ArticlePLoS pathogens2013
The HPV16 E6 oncoprotein causes prolonged receptor protein tyrosine kinase signaling and enhances internalization of phosphorylated receptor species.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 78 citations in OpenAlex.
- Erlotinib, erlotinib-sulindac versus placebo: a randomized, double-blind, placebo-controlled window trial in operable head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- Review
- Connexin 43 Expression as Biomarker of Oral Squamous Cell Carcinoma and Its Association with Human Papillomavirus 16 and 18.International journal of molecular sciences · 2025Article
- Targeted and untargeted metabolomics uncovering the effects of Jiawei Ermiao Granule on patients with persistent HPV infection.Frontiers in cellular and infection microbiology · 2025Article
- E7-mediated repression of miR-203 promotes LASP1-dependent proliferation in HPV-positive cervical cancer.Oncogene · 2024Article
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- Gut microbiota, an emergent target to shape the efficiency of cancer therapy.Exploration of targeted anti-tumor therapy · 2023Review
- Article
- Article
- The Dysregulation of MicroRNAs in the Development of Cervical Pre-Cancer-An Update.International journal of molecular sciences · 2022Review
- CD73 promotes cervical cancer growth via EGFR/AKT1 pathway.Translational cancer research · 2022Article
- The application of CRISPR/Cas9 system in cervical carcinogenesis.Cancer gene therapy · 2022Article
- PIK3CA Gene Mutations in HNSCC: Systematic Review and Correlations with HPV Status and Patient Survival.Cancers · 2022Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Therapeutic Effects of Natural Products on Cervical Cancer: Based on Inflammatory Pathways.Frontiers in pharmacology · 2022Review
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- The human papillomavirus oncoproteins: a review of the host pathways targeted on the road to transformation.The Journal of general virology · 2021Review
- Article
- Aristocratic human papillomavirus drove cervical cancer: a study of the therapeutic potential of the combination of interferon with zinc.Molecular and cellular biochemistry · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The high-risk human papillomavirus (HPV) E6 proteins are consistently expressed in HPV-associated lesions and cancers. HPV16 E6 sustains the activity of the mTORC1 and mTORC2 signaling cascades under conditions of growth factor deprivation. Here we report that HPV16 E6 activated mTORC1 by enhanced signaling through receptor protein tyrosine kinases, including epidermal growth factor receptor and insulin receptor and insulin-like growth factor receptors. This is evidenced by sustained signaling through these receptors for several hours after growth factor withdrawal. HPV16 E6 increased the internalization of activated receptor species, and the signaling adaptor protein GRB2 was shown to be critical for HPV16 E6 mediated enhanced EGFR internalization and mTORC1 activation. As a consequence of receptor protein kinase mediated mTORC1 activation, HPV16 E6 expression increased cellular migration of primary human epithelial cells. This study identifies a previously unappreciated mechanism by which HPV E6 proteins perturb host-signaling pathways presumably to sustain protein synthesis during the viral life cycle that may also contribute to cellular transforming activities of high-risk HPV E6 proteins.
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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.