ArticleOncogene2003
Transcription-independent triggering of the extrinsic pathway of apoptosis by human papillomavirus 18 E2 protein.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Who cites it
32 citing papers in PubMed, 80 citations in OpenAlex.
- Development of human papillomavirus and its detection methods (Review).Experimental and therapeutic medicine · 2024Review
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs.Nucleic acids research · 2022Article
- Cell death in head and neck cancer pathogenesis and treatment.Cell death & disease · 2021Review
- TIP60 represses telomerase expression by inhibiting Sp1 binding to the TERT promoter.PLoS pathogens · 2017Article
- HPV16-E2 protein modifies self-renewal and differentiation rate in progenitor cells of human immortalized keratinocytes.Virology journal · 2017Article
- The Replicative Consequences of Papillomavirus E2 Protein Binding to the Origin Replication Factor ORC2.PLoS pathogens · 2016Article
- Insights into the mechanism of human papillomavirus E2-induced procaspase-8 activation and cell death.Scientific reports · 2016Article
- Preclinical studies identify non-apoptotic low-level caspase-3 as therapeutic target in pemphigus vulgaris.PloS one · 2015Article
- Genome-wide analysis of high risk human papillomavirus E2 proteins in human primary keratinocytes.Genomics data · 2014Article
- E2 proteins of high risk human papillomaviruses down-modulate STING and IFN-κ transcription in keratinocytes.PloS one · 2014Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Localization of HPV-18 E2 at mitochondrial membranes induces ROS release and modulates host cell metabolism.PloS one · 2013Article
- Modulation of apoptotic pathways by human papillomaviruses (HPV): mechanisms and implications for therapy.Viruses · 2012Review
- Type-specific interaction between human papillomavirus type 58 E2 protein and E7 protein inhibits E7-mediated oncogenicity.The Journal of general virology · 2012Article
- Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development.Journal of oncology · 2012Article
- Oncolytic adenovirus armed with human papillomavirus E2 gene in combination with radiation demonstrates synergistic enhancements of antitumor efficacy.Cancer gene therapy · 2011Article
- The human papillomavirus E6 oncogene represses a cell adhesion pathway and disrupts focal adhesion through degradation of TAp63β upon transformation.PLoS pathogens · 2011Article
- HPV16 E2 could act as down-regulator in cellular genes implicated in apoptosis, proliferation and cell differentiation.Virology journal · 2011Article
- Growth inhibition of HeLa cells is a conserved feature of high-risk human papillomavirus E8^E2C proteins and can also be achieved by an artificial repressor protein.Journal of virology · 2011Article
- Expression of the HPV11 E2 gene in transgenic mice does not result in alterations of the phenotypic pattern.Transgenic research · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical carcinomas are most frequently associated with human papillomaviruses (HPV), whose E6 and E7 oncogenes products induce cellular immortalization. The papillomavirus E2 protein is a transcription factor, which represses the expression of the viral oncogenes, and activates viral DNA replication during the vegetative viral cycle. This protein is specifically inactivated in HPV18-associated carcinoma cells, suggesting that E2 functions prevent carcinogenic progression. Indeed, ectopic expression of E2 in cervical carcinoma cells strongly inhibits cell proliferation. Here we show that above a threshold level of expression, the E2 protein induces apoptosis, independently of other viral functions. The amino-terminal domain is responsible for this apoptotic activity, but surprisingly with no involvement of its transcriptional functions. The death pathway triggered by E2 relies on activation of the initiator caspase 8, specific of the extrinsic pathway of apoptosis. E2 itself is cleaved by caspases during cell death, providing an example of an apoptotic inducer that is itself a target for caspase processing. The autonomous proapoptotic activity of HPV18 E2 described here may counteract the proliferative functions of viral oncogenes, and renders the inactivation of E2 crucial for carcinogenic progression.
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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.