The role of barrier genes in epidermal malignancy

The outermost layer of the mammalian skin, the epidermis, forms a protective barrier against pathogenic microbes and tissue dehydration. This barrier is formed and maintained by complex genetic networks that connect cellular differentiation processes, enzymatic activities and cellular junctions. Dis...

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Bibliographic Details
Published in:Oncogene 2016-11, Vol.35 (44), p.5705-5712
Main Authors: Darido, C, Georgy, S R, Jane, S M
Format: Article
Language:English
Subjects:
Animals
Cancer
Carcinogenesis
Cell Differentiation - genetics
Cell growth
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Cellular biology
Cellular Microenvironment - genetics
Cellular Microenvironment - immunology
Dehydration
Development and progression
Enzymatic activity
Epidermis
Epidermis - metabolism
Epidermis - pathology
Genes
Genetic aspects
Genetic Predisposition to Disease
Genotypes
Health aspects
Humans
Hyperplasia
Inflammation
Inflammation - complications
Inflammation - etiology
Keratinocytes - cytology
Keratinocytes - metabolism
Malignancy
Skin Neoplasms - etiology
Skin Neoplasms - metabolism
Skin Neoplasms - pathology
Squamous cell carcinoma
Tumors
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Summary:The outermost layer of the mammalian skin, the epidermis, forms a protective barrier against pathogenic microbes and tissue dehydration. This barrier is formed and maintained by complex genetic networks that connect cellular differentiation processes, enzymatic activities and cellular junctions. Disruption in these networks affects the balance between keratinocyte proliferation and differentiation resulting in barrier function impairment, epidermal hyperproliferation and in some cases, squamous cell carcinoma (SCC). Recent studies in wound-induced inflammation-mediated cancers in mice have identified dysregulation of core barrier components as tumor drivers. We therefore propose a hypothesis in which loss of key barrier genes, induce barrier dysfunction, and promote inflammation-driven epidermal hyperplasia and carcinogenesis over time. This emerging vision suggests that under specific genetic circumstances, localized barrier impairment could be considered as a hallmark of initiating lesions in epidermal SCC.
ISSN:0950-9232
1476-5594
DOI:10.1038/onc.2016.84