The process involved relationship between your promoter region of the gene and specificmiRNA. We also ignored this possible mechanism by blasting miR 199a 5p and the promoter sequence of DRAM1 and Beclin1, and we found there have been no potential binding sites. Steitz and Vasudevan performed a number of studies to show the ability of miRNAs to stimulate gene interpretation by targeting the 30UTR. The authors demonstrated that cell cycle tips determine whether miRNAs stimulate or repress target order FK228 genes. They suggested that miRNAs could activate gene translation in quiescent cycle, which was set off by serum starvation o-r contact inhibition, and repress translation within the later stages of the cell cycle. Such phenomenon has been found to happen naturally in Xenopus laevis oocytes. Out of this perspective, we sought to investigate whether miR 199a 5p induces G0/G1 arrest so as to up manage its target genes. Nevertheless, we found that miR 199a 5p induced accumulation of cells at G2/M peak in MDA MB 231 but not in MCF7 cell line. After exposing both cell lines to IR, percentage of cells increased at G2/M and reduced at G0/G1, such event was com-pletely reversed upon overexpression of miR 199a 5p in both cell lines. The risk believes that miRNA mediated gene activation could be cell line specific feature. In MIA PaCa 2 pancreatic cancer cells, MiR 21 ectopic overexpression led to substantial upregulation of Bcl 2 target gene expression by targeting the 30UTR of Bcl 2 mRNA, although it was documented that miR 21 inhibits Bcl 2 expression in breast cancer cells Ribonucleic acid (RNA) also via targeting Bcl 2 30UTR. Similarly, via direct action on 30UTR of Kr ppel like factor 4 mRNA, overexpression of miR 206 endorsed KLF4 gene expression in MCF10A mammary epithelial cells, while it suppressed expression of KLF4 in MDA MB 231 breast cancer cells. Collectively, it seems that the influence of miR 199a 5p on DRAM1 and Beclin1 genes could be also cell line specific. Naturally, further complete investigations are warranted. Overall our results add more interest and concern to further comprehend the mechanisms of miRNAs, specially regarding how miRNAs determine the gene expression that is still largely illusive. Next we showed that IR up regulated miR 199a 5p expression in MCF7 Dinaciclib 779353-01-4 and down regulated miR 199a 5p expression inMDA MB 231cells. After transfection with mimic, miR 199a 5p appearance was enhanced pre IR and further enhanced post IR in MCF7 cells. Nevertheless, we didn’t see a loss of miR 199a 5p in MDA MD 231 cell line in reaction to IR probably due to very high degrees of miR 199a5p after transfection with copy, just like.