Evidence map›Paper›PMID 26804167›Full record

ArticleOncogene2016

The fibronectin/α3β1 integrin axis serves as molecular basis for keratinocyte invasion induced by βHPV.

S Heuser, M Hufbauer, J Steiger, J Marshall, A Sterner-Kock, C Mauch, P Zigrino, B Akgül

Abstract read
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In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

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  5. [Role of human papillomavirus (HPV) in the development of skin cancer].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

S HeuserInstitute of Virology, University of Cologne, Cologne, Germany.
M HufbauerInstitute of Virology, University of Cologne, Cologne, Germany.
J SteigerDepartment of Dermatology and Venerology, University of Cologne, Cologne, Germany.
J MarshallBarts Cancer Institute, Centre for Tumour Biology, Queen Mary University of London, John Vane Science Centre, London, UK.
A Sterner-KockCenter for Experimental Medicine, University Hospital, University of Cologne, Cologne, Germany.
C MauchDepartment of Dermatology and Venerology, University of Cologne, Cologne, Germany.
P ZigrinoDepartment of Dermatology and Venerology, University of Cologne, Cologne, Germany.
B AkgülInstitute of Virology, University of Cologne, Cologne, Germany.
University of Cologne · DEQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Organ-transplant-recipients exhibit cancerization of the skin from which multiple human papillomavirus (HPV)-positive squamous cell carcinomas (SCCs) arise. However, the molecular basis for HPV-induced invasion of skin keratinocytes is not known. We generated a transgenic mouse model expressing the E7 oncoprotein of HPV8 in the murine epidermis under the control of the keratin-14 promoter and showed that E7 is carcinogenic in mice. We further showed that both, the E7-expressing keratinocyte and mesenchymal components of the extracellular matrix as critical in eliciting the invasive behavior. E7 expression in basal keratinocytes, grown on fibronectin, led to epithelial-mesenchymal transition mediated by a cadherin switch. E7-positive keratinocytes displayed enhanced EDA-fibronectin expression and secretion and stimulated dermal fibroblasts to express EDA-fibronectin. Deposition of fibronectin was also detected in the peritumoral stroma of HPV8-positive skin SCC. When grown on fibronectin, E7-positive keratinocytes, in particular stem cell-like cells, exhibited increased cell surface levels of the α3-integrin chain. Functional blocking confirmed α3 as a critical molecule sufficient to induce E7-mediated invasion. This mechanistic link is further supported by expression of an E7-mutant, impaired in targeting α3 to the cell surface. These findings highlight the importance of epithelial-extracellular matrix interaction required for keratinocyte invasion and provide further mechanistic evidence for a role of HPV in skin carcinogenesis.

Indexed as

AnimalsCells, CulturedEpithelial-Mesenchymal TransitionExtracellular Matrix ProteinsFibronectinsIntegrin alpha3beta1KeratinocytesMicePapillomavirus E7 ProteinsSkin NeoplasmsExtracellular Matrix ProteinsFibronectinsIntegrin alpha3beta1Papillomavirus E7 Proteins

Identifiers

PMID26804167
OpenAlexW2473490130

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.