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Molecular Cancer Therapeutics
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Research Articles: Therapeutics, Targets, and Development

Calcitrol (1α,25-dihydroxyvitamin D3) inhibits androgen glucuronidation in prostate cancer cells

Jenny Kaeding, Julie Bélanger, Patrick Caron, Mélanie Verreault, Alain Bélanger and Olivier Barbier
Jenny Kaeding
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Julie Bélanger
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Patrick Caron
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Mélanie Verreault
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Alain Bélanger
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Olivier Barbier
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DOI: 10.1158/1535-7163.MCT-07-0455 Published February 2008
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Abstract

Calcitriol (1α,25-dihydroxyvitamin D3), the active metabolite of vitamin D, has recently emerged as a promising therapeutic agent in the treatment of prostate cancer, the second most common cause of cancer death in American males. In the present study, we have analyzed the effects of calcitriol treatment on the expression and activity of the UDP-glucuronosyltransferase (UGT) 2B15 and 2B17 in prostate cancer LNCaP and 22Rv1 cells. These two enzymes share a crucial role in the inactivation of androgens in the human prostate. We report that calcitriol treatment results in lower glucuronide conjugation of the active androgen dihydrotestosterone and its reduced metabolites androstane-3α-diol and androsterone in LNCaP cells. The same treatment also drastically decreased the mRNA and protein levels of UGT2B15 and UGT2B17 in LNCaP and 22Rv1 cells. Using casodex, an androgen receptor (AR) antagonist, and AR-specific small interfering RNA probes, we show that calcitriol requires a functional AR to inhibit the expression of the UGT2B17 gene in LNCaP cells. By contrast, transient transfection and site-directed mutagenesis experiments revealed that calcitriol down-regulates UGT2B15 promoter activity through a responsive region between positions -171 and -113 bp. In conclusion, the present study identifies the vitamin D receptor activator calcitriol as a negative regulator of the UGT2B15- and UGT2B17-dependent inactivation of androgens in prostate cancer LNCaP cells. Androgens promote prostate cancer cell proliferation; thus, the reduction of their inactivation could have a limiting effect of the calcitriol antiproliferative properties in prostate cancer cells. [Mol Cancer Ther 2008;7(2):380–90]

Keywords:
  • Vitamin D
  • Prostate cancer cells
  • Androgen metabolism
  • Glucuronidation
  • Gene regulation

Footnotes

  • ↵4 Supplementary material for this article are available at Molecular Cancer Therapeutics Online (http://mct.aacrjournals.org/).

  • Grant support: Canadian Institutes for Health Research MOP 118446 (O. Barbier), Fonds pour la Recherche en Santé du Québec (O. Barbier), Faculty of Pharmacy of Laval University (M. Verreault and J. Kaeding), and Health Research Foundation of R&D-Canadian Institutes for Health Research (O. Barbier and J. Kaeding).

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted December 31, 2007.
    • Received July 7, 2007.
    • Revision received December 4, 2007.
  • American Association for Cancer Research
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Molecular Cancer Therapeutics: 7 (2)
February 2008
Volume 7, Issue 2
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Calcitrol (1α,25-dihydroxyvitamin D3) inhibits androgen glucuronidation in prostate cancer cells
Jenny Kaeding, Julie Bélanger, Patrick Caron, Mélanie Verreault, Alain Bélanger and Olivier Barbier
Mol Cancer Ther February 1 2008 (7) (2) 380-390; DOI: 10.1158/1535-7163.MCT-07-0455

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Calcitrol (1α,25-dihydroxyvitamin D3) inhibits androgen glucuronidation in prostate cancer cells
Jenny Kaeding, Julie Bélanger, Patrick Caron, Mélanie Verreault, Alain Bélanger and Olivier Barbier
Mol Cancer Ther February 1 2008 (7) (2) 380-390; DOI: 10.1158/1535-7163.MCT-07-0455
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Molecular Cancer Therapeutics
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