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

Biochem Biophys Res Commun. 2017 Jun 17;488(1):60-66. doi: 10.1016/j.bbrc.2017.05.007. Epub 2017 May 4.


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 miR-125b 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, miR-125b induced AML cells G2/M cell cycle arrest in vitro. Overexpression of miR-125b resulted in a significant decrease of the expression of p-IκB-α and inhibition of IκB-α degradation, and the nuclear translocation of NF-κB subunit p65 was abrogated by miR-125b simutaneously. To further verify that miR-125b targeted NF-κB signaling pathway, the NF-κB-regulated downstream genes that were associated with cell cycle arrest and apoptosis was also determined. The results showed that, miR-125b also affect NF-κB-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-κB signaling pathway, and thus it can be viewed as an promising therapeutic target for AML.

Keywords: Acute myeloid leukemia; Apoptosis; Invasion; NF-κB signaling pathway; Proliferation; miR-125b.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis* / genetics
  • Cell Cycle Checkpoints / genetics
  • Cell Proliferation / genetics
  • Cell Survival / genetics
  • Dose-Response Relationship, Drug
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / metabolism
  • Leukemia, Myeloid, Acute / pathology*
  • MicroRNAs / biosynthesis
  • MicroRNAs / genetics*
  • NF-kappa B / metabolism*
  • Signal Transduction* / genetics
  • Structure-Activity Relationship
  • Tumor Cells, Cultured


  • MIRN125 microRNA, human
  • MicroRNAs
  • NF-kappa B