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

The study investigated the role of Protein Kinase C epsilon (PKCɛ) in skin carcinogenesis using transgenic mouse models that overexpressed PKCɛ. These mice were highly susceptible to developing metastatic squamous cell carcinoma (mSCC) when exposed to ultraviolet radiation or a specific tumor promotion protocol. The research suggested that PKCɛ might contribute to cancer development through a paracrine mechanism involving the induction of cytokines like tumor necrosis factor–α (TNFα). Notably, PKCɛ was not expressed in the tumors themselves but was present in the surrounding uninvolved tissue, indicating that its overexpression in the epidermis could create a microenvironment conducive to cancer development. Similar patterns were observed in human squamous cell carcinoma, supporting the findings from the mouse model.