{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T22:22:37Z","timestamp":1780957357654,"version":"3.54.1"},"reference-count":56,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,3,7]],"date-time":"2014-03-07T00:00:00Z","timestamp":1394150400000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIH","award":["R01 AR055924"],"award-info":[{"award-number":["R01 AR055924"]}]},{"name":"DOD","award":["CA110338"],"award-info":[{"award-number":["CA110338"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Sunlight, vitamin D and skin cancer form a controversial brew. While too much sunlight exposure causes skin cancer, it is the major source of vitamin D from skin. We propose that these processes can be balanced. Vitamin D signalling (<jats:styled-content style=\"fixed-case\">VDS<\/jats:styled-content>) protects against skin cancer as demonstrated by the susceptibility of the skin to tumor formation in <jats:styled-content style=\"fixed-case\">VDR<\/jats:styled-content> null mice and protection from UVB\u2010induced mutations when VDR agonists are administered. The question is how is protection afforded. Previously, we have focused on the Wnt\/\u03b2\u2010catenin\/hedgehog and <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> damage repair (<jats:styled-content style=\"fixed-case\">DDR<\/jats:styled-content>) pathways. As <jats:styled-content style=\"fixed-case\">VDR<\/jats:styled-content> regulates hundreds of genes with thousands of <jats:styled-content style=\"fixed-case\">VDR<\/jats:styled-content> response elements (<jats:styled-content style=\"fixed-case\">VDRE<\/jats:styled-content>) throughout the genome, and many <jats:styled-content style=\"fixed-case\">VDRE<\/jats:styled-content>s are in non\u2010coding regions, we decided to explore long non\u2010coding <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s (lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>). Lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s are m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010like transcripts ranging from 200 bases ~100\u00a0kb lacking significant open reading frames. They are aberrantly expressed in human cancers and involved in a spectrum of tumorigenic\/metastatic processes (cell proliferation\/apoptosis\/angiogenesis). We discovered that <jats:styled-content style=\"fixed-case\">VDS<\/jats:styled-content> regulated the expression of certain lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s in a manner consistent with <jats:styled-content style=\"fixed-case\">VDS<\/jats:styled-content> protection against skin cancer. Given the huge variation in genes actively regulated by 1,25(OH)<jats:sub>2<\/jats:sub>D from different cell types, it is conceivable that our results could apply to personalized medicine based on the distinctive lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> profiles. These lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s could also serve as skin cancer biomarkers secreted into the blood or urine via exosomes as demonstrated in other cancer types (breast, prostate). Modulation of lnc<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> profile by <jats:styled-content style=\"fixed-case\">VDS<\/jats:styled-content> may also provide insight into regulating pathways such as Wnt\/\u00df\u2010catenin and hedgehog.<\/jats:p>","DOI":"10.1111\/exd.12341","type":"journal-article","created":{"date-parts":[[2014,2,6]],"date-time":"2014-02-06T07:14:43Z","timestamp":1391670883000},"page":"147-150","source":"Crossref","is-referenced-by-count":59,"title":["Lnc<scp>RNA<\/scp>: a new player in 1<i>\u03b1<\/i>, 25(<scp>OH<\/scp>)<sub>2<\/sub> vitamin D<sub>3<\/sub>\/<scp>VDR<\/scp> protection against skin cancer formation"],"prefix":"10.1111","volume":"23","author":[{"given":"Yan J.","family":"Jiang","sequence":"first","affiliation":[{"name":"Endocrine Research Unit (111N) Department of Medicine VAMC\/UCSF NCIRE San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel 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