Pediatric acute myeloid leukemia (AML) is a complex and heterogeneous disease. Several studies have shown the regulatory functions of microRNAs (miRNAs) in pediatric AML progression, and in this study, we aimed to evaluate the biological role of miR-206 in pediatric AML. The results demonstrated that miR-206 expression levels in the bone marrow and serum of pediatric AML patients were remarkably decreased than those in normal controls, and low serum miR-206 expression was closely associated with the unfavorable clinicopathological characteristics and prognosis of pediatric AML patients. In addition, in vitro functional experiments revealed that overexpression of miR-206 significantly inhibited AML cell proliferation partly through induction of cell cycle arrest. Further studies showed that Cyclin D1 might be a direct target of miR-206 in AML cells, and the impaired proliferation ability of miR-206-overexpressing AML cells was notably rescued by Cyclin D1 restoration. Accordingly, the findings of our study suggested that miR-206 might serve as a promising prognostic marker and a potential therapy target for patients with pediatric AML.
Keywords: Cell cycle; Cyclin D1; Pediatric acute myeloid leukemia; microRNA-206.
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