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MicroRNA-125a regulates proliferation and apoptosis of acute myeloid leukemia through targeting NF-κB pathway

M-Y Shen1, Y Wang, S-Y Cui

  • 1First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China. shandongxuruirong@163.com.

European Review for Medical and Pharmacological Sciences
|May 23, 2019
PubMed
Abstract

Insights

MicroRNA-125a significantly inhibits acute myeloid leukemia (AML) cell growth and invasion. This microRNA also induces apoptosis and cell cycle arrest by regulating the NF-κB pathway in AML cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy.
  • MicroRNAs play crucial roles in regulating gene expression and cellular processes.
  • Understanding the role of specific microRNAs in AML is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional role of microRNA-125a in the biological behavior of acute myeloid leukemia (AML) cells.
  • To elucidate the molecular mechanisms by which microRNA-125a affects AML cell proliferation, apoptosis, invasion, and cell cycle.
  • To determine the potential of microRNA-125a as a therapeutic target in AML.

Main Methods:

  • Transfection of microRNA-125a mimic into the HL60 AML cell line.
  • Assessment of cell viability using MTT assay.
  • Quantification of apoptosis and invasion via flow cytometry and Transwell assays, respectively.
  • Analysis of protein and mRNA expression levels of key genes involved in cell cycle, apoptosis, and signaling pathways (e.g., Bcl-2, caspase-3, p53, NF-κB) using Western blot and qRT-PCR.

Main Results:

  • Overexpression of microRNA-125a significantly inhibited HL60 cell viability and proliferation.
  • MicroRNA-125a promoted apoptosis by increasing caspase-3 and caspase-9 activities and upregulating pro-apoptotic genes (Bax, p53, caspase-8).
  • MicroRNA-125a reduced the invasive potential of AML cells and arrested the cell cycle in the G2/M phase, partly by downregulating cell cycle genes and the NF-κB pathway.

Conclusions:

  • MicroRNA-125a acts as a tumor suppressor in AML by inhibiting cell proliferation and invasion.
  • MicroRNA-125a induces apoptosis and G2/M cell cycle arrest in AML cells.
  • The regulatory effects of microRNA-125a involve modulation of the NF-κB signaling pathway, highlighting its therapeutic potential in AML treatment.

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