ArticleOncotarget2013
HPV16 E5 and KGFR/FGFR2b interplay in differentiating epithelial cells.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- FGF7 mitigates airway inflammation and epithelial injury in cigarette smoke-induced COPD model.Frontiers in immunology · 2026Article
- Virus-mediated immunosuppression in head and neck cancer.Oncogene · 2025Review
- The Expression of HPV-16 E5 Oncoprotein Impacts the Transcript Profiles of FGFR2 and EMT-Related Genes in Preneoplastic Anal Epithelium Lesions.International journal of molecular sciences · 2024Article
- Increased Gene Expression ofCells · 2023Article
- Unravelling the Immunomodulatory Effects of Viral Ion Channels, towards the Treatment of Disease.Viruses · 2021Review
- Expression of the E5 Oncoprotein of HPV16 Impacts on the Molecular Profiles of EMT-Related and Differentiation Genes in Ectocervical Low-Grade Lesions.International journal of molecular sciences · 2021Article
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- The aberrant expression in epithelial cells of the mesenchymal isoform of FGFR2 controls the negative crosstalk between EMT and autophagy.Journal of cellular and molecular medicine · 2021Article
- Role of PKCε in the epithelial-mesenchymal transition induced by FGFR2 isoform switch.Cell communication and signaling : CCS · 2020Article
- Suppression of Stromal Interferon Signaling by Human Papillomavirus 16.Journal of virology · 2019Article
- The Aberrant Expression of the Mesenchymal Variant of FGFR2 in the Epithelial Context Inhibits Autophagy.Cells · 2019Article
- The Known and Potential Intersections of Rab-GTPases in Human Papillomavirus Infections.Frontiers in cell and developmental biology · 2019Review
- Papillomaviruses and Endocytic Trafficking.International journal of molecular sciences · 2018Review
- Role of Fibroblast Growth Factor Receptor 2b in the Cross Talk between Autophagy and Differentiation: Involvement of Jun N-Terminal Protein Kinase Signaling.Molecular and cellular biology · 2018Article
- Role of FGFR2b expression and signaling in keratinocyte differentiation: sequential involvement of PKCδ and PKCα.Cell death & disease · 2018Article
- Expression of the FGFR2c mesenchymal splicing variant in human keratinocytes inhibits differentiation and promotes invasion.Molecular carcinogenesis · 2018Article
- Article
- The signaling involved in autophagy machinery in keratinocytes and therapeutic approaches for skin diseases.Oncotarget · 2016Review
- Expression of the FGFR2 mesenchymal splicing variant in epithelial cells drives epithelial-mesenchymal transition.Oncotarget · 2016Article
- The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E5 oncogenic protein of the human papillomavirus type 16 (HPV16 E5) cooperates in epithelial transformation perturbing the behaviour of differentiating suprabasal cells. Among the receptor tyrosine kinases deregulated by 16E5 expression, the key paracrine mediator of epithelial homeostasis keratinocyte growth factor receptor (KGFR/FGFR2b) is altered in its signaling and endocytic traffic in undifferentiated keratinocytes expressing 16E5 and it would represent a major target of the viral protein in differentiated cells. With the aim to specifically address the possible interplay of 16E5 with KGFR/FGFR2b in cells already committed to differentiation, we took advantage of an in vitro model for forced overexpression or depletion of KGFR in E5 expressing human keratinocytes under synchronous waves of differentiation. Quantitative RT-PCR, biochemical and immunofluorescence analysis showed that KGFR down-modulation is responsible for a E5-mediated decrease of the early differentiation marker K1 and that the receptor re-expression as well as triggering of its kinase activity and signaling are able to efficiently counteract the impairment of differentiation, providing a further demonstration of the tumor-suppressive role of KGFR in the new unexplored context of HPV16 E5-mediated carcinogenesis. In addition, KGFR induced a ligand-dependent decrease of p63 through a miR-203 independent mechanism and this effect was blocked by inhibition of the PI3K/Akt signaling, which is the main pathway involved in KGFR-dependent keratinocyte differentiation, suggesting that alterations of the KGFR/p63 crosstalk are responsible for the impairment of keratinocyte differentiation induced by 16E5 and that the opposite tumor-suppressive action of KGFR and oncogenic role of E5 might both involve p63.
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