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Skin-Derived Vitamin D3 Protects against Basal Cell Carcinoma

Maarten F Bijlsma1, Henk Roelink2

  • 1Laboratory for Experimental Oncology and Radiobiology, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam and Academic Medical Center, Amsterdam, The Netherlands.

The Journal of Investigative Dermatology
|November 25, 2017
PubMed

Insights

Sunlight-induced mutations cause skin cancer, but vitamin D3 produced in the skin offers protection. This skin-synthesized vitamin D3 inhibits cancer-driving Hedgehog signaling, unlike dietary vitamin D3.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Oncology

Background:

  • Ultraviolet radiation (UVR) in sunlight is a known mutagen that initiates skin cancer development.
  • Basal cell carcinoma incidence plateaus with prolonged UVR exposure, while other skin cancer types increase.
  • The role of vitamin D3 in mitigating UVR-induced skin damage and cancer is under investigation.

Purpose of the Study:

  • To investigate the protective mechanisms of UVR-induced skin vitamin D3 synthesis against oncogenesis.
  • To compare the effects of skin-produced vitamin D3 versus dietary vitamin D3 on UVR-driven skin cancer.
  • To elucidate the signaling pathways involved in UVR-induced skin carcinogenesis and vitamin D3's modulation thereof.

Main Methods:

  • Utilized a model system to study UVR-induced mutations and skin cancer development.
  • Quantified vitamin D3 production in the skin following UVR exposure.
  • Assessed the impact of both endogenously produced and exogenously supplied vitamin D3 on specific cancer-driving signaling pathways, including Hedgehog signaling.

Main Results:

  • UVR exposure leads to mutations that drive basal cell carcinomas, with incidence plateauing upon prolonged exposure.
  • Skin-produced vitamin D3, generated by UVR, was found to inhibit the oncogenic effects of UVR.
  • This protective effect of skin-produced vitamin D3 was mediated by the inhibition of Hedgehog signaling.
  • Dietary vitamin D3 did not exhibit similar protective effects against UVR-induced oncogenesis.

Conclusions:

  • Endogenously produced vitamin D3 in the skin acts as a protective agent against UVR-induced skin cancer.
  • Inhibition of Hedgehog signaling by skin-derived vitamin D3 is a key mechanism in preventing UVR-driven oncogenesis.
  • Dietary vitamin D3 supplementation does not replicate the protective benefits of UVR-induced skin vitamin D3 synthesis.

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