ArticleJournal of virology2014
Depletion of the cdk inhibitor p16INK4a differentially affects proliferation of established cervical carcinoma cells.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
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
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Meta-analysis of survival in patients with HNSCC discriminates risk depending on combined HPV and p16 status.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2016Pooled it
- Article
- Development and Evaluation of p16 based Double Antibody Sandwich ELISA for Detection of Cervical Precancer and Cancer.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Active enhancers strengthen insulation by RNA-mediated CTCF binding at chromatin domain boundaries.Genome research · 2023Article
- Antiproliferative and Pro-Apoptotic Effects of a Phenolic-Rich Extract fromMolecules (Basel, Switzerland) · 2022Article
- An interdependent network of functional enhancers regulates transcription and EZH2 loading at the INK4a/ARF locus.Cell reports · 2021Article
- Targeting P16INK4A in uterine serous carcinoma through inhibition of histone demethylation.Oncology reports · 2019Article
- Application of p16/Ki-67 dual-staining cytology in cervical cancers.Journal of Cancer · 2019Review
- Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer.EBioMedicine · 2016Review
- Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells.Virus genes · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledInfections with high-risk human papillomaviruses (hrHPV) contribute to cervical carcinoma. The cdk inhibitor and tumor suppressor p16INK4A is consistently upregulated in cervical carcinoma cells for reasons that are poorly understood. We report here that downregulation of p16INK4A gene expression in three different cervical carcinoma cell lines reduced expression of the E7 oncogene, suggesting a positive feedback loop involving E7 and p16INK4A. p16INK4A depletion induced cellular senescence in HeLa but not CaSki and MS-751 cervical carcinoma cells. IMPORTANCE: This study demonstrates that the cdk inhibitor p16INK4A, frequently used as surrogate marker for transforming infections by human papillomaviruses of the high-risk group, is required for high-level expression of the E7 oncoproteins of HPV-16, HPV-18, and HPV-45 in cervical carcinoma cells. It is also demonstrated that depletion of p16INK4A induces senescence in HeLa but not CaSki or MS-751 cervical carcinoma cells.
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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.