/ dysregulation predicts clinical outcome and facilitates leukemogenesis by activating PI3K/Akt signaling pathway in acute myeloid leukemia.

() has been reported as a significant cancer-associated microRNA, which was often epigenetically silenced and acted as a tumor suppressor gene in diverse human solid tumors. Conversely, recent studies show that overexpression was identified in both adult and pediatric acute myeloid leukemia (AML), suggesting that it might play an oncogenic role of in AML. However, the role of during leukemogenesis remains to be elucidated. / expression was detected by real-time quantitative PCR and/or western blot. Survival analysis was performed to explore the association between / expression and the prognosis, and further validated by public databases. Gain-of-function experiments determined by cell proliferation, apoptosis, and differentiation were conducted to investigate the biological functions of /. Herein, we found that expression, independent of its methylation, was significantly increased and negatively correlated with reduced expression in AML. Moreover, aberrant / expression independently affected chemotherapy response and leukemia-free/overall survival in patients with AML. Gain-of-function experiments in vitro showed the oncogenic role of by affecting cell apoptosis and proliferation in AML, and could be rescued by restoration. Mechanistically, we identified and verified that contributed to leukemogenesis through activating PI3K/Akt signaling pathway. Collectively, aberrant / expression was an independent prognostic biomarker in AML. / dysregulation facilitated leukemogenesis through the activation of PI3K/Akt signaling pathway.