Rajendra G. Mehta, , Xinjian Peng, Fatouma Alimirah, Genoveva Murillo, Rajeshwari Mehta
IIT Research Institute, 10 West 35th Street, Chicago, IL 60616 http://dx.doi.org/10.1016/j.canlet.2012.10.034,
The benefit of vitamin D in cancer prevention and to certain extent therapy has been well recognized. The active form of vitamin D, 1, 25-dihydroxycholecalciferol (1, 25(OH)2 D3) is a natural ligand for vitamin D receptor (VDR). Since 1,25(OH)2D3 exerts toxic effects at a concentration that is beneficial, nearly 1500 analogs of vitamin D have been synthesized and evaluated for their efficacy in a variety of carcinogenesis and human cancer models both in vitro and in vivo. Among these only a handful of them have been approved for evaluation in clinical trials for leukemia, breast, prostate and colon cancers. The mechanism of vitamin D action is mediated by the nuclear VDR and the signaling cascade for its action is extensively reported. In this review we focus on the newer concepts for vitamin D action.
- 1. differential effects of vitamin D in maintaining cell proliferation when the cells are under stress but suppressing cell growth when the cells are transformed;
- 2. Functional significance of VDR polymorphism in potential vitamin D responsiveness;
- 3. Regulation of constitutive splicing of vitamin D target gene, CYP24a by the hormone and its significance;
- 4. Regulation of microRNA by vitamin D in breast cancer.
It is anticipated that the new work in these selective areas would expand the understanding of vitamin D in breast cancer prevention and therapy.
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