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Regulation of estrogen receptor-α gene expression by 1,25-dihydroxyvitamin D in MCF-7 cells

✍ Scribed by Adriana Stoica; Miguel Saceda; Amina Fakhro; Harrison B. Solomon; Bradley D. Fenster; Mary Beth Martin

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
205 KB
Volume
75
Category
Article
ISSN
0730-2312

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✦ Synopsis

This report describes an investigation of the role of 1,25-dihydroxyvitamin D (VD 3 ) in the regulation of estrogen receptor-␣ (ER) in the ER-positive breast cancer cell line, MCF-7. Treatment of cells with 10 nM VD 3 resulted in a 50% decline in the concentration of ER protein at 24 h. Scatchard analysis showed a corresponding decrease in the number of estradiol binding sites and no alteration in the binding affinity of estradiol for the ER (K d ϭ 0.08 nM in VD 3 -treated cells compared with K d ϭ 0.07 nM in control cells). Vitamin D treatment also caused a 50% decrease in the steady state amount of ER mRNA, which was maximal by 18 h. In vitro transcription run-on experiments demonstrated a decrease of approximately 60% in transcription of the estrogen receptor gene. Transient transfections using an ER promoter-CAT construct also demonstrated a 40% decrease in CAT activity after VD 3 treatment. Sequence analysis identified a potential vitamin D response element (nVDRE) within the ER promoter. When this element was mutated, the ability of VD 3 to block transcription from the ER promoter was lost. When the nVDRE was placed upstream of a heterologous promoter, nVDRE-SV40-CAT, treatment with VD 3 resulted in a 50% decrease in CAT activity. Interestingly, co-transfection of either the ER promoter-CAT or the nVDRE-SV40-CAT construct and a vitamin D receptor expression vector into COS-1 or CV-1 cells showed an approximately 4-fold increase in CAT activity after VD 3 treatment. Taken together these data suggest that VD 3 inhibition of ER gene transcription is mediated through a nVDRE in the ER promoter. Inhibition appears to be cell specific.

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