Email address details are different from the prior report that the quantities of mRNA and ATM protein were afflicted with DNAPKcs, which might be as a result of different cell lines that we noticed. We next examined the post translational destruction of ATM by evaluating the effects of cycloheximide Dizocilpine MK 801 on ATM protein level changes at different times between M059J and M059K cells. The results showed there clearly was no clear difference in the ATM level change between M059J and M059K cells, indicating that the low level of ATM in M059J cells might not be due to the post translational modification. These results led us to take into account whether epigenetic change plays any part in the reduced expression ofATMin M059J cells. The epigenetic modification generally contains methylation and miRNA modification. We first tested the hypothesis that miRNAs may play a role in the low expression of ATM in M059J cells. For this purpose, we searched three databases for the miRNA prospects which could target the 3_ UTR of ATM. As we found significantly more than twenty miRNAs that could be individuals, a result. After evaluating the expression levels of these miRNAs between Inguinal canal M059J and M059K cells by using a real time PCR approach, we discovered that only miR 100 was over expressed in M059J cells as weighed against M059K cells, suggesting that ATM could be the mark of miR 100. The expression of miR 100 in M059J cells was further verified by an RNase protection assay. These results claim that ATM might be the goal of miR 100. You will find three putative miR 100 binding web sites of the ATM 3_UTR place. We built the constructs encoding the ATM 3_ UTR place carrying a miR 100 binding site and we described them as b1, b2 or b3, and the constructs containing a related mutated site, we named CX-4945 1009820-21-6 as mb1, mb2 or mb3. To research whether ATM was the prospective of miR 100, we examined the effects of miR 100 on translation inhibition using a luciferase assay with the vector encoding the putative or mutant miR 100 binding site of ATM 3_ UTR. The results showed that the translation activity was substantially inhibited by the putative website of 3_ UTR of ATM, b1, otherwise, the translation activity wasn’t affected at all by b2, b3 or mb1?mb3 that wasmutated at the feed location. These results claim that miR 100 restricted ATM expression in M059J cells by targeting the particular b1 site of the 3_ UTR of ATM. We examined the consequences of the miR 100 inhibitor or Dicer siRNA on the ATM expression in M059J and M059K cells, to investigate whether the over expressed miR 100 in M059J cells may be the major reason to prevent ATM expression. The results showed that when the expression of miR 100 or the miRNA building process was restricted in M059J, ATM was up regulated, showing that ATM could be the target of miR 100.