Vitamin D - Metabolism in the Human Breast Cancer Cell Line MCF-7

• Published in: Anticancer research 2006-07, Vol.26 (4A), p.2755-2759
• Main Authors: DIESING, Dagmar, CORDES, Tim, FISCHER, Dorothea, DIEDRICH, Klaus, FRIEDRICH, Michael
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Breast Neoplasms - enzymology; Breast Neoplasms - metabolism; Calcifediol - metabolism; Calcifediol - pharmacology; Calcitriol - analogs & derivatives; Calcitriol - metabolism; Calcitriol - pharmacology; Cell Line, Tumor; Cholestanetriol 26-Monooxygenase; Gynecology. Andrology. Obstetrics; Humans; Mammary gland diseases; Medical sciences; Steroid Hydroxylases - metabolism; Tumors; Vitamin D - metabolism; Vitamin D3 24-Hydroxylase
• ISSN: 0250-7005; 1791-7530

Background: The three main vitamin D metabolizing enzymes, vitamin D 3 -25-hydroxylase (25-OHase, 25-hydroxylase), 25-hydroxyvitamin D 3 -1α-hydroxylase (1α-OHase, 1α-hydroxylase) and 25-hydroxyvitamin D 3 -24-hydroxylase (24-OHase, 24-hydroxylase), have been described in malignant breast tissue. This in vitro study aimed to obtain more information regarding the regulation of these enzymes in the human breast cancer cell line MCF-7. Materials and Methods: Vitamin D receptor (VDR)- positive MCF-7 cells in culture were stimulated with the vitamin D metabolites vitamin D 3 , 25-hydroxyvitamin D 3 and 1,25-dihydroxyvitamin D 3 for 24, 48; 72 and 96 hours in physiological and supraphysiological concentrations. The expressions of 25-hydroxylase, 1α-hydroxylase and 24-hydroxylase and their changes after stimulation were assessed by real-time PCR. Results: The expression of 25-hydroxylase was slightly influenced by vitamin D 3 . The expression of 1α-hydroxylase was induced after stimulation with vitamin D 3 and 25-hydroxyvitamin D 3 . Stimulation with 1,25-dihydroxyvitamin D 3 markedly increased the expression of 24-hydroxylase time- and dose-dependently. Conclusion: Our results demonstrated that MCF-7 cells are able to regulate the expression of 24-hydroxylase. This might be a mechanism for these tumor cells to protect themselves against the antiproliferative and apoptosis-inducing effects of calcitriol.