ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2015
Expression of the Ly6/uPAR-domain proteins C4.4A and Haldisin in non-invasive and invasive skin lesions.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- AP-1 and TGFß cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma.Nature communications · 2020Article
- Crystal Structures of Human C4.4A Reveal the Unique Association of Ly6/uPAR/α-neurotoxin Domain.International journal of biological sciences · 2020Article
- Evolution and Medical Significance of LU Domain-Containing Proteins.International journal of molecular sciences · 2019Review
- Prognostic value of uPAR expression and angiogenesis in primary and metastatic melanoma.PloS one · 2019Article
- Expression and crystallographic studies of the D1D2 domains of C4.4A, a homologous protein to the urokinase receptor.Acta crystallographica. Section F, Structural biology communications · 2017Article
- Expression of C4.4A in an In Vitro Human Tissue-Engineered Skin Model.BioMed research international · 2017Article
- Local Adaptation of Sun-Exposure-Dependent Gene Expression Regulation in Human Skin.PLoS genetics · 2016Article
- C4.4A gene ablation is compatible with normal epidermal development and causes modest overt phenotypes.Scientific reports · 2016Article
- Organization, evolution and functions of the human and mouse Ly6/uPAR family genes.Human genomics · 2016Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C4.4A and Haldisin belong to the Ly6/uPAR/α-neurotoxin protein domain family. They exhibit highly regulated expression profiles in normal epidermis, where they are confined to early (C4.4A) and late (Haldisin) squamous differentiation. We have now explored if dysregulated expressions occur in non-invasive and invasive skin lesions. In non-invasive lesions, their expression signatures were largely maintained as defined by that of normal epidermis. The scenario was, however, markedly different in the progression towards invasive squamous cell carcinomas. In its non-invasive stage (carcinoma in situ), a pronounced attenuation of C4.4A expression was observed, but upon transition to malignant invasive squamous cell carcinomas, the invasive fronts regained high expression of C4.4A. A similar progression was observed for the early stages of benign infiltrating keratoacanthomas. Interestingly, this transition was accompanied by a shift in the predominant association of C4.4A expression with CK1/10 in the normal epidermis to CK5/14 in the invasive lesions. In contrast, Haldisin expression maintained its confinement to the most-differentiated cells and was hardly expressed in the invasive lesions. Because this altered expression of C4.4A was seen in the invasive front of benign (keratoacanthomas) and malignant (squamous cell carcinomas) neoplasms, we propose that this transition of expression is primarily related to the invasive process.
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