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Abstract

Alterations of Vitamin D Receptor (VDR) Expression Profile in Normal and Malignant Breast Tissues by Naghmeh Zhalehjoo, Yadollah Shakiba, Mojtaba Panjehpour

Background: The actions of Vitamin D in different tissues, including breast tissue, are mediated by vitamin D receptor (VDR). Vitamin D has antitumor functions in the body; any changes in VDR expression can therefore affect the anticancer activities of Vitamin D. The present study was conducted to compare expression levels of VDR mRNA and protein in normal and tumor breast tissues.
Methods: Tumor and adjacent normal tissue samples from 30 patients with breast cancer were procured from the Iran National Tumor Bank of the Cancer Institute. After the extraction of RNA and cDNA synthesis, expression of the VDR gene was analyzed using Real Time RT-PCR based on TaqMan method. The expression of VDR protein was also assessed using the western blotting method. The results were quantified and analyzed in Alpha Ease, SPSS, and Excel.
Results: VDR mRNA and protein expression was significantly greater in tumor tissues compared to in the adjacent normal tissues (p < 0.01). Comparison of the relationship between the VDR gene mRNA expression level in tumor tissues and the clinicopathological parameters (including tumor stage, grade, size, patients' age groups, and the presence or absence of lymphatic invasion) showed VDR gene expression to be significantly related to tumor size and stage (p < 0.05). However, no relationships were observed between the expression of VDR protein in the tumor tissues and either of the parameters examined.
Conclusions: The results suggest possible changes in the vitamin D signaling pathway associated with carcinogenesis of the breast, which can affect the anticancer activities of vitamin D. The study of blood vitamin D concentrations and expression changes of its anabolic and catabolic pathway enzymes can probably promote our understanding of the effects of vitamin D and its changes during breast tumorigenesis.

DOI: 10.7754/Clin.Lab.2016.151205