Protein Kinase C Epsilon Signals Ultraviolet Light-Induced Cutaneous Damage and Development of Squamous Cell Carcinoma Possibly Through Induction of Specific Cytokines in a Paracrine Mechanism
January 2005
in “
Photochemistry and Photobiology
”
Studysummary This study found that overexpression of PKCepsilon in mouse epidermis was associated with increased susceptibility to metastatic squamous cell carcinoma, potentially through a mechanism involving tumor necrosis factor-alpha. Our plain-language summary of this paper — not a Tressless recommendation.
The study investigated the role of Protein kinase C epsilon (PKCepsilon) in skin carcinogenesis using transgenic mice that overexpressed PKCepsilon. These mice showed increased sensitivity to developing metastatic squamous cell carcinoma (mSCC) when exposed to ultraviolet radiation or a tumor promotion protocol. The development of squamous cell carcinoma was linked to PKCepsilon-mediated induction of the cytokine tumor necrosis factor-alpha (TNFalpha). Interestingly, PKCepsilon was not expressed in the tumors themselves but was present in the surrounding uninvolved tissue, suggesting a paracrine mechanism. Similar patterns were observed in human squamous cell carcinoma, indicating that PKCepsilon overexpression in the epidermis may create a microenvironment conducive to mSCC development through specific cytokines.