Personalized and Precision Medicine Journal

Abstract Vitamin D (Vit D) ,as an antioxidant contributes to a wide range of diseases including obesity, type 2 diabetes, multiple sclerosis, and certain cancers that oxidative stress plays a vital role in their development. Excessive oxidative stress can damage to DNA and nucleotide pool. Base excision repair and house-cleaning enzymes can protect genome so that any disruption in expression of these genes indicates enhanced susceptibility risk for diseases like cancer. The present study was conducted aimed at evaluating the effect of Vit D on the expression of MYH and MTH1 as DNA repair genes, as well as effect of ViD treatment in Human Umbilical Vein Endothelial Cells (HUVEC) cell line. To do this, bioinformatics tools were used to predict the interaction of MTH1 and MYH with VDR as a specific transcription factor (TF) for  Vit D. The cell line was treated with VitD. Next, viability was evaluated using MTT assay. The mRNA expression of MTH1 and MYH was assessed using real-time PCR at 48h post-treatment with Vit D.  
Results of the study revealed that Vit D could regulate MTH1 and MYH  transcript expression directly through its specific TF; VDR. In response to VitD treatment a different alteration was observed in DNA repair, and non-canonical nucleotide repair genes. Findings of this study showed a new regulation of DNA repair genes in Vit D signaling pathway, and it may be a new perspective for the therapeutic effect of Vit D on related diseases. Variation in interested genes may affect the vitD signaling and personalized medicine should be considered.  

Abstract One of the key molecular mechanisms contributing to the metastatic progression is epithelial to mesenchymal transition (EMT), which drives invasion and migration of various cancer including breast cancer.During tumorigenesis, changes in EMT regulatory pathways lead to a loss of cellular adhesions, changes in the polarization of the cell and cytoskeleton, detachment, migration, intra-vasation, and survival in the vascular system; extravasation, and finally, metastasis.EMT is largely mediated by a core set of EMT-activating transcription factors. The master regulators of the EMT include many pathways, however the primary mediators of the EMT include signaling through TGF-, Notch and Wnt.  The role of EMT in breast cancer has  been demonstrated via numerous in vitro studies in  normal and malignant mammary epithelial cells and via in vivo studies using mouse models of breast cancers. Studying the regulatory pathways of the EMT process can be used as a tool for cancer monitoring ,treatment and possible direct targets for new-combination anticancer personalized medicine.