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Endocrinology, Vol 132, 1952-1960, Copyright © 1993 by Endocrine Society

ARTICLES

Vitamin D and prostate cancer: 1,25 dihydroxyvitamin D3 receptors and actions in human prostate cancer cell lines

RJ Skowronski, DM Peehl and D Feldman
Department of Medicine, Stanford University School of Medicine, California 94305.

It has been suggested that vitamin D deficiency may promote prostate cancer, although the mechanism is not understood. In this study three human prostate carcinoma cell lines, LNCaP, DU-145, and PC-3, were examined both for the presence of specific 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] receptors (VDRs) and also employed to study the effects of hormone on cell proliferation and differentiation. Ligand binding experiments demonstrated classical VDR in all three cell lines examined with an apparent dissociation constant of 7.5, 5.4, and 6.3 x 10(-11) M for LNCaP, DU-145, and PC-3 cells, respectively. Corresponding binding capacity for the three prostate carcinoma cell lines were 27, 31, and 78 fmol/mg protein, respectively. The presence of VDR in the three cell lines was also confirmed by immunocytochemistry. In addition, one major 4.6-kilobase messenger RNA transcript hybridizing with a specific human VDR complementary DNA probe was identified in all three cell lines. Interestingly, both DU-145 and PC-3 but not LNCaP cell lines exhibited 1,25(OH)2D3-stimulated induction of 24-hydroxylase messenger RNA employed as a marker of 1,25(OH)2D3 action. Physiological levels of 1,25(OH)2D3 dramatically inhibited proliferation of the LNCaP and PC-3 cell lines. However, in spite of the presence of high affinity VDR, proliferation of DU-145 cells was not inhibited by 1,25(OH)2D3 at the doses tested. Treatment with 1,25(OH)2D3 caused a dose-dependent stimulation of prostate-specific antigen secretion by LNCaP cells. In conclusion, these results demonstrate that these three human prostate carcinoma cell lines all possess specific VDR and that 1,25(OH)2D3 treatment can elicit both an antiproliferative and a differentiating action on these cancer cells. The findings lend support to the hypothesis that vitamin D might exert beneficial actions on prostate cancer risk.


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S.-H. Zhuang and K. L. Burnstein
Antiproliferative Effect of 1{alpha},25-Dihydroxyvitamin D3 in Human Prostate Cancer Cell Line LNCaP Involves Reduction of Cyclin-Dependent Kinase 2 Activity and Persistent G1 Accumulation
Endocrinology, March 1, 1998; 139(3): 1197 - 1207.
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X.-Y. Zhao, L. H. Ly, D. M. Peehl, and D. Feldman
1{alpha},25-Dihydroxyvitamin D3 Actions in LNCaP Human Prostate Cancer Cells Are Androgen-Dependent
Endocrinology, August 1, 1997; 138(8): 3290 - 3298.
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S. E. Blutt, E. A. Allegretto, J. W. Pike, and N. L. Weigel
1,25-Dihydroxyvitamin D3 and 9-cis-Retinoic Acid Act Synergistically to Inhibit the Growth of LNCaP Prostate Cells and Cause Accumulation of Cells in G1
Endocrinology, April 1, 1997; 138(4): 1491 - 1497.
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I. M. Musiol and D. Feldman
1,25-Dihydroxyvitamin D3 Induction of Nerve Growth Factor in L929 Mouse Fibroblasts: Effect of Vitamin D Receptor Regulation and Potency of Vitamin D3 Analogs
Endocrinology, January 1, 1997; 138(1): 12 - 18.
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S. A. Gardezi, C. Nguyen, P. J. Malloy, G. H. Posner, D. Feldman, and S. Peleg
A Rationale for Treatment of Hereditary Vitamin D-resistant Rickets with Analogs of 1alpha ,25-Dihydroxyvitamin D3
J. Biol. Chem., July 27, 2001; 276(31): 29148 - 29156.
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