Abstract
Vitamin D deficiency and insufficiency are associated with an increased risk of colon cancer. The active form of vitamin D, 1α,25-dihydroxyvitamin D3[1,25(OH)2D3], inhibits proliferation and/or induces differentiation in cells derived from myeloid leukemia, colon cancer, breast cancer, prostate cancer and other malignancies. 1,25(OH)2D3 and its synthetic derivatives activate vitamin D receptor(VDR), a member of the nuclear receptor superfamily, and exhibit antitumor effects by regulating genes involved in cell cycle, differentiation, apoptosis, inflammation and angiogenesis. VDR activation also enhances metabolism of toxic bile acids, likely preventing colon carcinogenesis. Although many cell culture and animal experiments show that VDR is a promising drug target in the treatment of malignancy and many VDR ligands have been developed, a principal adverse effect of hypercalcemia has limited their clinical application. The development of VDR ligands with less calcemic activity is needed to expand clinical application of VDR-targeting therapy.
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