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- Title
Shedding new light on the role of the sunshine vitamin D for skin health: the lnc RNA-skin cancer connection.
- Authors
Holick, Michael F.
- Abstract
Throughout evolution, vertebrates including humans have depended on the sunshine vitamin D for their calcified skeletons. As our hunter gatherer forefathers ventured from the equator, their skin tone became much lighter in order to permit an adequate amount of ultraviolet B radiation to enter the skin to produce the vitally important vitamin D. Although sensible sun exposure does not significantly increase risk of skin cancer, it has remained a mystery as to why. Jiang and Bikle in their viewpoint provide a novel insight as to how Mother Nature was able to balance the need for receiving adequate sun exposure to produce vitamin D while limiting damage caused by the DNA absorbing the ultraviolet B radiation. Long non-coding RNAs which are plentiful in cells have a dual personality. Some enhance malignancy, while others act as tumor suppressors. Jiang and Bikle provide compelling evidence that these long non-coding RNAs in skin cells are responsive to 1,25-dihydroxyvitamin D3 by decreasing their carcinogenic activity while enhancing their tumor suppression function presumably as a strategy for reducing ultraviolet-induced non-melanoma skin cancer. Mother Nature got it right. Sensible sun exposure is important for maintaining an adequate vitamin D status. Once formed in the skin, vitamin D can exit into the circulation to carry out its physiologic functions on calcium and bone metabolism. Some vitamin D however remains in the skin and is activated to interact with its vitamin D receptor to control cell proliferation using a variety of strategies including interacting with long non-coding RNAs to reduce risk of photocarcinogenesis.
- Subjects
SKIN cancer; VITAMIN D; CALCIFICATION; PHYSIOLOGICAL effects of ultraviolet radiation; NON-coding RNA; DNA
- Publication
Experimental Dermatology, 2014, Vol 23, Issue 6, p391
- ISSN
0906-6705
- Publication type
Article
- DOI
10.1111/exd.12386