expression.PLoS pathogens · 2021Article
- Heterogeneous Nuclear Ribonucleoprotein A1 (hnRNP A1) and hnRNP A2 Inhibit Splicing to Human Papillomavirus 16 Splice Site SA409 through a UAG-Containing Sequence in the E7 Coding Region.Journal of virology · 2020Article
- Human papillomavirus type 16 infection activates the host serine arginine protein kinase 1 (SRPK1) - splicing factor axis.The Journal of general virology · 2020Article
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer.Frontiers in oncology · 2020Review
- 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
- Viral modulation of cellular RNA alternative splicing: A new key player in virus-host interactions?Wiley interdisciplinary reviews. RNA · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The most prevalent human papillomaviruses (HPVs) causing cervical disease are the 'high-risk' HPV types 16 and 18. All papillomaviruses express a transcription factor, E2, that can regulate viral and cellular gene expression. Recently, we demonstrated high-risk HPV E2-mediated transcriptional transactivation of SF2/ASF. This essential oncoprotein is a key member of a family of proteins, the SR proteins, that regulate constitutive and alternative splicing. Tight control of RNA splicing is necessary for the production of wild-type proteins. So, aberrant expression of SR proteins is involved in the aetiology of a range of human diseases, including cancer. Here we demonstrate epithelial differentiation-specific control of SF2/ASF in HPV16-infected keratinocytes in organotypic raft culture and in low-grade cervical lesions (CIN1). Further, we demonstrate HPV16 infection/differentiation-induced up-regulation of a specific subset of SR proteins and present evidence that HPV16 E2 controls expression of SRp20, SC35 and SRp75. Using a series of cell lines that model cervical tumour progression, we show that SF2/ASF, SRp20 and SC35 are specifically up-regulated in a model of cervical tumour progression. These SR proteins are also over-expressed in high-grade cervical lesions, indicating that they may all have oncogenic functions. SR proteins could be useful biomarkers for HPV-associated disease.
Indexed as
Identifiers
What OpenQuestion holds
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.