ArticleThe EMBO journal2000
Papillomavirus E2 induces senescence in HPV-positive cells via pRB- and p21(CIP)-dependent pathways.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed.
- Disruption of Human Papillomavirus 16 E6/E7 Genes Using All-in-One Adenovirus Vectors Expressing Eight Double-Nicking Guide RNAs.International journal of molecular sciences · 2025Article
- Structural and functional roles of conserved residues of human papillomavirus (HPV) E2 protein and biological consequences.Virology journal · 2025Article
- Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells.Journal of medical virology · 2025Article
- Hypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.Journal of medical virology · 2025Article
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- Resolution of oncogene-induced senescence markers in HPV-infected cervical cancer tissue.BMC cancer · 2025Article
- Variable Expression of Oncogene-Induced Senescence/SASP Surrogates in HPV-Associated Precancerous Cervical Tissue.Current issues in molecular biology · 2024Article
- Article
- Human Papillomavirus Infection in Penile Cancer: Multidimensional Mechanisms and Vaccine Strategies.International journal of molecular sciences · 2023Review
- Topical Protease Inhibitor Decreases Anal Carcinogenesis in a Transgenic Mouse Model of HPV Anal Disease.Viruses · 2023Article
- Network-informed discovery of multidrug combinations for ERα+/HER2-/PI3Kα-mutant breast cancer.Cellular and molecular life sciences : CMLS · 2023Article
- Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells.International journal of molecular sciences · 2022Review
- HPV16 E7 Nucleotide Variants Found in Cancer-Free Subjects Affect E7 Protein Expression and Transformation.Cancers · 2022Article
- Identification of MicroRNAs That Stabilize p53 in Human Papillomavirus-Positive Cancer Cells.Journal of virology · 2022Article
- Delineating the Switch between Senescence and Apoptosis in Cervical Cancer Cells under Ciclopirox Treatment.Cancers · 2021Article
- Article
- The Role of Senescent Cells in Acquired Drug Resistance and Secondary Cancer in BRAFi-Treated Melanoma.Cancers · 2021Review
- HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins.Cancers · 2021Article
- PI3K/AKT/mTOR Signaling Regulates the Virus/Host Cell Crosstalk in HPV-Positive Cervical Cancer Cells.International journal of molecular sciences · 2019Review
- Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
A hallmark of human papillomavirus (HPV) associated carcinogenesis is the integration of the viral DNA into the cellular genome, usually accompanied by the loss of expression of the viral E2 gene. E2 binds to and represses the viral promoter directing expression of the E6 and E7 oncogenes. The re-introduction and expression of exogenous E2 in HPV-positive cancer cells results in cellular growth arrest, while growth in the context of exogenous E2 can be restored through the expression of exogenous E6 and E7. Here we examine the individual contributions of the viral E6 and E7 genes to this phenotype. E6 alone displays moderate activity, whereas both E7 and adenovirus E1A display high activity in reversing E2-mediated cellular growth suppression. Using defined mutants of E7 and E1A, we show that an intact retinoblastoma interaction domain is required for this function. In addition, we show that the E2-mediated growth arrest of HPV-positive cells results in cellular senescence, and implicate the cyclin/cdk inhibitor p21(CIP) as a downstream E2 effector in this phenotype.
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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.