VDR

Vitamin D is well known as being essential for bone health. It is a group of fat-soluble
prohormones, which are converted in the body into a number of biologically active metabolites that function as true hormones, circulating in the blood and regulating the activities of various cell types - both calcemic and noncalcemic effects1. Cell responsiveness to 1,25(OH)2D3 mainly relays on VDR expression levels. The liganded VDR forms a heterodimer with retinoid X receptor (RXR) and binds to vitamin D response element (VDRE) to modulate the gene expression. The presence of
VDR in cells other than those of the intestine, bone, kidney, and parathyroid gland led to the recognition of noncalcemic actions of VDR ligands. VDR protein is expressed in almost all normal human cell types and tissues, and also in cancer cell lines and tumors of several origins. VDR downregulation has been observed in a proportion
of melanomas and colon, breast, lung, and ovarian tumors, which may jeopardize the response to therapy with vitamin D, 1,25(OH)2D3, or its analogs. 1,25(OH)2D3, and its synthetic analogs, is therapeutic efficacy in skin diseases involving Vitamin D is well known as being essential for bone health. It is a group of fat-soluble prohormones, which are converted in the body into a number of biologically active metabolites that
function as true hormones, circulating in the blood and regulating the activities of various cell types - both calcemic and noncalcemic effects1. Cell responsiveness to 1,25(OH)2D3 mainly relays on VDR expression levels. The liganded VDR forms a
heterodimer with retinoid X receptor (RXR) and binds to vitamin D response element (VDRE) to modulate the gene expression. The presence of VDR in cells other than those of the intestine, bone, kidney, and parathyroid gland led to the recognition of noncalcemic actions of VDR ligands. VDR protein is expressed in almost all normal
human cell types and tissues, and also in cancer cell lines and tumors of several origins. VDR downregulation has been observed in a proportion of melanomas and colon, breast, lung, and ovarian tumors, which may jeopardize the response to
therapy with vitamin D, 1,25(OH)2D3, or its analogs. 1,25(OH)2D3, and its synthetic analogs, is therapeutic efficacy in skin diseases involving defective keratinocyte differentiation, such as psoriasis, seborhheic dermatitis, and ichthyosis2. Promotion of epithelial differentiation by VDR ligands also provides a mechanistic basis for their
potential use in the treatment of actinic keratosis, head and neck squamous cell carcinoma (HNSCC), basal cell carcinoma3'4'56 (BCC) and melanomas.
So-called, non-genomic mechanism of rapid vitamin D response has been described recently. This mechanism does not directly affect VDR, its expression, gene expression of target proteins or require additional protein synthesis75.