The population-based association between low vitamin D status and increased cancer risk can be inconsistent, but it is now generally accepted. These relationships link low serum 25OHD (25-hydroxyvitamin D) levels to cancer, whereas cell-based studies show that the metabolite 1,25(OH)2D (1,25-dihydroxyvitamin D) is a biologically active metabolite that works through vitamin D receptor to regulate gene transcription. In the present review we discuss the literature relevant to the molecular events that may account for the beneficial impact of vitamin D on cancer prevention or treatment. These data show that although vitamin D-induced growth arrest and apoptosis of tumour cells or their non-neoplastic progenitors are plausible mechanisms, other chemoprotective mechanisms are also worthy of consideration. These alternative mechanisms include enhancing DNA repair, antioxidant protection and immunomodulation. In addition, other cell targets, such as the stromal cells, endothelial cells and cells of the immune system, may be regulated by 1,25(OH)2D and contribute to vitamin D-mediated cancer prevention.
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Review Article| December 14 2011
Vitamin D and cancer: a review of molecular mechanisms
James C. Fleet;
*Department of Nutrition Science, Purdue University, West Lafayette, IN 47907-2059, U.S.A.
†Purdue Center for Cancer Research, Purdue University, West Lafayette, IN 47907-2059, U.S.A.
1To whom correspondence should be addressed (email email@example.com).
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James C. Fleet, Marsha Desmet, Robert Johnson, Yan Li; Vitamin D and cancer: a review of molecular mechanisms. Biochem J 1 January 2012; 441 (1): 61–76. doi: https://doi.org/10.1042/BJ20110744
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