ArticleJournal of virology2002
Inactivation of both the retinoblastoma tumor suppressor and p21 by the human papillomavirus type 16 E7 oncoprotein is necessary to inhibit cell cycle arrest in human epithelial cells.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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.
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Who cites it
57 citing papers in PubMed, 114 citations in OpenAlex.
- Resolution of oncogene-induced senescence markers in HPV-infected cervical cancer tissue.BMC cancer · 2025Article
- Surgical Advancements, Immunotherapy, Targeted and Conventional Therapies, Biopsy, Colposcopy, and Pap Smear Integration in the Management of Cervical Cancer.Current medicinal chemistry · 2025Review
- Immunotherapies landscape and associated inhibitors for the treatment of cervical cancer.Medical oncology (Northwood, London, England) · 2023Review
- Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells.International journal of molecular sciences · 2022Review
- Regulation of HPV E7 Stability by E6-Associated Protein (E6AP).Journal of virology · 2022Article
- Genomic Risk Factors for Cervical Cancer.Cancers · 2021Review
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
- FNDC3B and BPGM Are Involved in Human Papillomavirus-Mediated Carcinogenesis of Cervical Cancer.Frontiers in oncology · 2021Article
- Review
- HPV Oncoproteins and the Ubiquitin Proteasome System: A Signature of Malignancy?Pathogens (Basel, Switzerland) · 2020Review
- Human Papillomavirus 16 E7 Stabilizes APOBEC3A Protein by Inhibiting Cullin 2-Dependent Protein Degradation.Journal of virology · 2018Article
- p53 controls expression of the DNA deaminase APOBEC3B to limit its potential mutagenic activity in cancer cells.Nucleic acids research · 2017Article
- HPV/E7 induces chemotherapy-mediated tumor suppression by ceramide-dependent mitophagy.EMBO molecular medicine · 2017Article
- Involvement of TP53 and TP16 expression in human papillomavirus-associated non-small cell lung cancer.Oncology letters · 2016Article
- Article
- The role of the PI3K/Akt/mTOR signalling pathway in human cancers induced by infection with human papillomaviruses.Molecular cancer · 2015Review
- p38MAPK and MK2 pathways are important for the differentiation-dependent human papillomavirus life cycle.Journal of virology · 2015Article
- Attenuated Recombinant Influenza A Virus Expressing HPV16 E6 and E7 as a Novel Therapeutic Vaccine Approach.PloS one · 2015Article
- Restoration of MAGI-1 expression in human papillomavirus-positive tumor cells induces cell growth arrest and apoptosis.Journal of virology · 2014Article
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The human papillomavirus (HPV) type 16 E7 oncoprotein must inactivate the retinoblastoma tumor suppressor (Rb) pathway to bypass G(1) arrest. However, E7 C-terminal mutants that were able to inactivate Rb were unable to bypass DNA damage-induced G(1) arrest and keratinocyte senescence, suggesting that the E7 C terminus may target additional G(1) regulators. The E7 C-terminal mutant proteins E7 CVQ68-70AAA and E7 Delta79-83 (deletion of positions 79 through 83) were further tested in several models of cell cycle arrest associated with elevated levels of p21. C-terminal mutations rendered E7 unable to induce S phase and endoreduplication in differentiated keratinocytes and rendered it less efficient in delaying senescence of human mammary epithelial cells. Interestingly, when cell cycle arrest was induced with a peptide form of p21, the E7 C-terminal mutants were deficient in overcoming arrest, whereas a mutant defective in Rb binding was competent in inhibiting G(1) arrest. These results suggest that the inactivation of both p21 and Rb by E7 contributes to subversion of cell cycle control in normal human epithelia but that neither p21 nor Rb inactivation alone is sufficient.
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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.