Overexpression of Hedgehog Signaling Is Associated With Epidermal Tumor Formation in Vitamin D Receptor-Null Mice

August 2011 in “ Journal of Investigative Dermatology ”

Arnaud Teichert, Hashem Elalieh, Peter M. Elias, JoEllen Welsh, Daniel D. Bikle

vitamin D receptor Hedgehog signaling pathway epidermal tumor 1,25 dihydroxyvitamin D3 skin carcinogenesis VDR Hh pathway vitamin D3

TLDR Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

The study explored the role of the vitamin D receptor (VDR) in skin tumor formation, focusing on the hedgehog (Hh) signaling pathway. VDR-null mice showed increased skin tumor formation when exposed to carcinogens, with overexpression of Hh pathway components. The absence of VDR led to hyperproliferation and decreased differentiation in the epidermis, predisposing the skin to tumors. Treatment with 1,25 dihydroxyvitamin D3 downregulated some Hh pathway members, indicating that VDR and its ligand played a protective role against skin carcinogenesis by regulating the Hh pathway.

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Overexpressing GLI-1 in mice skin can cause tumors like human basal cell carcinomas.

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