Protein Kinase C δ Overexpressing Transgenic Mice Are Resistant to Chemically but not to UV Radiation–Induced Development of Squamous Cell Carcinomas: A Possible Link to Specific Cytokines and Cyclooxygenase-2

January 2006 in “ Cancer Research ”

Moammir Hasan Aziz, Deric L. Wheeler, Bhushan Bhamb, Ajit Kumar Verma

Protein Kinase C δ PKCδ squamous cell carcinoma SCC cytokines cyclooxygenase-2 COX-2 apoptosis UV radiation chemical carcinogens

TLDR Mice with extra PKCδ resist chemical-induced skin cancer but not UV-induced.

The study examined the role of Protein Kinase C δ (PKCδ) in squamous cell carcinoma (SCC) development using transgenic mice overexpressing PKCδ. These mice were resistant to SCCs induced by chemical carcinogens but not to those caused by UV radiation, suggesting a protective mechanism against chemical carcinogenesis. This resistance was linked to enhanced apoptosis and suppression of cytokines and COX-2 expression in response to chemical exposure, but not UV radiation. The findings highlighted different molecular mechanisms in SCC development via chemical and UV exposure, emphasizing the complexity of cancer resistance and potential pathways for targeted prevention.

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research 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¶

28 citations , January 2005 in “Photochemistry and Photobiology”

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.

research Protein kinase Cepsilon is linked to 12-O-tetradecanoylphorbol-13-acetate-induced tumor necrosis factor-alpha ectodomain shedding and the development of metastatic squamous cell carcinoma in protein kinase Cepsilon transgenic mice.

79 citations , October 2003 in “PubMed”

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