ArticleOncogene2002
Identification of a novel activity of human papillomavirus type 16 E6 protein in deregulating the G1/S transition.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- MAGT1 is required for HeLa cell proliferation through regulating p21 expression, S-phase progress, and ERK/p38 MAPK MYC axis.Cell cycle (Georgetown, Tex.) · 2021Article
- Relevance of Human Papillomaviruses in Head and Neck Cancer-What Remains in 2021 from a Clinician's Point of View?Viruses · 2021Review
- HPV16-LINC00393 Integration Alters Local 3D Genome Architecture in Cervical Cancer Cells.Frontiers in cellular and infection microbiology · 2021Article
- PDZ Domain-Containing Protein NHERF-2 Is a Novel Target of Human Papillomavirus 16 (HPV-16) and HPV-18.Journal of virology · 2019Article
- In vitro 3-dimensional tumor model for radiosensitivity of HPV positive OSCC cell lines.Cancer biology & therapy · 2015Article
- Article
- Restoration of tumor suppressor p53 by differentially regulating pro- and anti-p53 networks in HPV-18-infected cervical cancer cells.Oncogene · 2012Article
- RNA interference for the treatment of papillomavirus disease.The open virology journal · 2012Article
- Review
- HPV infection and p53 inactivation in pterygium.Molecular vision · 2009Article
- Identification of inhibitors to papillomavirus type 16 E6 protein based on three-dimensional structures of interacting proteins.Antiviral research · 2006Article
- Skin hyperproliferation and susceptibility to chemical carcinogenesis in transgenic mice expressing E6 and E7 of human papillomavirus type 38.Journal of virology · 2005Article
- Human papillomavirus type 16 E6 promotes retinoblastoma protein phosphorylation and cell cycle progression.Journal of virology · 2004Article
- Article
- Human papillomavirus type 16 E6 activates TERT gene transcription through induction of c-Myc and release of USF-mediated repression.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we show that E6 of human papillomavirus has the ability to deregulate the cell cycle G1/S transition. In rodent immortalized fibroblasts (NIH3T3) serum deprivation or over-expression of the cyclin-dependent kinase inhibitors, p16(INK4a) or p27(KIP1), leads to G1 cell cycle arrest. HPV16 E6 overcomes the antiproliferative signals, gaining the ability to drive serum-deprived and p16(INK4a) or p27(KIP1) over-expressing cells into S phase. E6 protein from the benign HPV type 1 displays a similar activity to HPV16 E6 to deregulate the G1/S transition. Thus, this activity appears to be conserved between E6 proteins from non-oncogenic and oncogenic HPV types. Furthermore, we show that HPV16 E6 is not able to circumvent a G1 arrest imposed by pRb mutant in which all CDK phosphorylation sites have been mutated. These data indicate that the viral protein acts upstream of pRb and its mechanism in promoting cell cycle progression is dependent on pRb phosphorylation. In summary, this study describes a novel biological function of HPV E6 and shows that the S phase entry, required for viral DNA replication, is not exclusively controlled by E7, but that E6 also is involved in this event.
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