studies demonstrate that DRAM1 goes to an evolutionarily conserved family of proteins, and encodes some p53 inducible splice variants, part of which localize to peroxisomes and autophagosomes and are required for p53 induced autophagy. probably as a result of low basal autophagic activity in MCF7, we’re able to not discover a clear reduction in percent of puncta positive cells or in LC3 II by overexpressing miR 199a 5p pre IR. Using in silico analysis, we found Beclin1 and DRAM1 were possible targets of miR199a 5p. The ATP-competitive ALK inhibitor other putative target gene, Beclin1/ ATG6 is the commonly studied autophagy associated gene. As a vital autophagy promoting gene beclin1 includes a central position in machinery and play, including IR caused autophagy. Using Western blotting and luciferase assay, we showed that both DRAM1 and Beclin1 are novel target genes for miR 199a 5p. Overexpression of miR 199a 5p in MCF7 cells suppressed the expression of DRAM1 and Beclin1 via targeting the 30UTR of those genes. Added to this, miR 199a 5p may successfully control the expression of DRAM1 and Beclin1 proteins in MCF7 cells in the pres-ence or absence of IR. Jointly, these finding imply miR 199a 5p potently suppresses IR induced autophagy in MCF7 cells through its inhibitory impact on Beclin1 and DRAM1 a minimum of partially, because one miRNA might target many genes simultaneously. Very recently, it has been noted Cellular differentiation that miR 199a 5p targets and inhibits autophagy related gene 7 to suppress Cisplatin induced autophagy in liver cancer cells. In MDA MB 231, which can be characterized by being highly invasive estrogen receptor negative breast cancer cell line, while MCF7 are low invasive estrogen receptor negative cells, we showed that miR 199a 5p operated in an entirely opposite tendency. Overexpression of miR 199a 5p increased both basal and IR induced autophagy within this cell line. CTEP Similarly, miR 199a 5p ectopic overexpression triggered sharp up regulation of DRAM1 and Beclin1 target genes appearance through immediately targeting 30UTR of DRAM1 o-r Beclin1 mRNA in MDA MB 231 cells. In the human body of literature in the area of miRNAs, we found only countable number of studies reported that miRNAs might, through various mechanisms, up regulate instead of control gene expression. In human liver cells, miR 122 was found to bind to 50UTR of hepatitis C virus RNA and trigger its translation. MiR 10a was observed to bind to 50UTRsegment of ribosomal protein mRNA, leading to stimulation of ribosome biogenesis and ribosomal protein mRNA translation and finally up control global protein synthesis. We ignored this possible mechanism by raging miR 199a 5p and the 50UTR series of DRAM1 and Beclin1, and we found there have been no potential binding sites.