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Cited by 62Dermatology and Skin DiseasesContact Dermatitis and AllergiesSkin and Cellular Biology Research

Epidermal barrier defects link atopic dermatitis with altered skin cancer susceptibility

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Cipolat, Sara, Hoste, Esther, Natsuga, Ken, Quist, Sven R, Watt, Fiona M·2014·eLife
DOI 10.7554/elife.01888PMC PMC4007207
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Abstract

Atopic dermatitis can result from loss of structural proteins in the outermost epidermal layers, leading to a defective epidermal barrier. To test whether this influences tumour formation, we chemically induced tumours in EPI−/− mice, which lack three barrier proteins—Envoplakin, Periplakin, and Involucrin. EPI−/− mice were highly resistant to developing benign tumours when treated with 7,12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). The DMBA response was normal, but EPI−/− skin exhibited an exaggerated atopic response to TPA, characterised by abnormal epidermal differentiation, a complex immune infiltrate and elevated serum thymic stromal lymphopoietin (TSLP). The exacerbated TPA response could be normalised by blocking TSLP or the immunoreceptor NKG2D but not CD4+ T cells. We conclude that atopy is protective against skin cancer in our experimental model and that the mechanism involves keratinocytes communicating with cells of the immune system via signalling elements that normally protect against environmental assaults.

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  • Either too much or too little EGFR activity at TJs will impair barrier function and alter cytokine expression, both of which contribute to skin inflammatory skin diseases as well as skin cancer.

    “Either too much or too little EGFR activity at TJs will impair barrier function and alter cytokine expression, both of which contribute to skin inflammatory skin diseases3 as well as skin cancer54.”

    From E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning (2017) · cites this paper as [54]

    The Results and Discussion report that mice lacking three epidermal barrier proteins had altered cytokine production and were protected against chemically induced skin tumours. That supports a link between barrier defects, immune signalling and skin cancer, but the paper does not establish that either excessive or insufficient EGFR activity at tight junctions causes those changes. (LLM, conf=0.86)

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Cited by

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Authors
Cipolat, S., Hoste, E., Natsuga, K., Quist, S. R., & Watt, F. M.
Affiliations
  • King's College London (GB)
  • Hokkaido University (JP)
  • Cancer Research UK (GB)
Corresponding author
Watt, Fiona M
ORCID
Venue
eLife
Publisher
eLife Sciences Publications, Ltd
Published
2014-05-06
Volume
3
Pages
e01888-e01888
ISSN
2050-084X (ISSN-L)
DOI
10.7554/elife.01888
PMC
PMC4007207
OpenAlex
W2153454205
Cited by
62
References
1
Citations by year
2026: 3 · 2025: 1 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 10 · 2015: 5 · 2014: 3 · 2013: 2
FWCI
8.01
Type
journal article
Language
en
Open access
Licence
Locations
  • eLife (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (publishedVersion, other-oa)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Medical Research Council
  • Wellcome Trust
  • European Union
  • Cancer Research UK
Topics
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
Keywords
atopic dermatitis, skin barrier, skin cancer predisposition, envoplakin, periplakin, involucrin, thymic stromal lymphopoietin, NKG2D, epidermal differentiation, immune cell infiltration
MeSH terms
Thymic Stromal Lymphopoietin, Animals, Carcinoma, Squamous Cell, Cell Communication, Cell Differentiation, Cell Transformation, Neoplastic, Dermatitis, Atopic, Disease Models, Animal, Epidermis, Membrane Proteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Nude, Papilloma, Permeability, Protein Precursors, Skin Neoplasms, Tetradecanoylphorbol Acetate, Time Factors, 9,10-Dimethyl-1,2-benzanthracene, Signal Transduction, Keratinocytes, Cytokines, Mice, Knockout, Plakins, NK Cell Lectin-Like Receptor Subfamily K, Mice, 129 Strain

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