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=====Vitamin D Receptor===== | =====Vitamin D Receptor===== | ||
One of the most important parts of the vitamin D pathway is the [[vitamin D receptor]] (VDR). This receptor is a ligand regulated [[transcription]] factor that has several hundred direct target genes. The VDR is present in over thirty human tissues including the mammary gland. During glandular development, which occurs during puberty, pregnancy and involution, VDR expression is regulated. Two ligands that bind to the VDR are calcidiol and calcitriol. Once bound, the VDR protein levels start to increase because the ligands cause an increase in the transcription of the VDR gene. The increased protein levels correlate with an increase in the antitumor efficacy of the VDR. If the VDR is disrupted in any way, the cell’s ability to stop the progression of cancer is greatly inhibited favoring tumor growth. When a ligand is bound to the vitamin D receptor, it has an influence over [[cell cycling]], proliferation, differentiation and [[apoptosis]] in the cells. | |||
====Case Studies==== | ====Case Studies==== | ||
Revision as of 20:14, 7 November 2010
Vitamin D
In recent years, vitamin D has been shown to decrease the risk of getting breast cancer. When different mechanisms of the vitamin D pathway are inhibited, breast cancer formation is favored. The two major forms of vitamin D, calcidiol and calcitriol, play a role in prevention. Vitamin D in the body can be measured by the serum concentration of calcidiol.
Mechanisms
Genes
Two important genes relating to the vitamin D pathway are CYP24A1 and CYP27B1. CYP24A1 is responsible for metabolizing both calicidiol and calcitriol. The other gene, CYP27B1, is responsible for converting calcidiol into the more active metabolite calcitriol. Both of the genes are responsible for the local concentration of vitamin D in the breast tissue. As the breast tumor progresses, the expression of CYP24A1 is increased whereas the expression of CYP27B1 is decreased. The result is that less calcidiol is converted to the active form and also that catabolism of vitamin D is increased. This result has detrimental effects on the cells in the breast tissue and favors tumor progression and formation.
Calcidiol and Calcitriol
Calcidiol is important in protecting breast cells against cellular stress.[1] Cellular stress is implicated in starting the tumor process. Calcitriol, once bound to the vitamin D receptor, is involved with modulation of cell proliferation, differentiation, cancer metastasis and angiogenesis. The effective concentration of calcitriol for cell protection is 10nmol/L whereas the most effective concentration for calcidiol is 250nmol/L.[1] The difference in effective concentrations is caused by how tightly the two ligands bind to the vitamin D receptor with calcitriol binding tighter to the vitamin D receptor.
Vitamin D Receptor
One of the most important parts of the vitamin D pathway is the vitamin D receptor (VDR). This receptor is a ligand regulated transcription factor that has several hundred direct target genes. The VDR is present in over thirty human tissues including the mammary gland. During glandular development, which occurs during puberty, pregnancy and involution, VDR expression is regulated. Two ligands that bind to the VDR are calcidiol and calcitriol. Once bound, the VDR protein levels start to increase because the ligands cause an increase in the transcription of the VDR gene. The increased protein levels correlate with an increase in the antitumor efficacy of the VDR. If the VDR is disrupted in any way, the cell’s ability to stop the progression of cancer is greatly inhibited favoring tumor growth. When a ligand is bound to the vitamin D receptor, it has an influence over cell cycling, proliferation, differentiation and apoptosis in the cells.