ArticleCancer research2012
Inactivating all three rb family pocket proteins is insufficient to initiate cervical cancer.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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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
28 citing papers in PubMed, 37 citations in OpenAlex.
- The R2TP complex stabilises E7 to drive human papillomavirus-mediated pathogenesis in cellular models of cervical cancer.Virology journal · 2026Article
- Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026Review
- MmuPV1 E7 promotes phenotypes associated with "high-risk" HPV infection in mouse keratinocytes.Journal of virology · 2025Article
- Review
- Non-Metabolic Functions of PKM2 Contribute to Cervical Cancer Cell Proliferation Induced by the HPV16 E7 Oncoprotein.Viruses · 2021Article
- Restoring the DREAM Complex Inhibits the Proliferation of High-Risk HPV Positive Human Cells.Cancers · 2021Article
- The role of Hippo-YAP signaling in squamous cell carcinomas.Cancer science · 2021Review
- Endogenous YAP1 activation drives immediate onset of cervical carcinoma in situ in mice.Cancer science · 2020Article
- Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies.Viruses · 2020Review
- Article
- MicroRNA-18a targeting of the STK4/MST1 tumour suppressor is necessary for transformation in HPV positive cervical cancer.PLoS pathogens · 2020Article
- Article
- Mus musculus Papillomavirus 1: a New Frontier in Animal Models of Papillomavirus Pathogenesis.Journal of virology · 2020Review
- Review
- PTPN14 degradation by high-risk human papillomavirus E7 limits keratinocyte differentiation and contributes to HPV-mediated oncogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Cdc6 contributes to abrogating the G1 checkpoint under hypoxic conditions in HPV E7 expressing cells.Scientific reports · 2017Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Ablating all three retinoblastoma family members in mouse lung leads to neuroendocrine tumor formation.Oncotarget · 2017Article
- Article
- HPV18 E7 induces the over-transcription of eIF4E gene in cervical cancer.Iranian journal of basic medical sciences · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human papillomavirus-16 (HPV-16) is associated etiologically with many human cervical cancers. It encodes 3 oncogenes E5, E6, and E7. Of these oncogenes, E7 has been found to be the dominant driver of cervical cancer in mice. More than 100 cellular proteins have been reported to associate with HPV-16 E7, which is thought to dysregulate the cell cycle in part by binding and inducing the degradation of pRb and its related pocket protein family members, p107 and p130. The ability of E7 to inactivate the pRb family correlates with its ability to induce head and neck cancers in mice. We previously showed that the inactivation of pRb is itself not sufficient to recapitulate the oncogenic properties of E7 in cervical carcinogenesis. In this study, we evaluated mice that were deficient in multiple pocket proteins, including mice that lacked pRb, p107, and p130. Strikingly, combined loss of two or all 3 pocket proteins resulted in development of high-grade cervical intraepithelial neoplasia, but not frank cervical carcinoma. These findings strongly argue that the oncogenic properties of HPV-16 E7 in human cervical carcinogenesis may involve disruption of E7 binding proteins beyond simply the pRb family members.
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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.