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miR-26b-5p Affects the Progression of Acute Myeloid Leukemia by Regulating the USP48-Mediated Wnt/β-Catenin Pathway

Yu Xie1, Lin Tan1, Kun Wu2

  • 1Department of Hematology, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China.

Critical Reviews in Eukaryotic Gene Expression
|March 20, 2024
PubMed

Insights

MicroRNA-26b-5p (miR-26b-5p) negatively regulates USP48, impacting acute myeloid leukemia (AML) progression. Targeting the miR-26b-5p/USP48 axis offers a potential therapeutic strategy for AML treatment.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Acute myeloid leukemia (AML) is a complex and heterogeneous hematologic malignancy.
  • Understanding AML pathogenesis is crucial for developing effective therapeutic strategies.
  • The role of specific microRNAs and their target genes in AML progression requires further elucidation.

Purpose of the Study:

  • To investigate the functional role of miR-26b-5p and its target USP48 in acute myeloid leukemia (AML).
  • To explore the underlying molecular mechanisms, including the Wnt/β-catenin signaling pathway, by which miR-26b-5p affects AML cell behavior.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot were used to measure gene and protein expression levels.
  • Cell Counting Kit-8 (CCK-8) and flow cytometry assessed cell viability, proliferation, and apoptosis.
  • Coimmunoprecipitation examined the interaction between USP48 and Wnt5a.
  • Bioinformatics analysis predicted correlations between miR-26b-5p, USP48, and patient prognosis.

Main Results:

  • High miR-26b-5p and low USP48 levels correlated with poor prognosis in AML patients.
  • miR-26b-5p was found to negatively regulate USP48 expression.
  • Downregulation of miR-26b-5p inhibited epithelial-mesenchymal transition (EMT), viability, and proliferation while promoting apoptosis in AML cells.
  • USP48 knockdown and miR-26b-5p inhibition effects on AML progression were reversible by a Wnt/β-catenin inhibitor.

Conclusions:

  • miR-26b-5p plays a significant role in regulating AML progression.
  • The miR-26b-5p/USP48 axis potentially influences AML cell behavior via the Wnt/β-catenin signaling pathway.
  • This study highlights miR-26b-5p as a potential therapeutic target for AML.

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