Acute myeloid leukemia (AML) is the most common pediatric malignancy and a major cause of morbidity and mortality in children. miR-100 is associated with progression of various diseases including AML. The aim of this study was to explore the underlying molecule mechanisms of miR-100 involved in AML. The expressions of miR-100 and ataxia telangiectasia mutated (ATM) in pediatric AML patients and cell lines were monitored using qRT-PCR and western blot assays. MTT assay was carried to evaluate cell viability. Cell apoptosis was measured by flow cytometry. The binding sites between miR-100 and ATM were predicted by mirtarbase database. Luciferase reporter assay was used to confirm the relationship between miR-100 and ATM. miR-100 expression was highly expressed in bone marrow of AML patients and cell lines. Moreover, Knockdown of miR-100 led to the inhibition of viability and promotion of apoptosis in Kasumi-1 and MV-4-11 cells. miR-100 harbored the 3'UTR of ATM. Meanwhile, the expression of ATM was downregulated in bone marrow of AML patients and AML cell lines. Subsequently, a negative correlation between miR-100 and ATM in bone marrow of AML patients was also observed. Furthermore, ectopic expression of ATM repressed cell viability while enhanced apoptosis. Notably, loss of ATM attenuated the effect of miR-100 depletion on cell viability and apoptosis in AML cells. miR-100 participates in cell viability and apoptosis by targeting ATM in pediatric AML. (C) 2019 Elsevier Inc. All rights reserved.