miR-181a promotes G1/S transition and cell proliferation in pediatric acute myeloid leukemia by targeting ATM.

摘要: Abnormal expression of miRNAs is intimately related to a variety human cancers. The purpose this study confirm the miR-181a and elucidate its physiological function mechanism in pediatric acute myeloid leukemia (AML). Pediatric AML patients healthy controls were enrolled, ataxia telangiectasia mutated (ATM) tissues examined using quantitative PCR. Moreover, cell proliferation cycle evaluated several lines (HL60, NB4 K562) by flow cytometry after transfected with mimics inhibitors, or ATM siRNA control siRNA. Finally, as potential target protein was examined. We found that significantly increased AML, which showed an inverse association expression. Overexpressed enhanced proliferation, well ratio S-phase cells transfection vitro. Luciferase activity reporter construct identified direct molecular miR-181a. results revealed novel through regulates G1/S transition regulating tumor suppressor ATM, providing insights into AML.