Title:The Anti-cancer Actions of Vitamin D
Volume: 13
Issue: 1
Author(s): Kun-Chun Chiang and Tai C. Chen
Affiliation:
Keywords:
Cancer, Vitamin D, Cell cycle, Hedgehog, Growth factors, Apoptosis, Angiogenesis, Differentiation, Kinases, Transcription factors, Metastasis
Abstract: Vitamin D3 is biologically inert. To become active, it requires two successive hydroxylation steps catalyzed by two
cytochrome P450 enzymes, first to synthesize the pro-hormone 25-hydroxyvitamin D3 [25(OH)D3] and then the active hormone 1α,25-
dihydroxyvitamin D3 [1α,25(OH)2D3]. 1α,25(OH)2D3 has high affinity for the vitamin D receptor (VDR), a transcription factor and a
member of the steroid receptor superfamily. Through VDR, 1α,25(OH)2D3 regulates more than 200 genes in mammals, including those
involved in the calcium and phosphorus homeostasis, immune function, reproduction, cardiovascular, central nerve system,
inflammation, angiogenesis, and cellular proliferation, differentiation and apoptosis. Due to its versatile roles in maintaining and
regulating normal cellular phenotypes and functions, 1α,25(OH)2D3 has been implicated as an anti-cancer agent. In fact, ecological and
epidemiologic data have linked vitamin D deficiency with the incidence and mortality of many types of cancer. More importantly, in
vitro and in vivo animal model studies have clearly demonstrated the anti-tumor effects of vitamin D. In this review, we describe the anticancer
actions of vitamin D, with special emphasis on different pathways underlying the VDR-mediated genomic as well as less-defined
non-genomic actions of vitamin D.
