1,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3], the bioactive form of vitamin D, has been shown to possess significant anti-tumor potential. While most studies so far have focused on the ability of this molecule to influence the proliferation and apoptosis of cancer cells, more recent data indicate that 1,25(OH)(2)D-3 also impacts energy utilization in tumor cells. In this article, we summarize and review the evidence that demonstrates the targeting of metabolic aberrations in cancers by 1,25(OH)(2)D-3, and highlight potential mechanisms through which these effects may be executed. We shed light on the ability of this molecule to regulate metabolism-related tumor suppressors and oncogenes, energy- and nutrient-sensing pathways, as well as cell death and survival mechanisms such as autophagy.
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vitamin D,cancer,metabolism,autophagy,AMPK (AMP-activated protein kinase),mTOR (Mammalian target of rapamycin),TXNIP (Thioredoxin-interacting protein),p53,HIF1a (Hypoxia-inducible factor 1a),c-Myc