Overexpression of microRNA-125b inhibits human acute myeloid leukemia cells invasion, proliferation and promotes cells apoptosis by targeting NF-kB signaling pathway

microRNA-125b has been reported to play an novel biological function in the progression and development of several kinds of leukemia. However, the detail role of miR-125b in acute myeloid leukemia (AML) is remains largely unknown. The present study aimed to investigate the biological role of miR125b in AML and the potential molecular mechanism involved in this process. Our results showed that overexpression of miR-125b suppressed AML cells proliferation, invasion and promotes cells apoptosis in a dose-dependent manner, while the miR-NC did not show the same effect. In addition, miR125b induced AML cells G2/M cell cycle arrest in vitro. Overexpression of miR-125b resulted in a significant decrease of the expression of p-IKB-alpha and inhibition of IKB-alpha degradation, and the nuclear translocation of NF-kappa B subunit p65 was abrogated by miR-125b simutaneously. To further verify that miR-125b targeted NF-kappa B signaling pathway, the NF-kappa B-regulated downstream genes that were associated with cell cycle arrest and apoptosis was also determined. The results showed that, miR-125b also affect NF-kappa B-regulated genes expression involved in cell cycle arrest and apoptosis. In conclusion, the present work certificates that miR-125b can significantly inhibit human AML cells invasion, proliferation and promotes cells apoptosis by targeting the NF-kappa B signaling pathway, and thus it can be viewed as an promising therapeutic target for AML. (C) 2017 Published by Elsevier Inc.