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Updated: Apr 27, 2026

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
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Dual mechanisms by which miR-125b represses IRF4 to induce myeloid and B-cell leukemias

Alex Yick-Lun So1, Reeshelle Sookram1, Aadel A Chaudhuri2

  • 1Department of Biology, California Institute of Technology, Pasadena, CA;

Blood
|July 10, 2014
PubMed

Insights

MicroRNA-125b (miR-125b) drives myeloid and B-cell leukemia by promoting cancer in blood stem cells. It inhibits IRF4 through different mechanisms, leading to distinct leukemias.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • MicroRNA-125b (miR-125b) is an oncomir implicated in various human blood cancers.
  • Constitutive miR-125b upregulation in mice can lead to myeloid and B-cell leukemia.

Purpose of the Study:

  • To investigate the role of miR-125b in inducing tumorigenesis in hematopoietic progenitor cells.
  • To elucidate the distinct mechanisms by which miR-125b drives myeloid and B-cell leukemia.

Main Methods:

  • Functional and genetic analyses were employed.
  • Investigated miR-125b's impact on hematopoietic progenitor cells and stem cells.

Main Results:

  • miR-125b promotes myeloid and B-cell neoplasm by inducing tumorigenesis in hematopoietic progenitor cells.
  • miR-125b enhances myeloid progenitor output, immortality, self-renewal, and tumorigenesis.
  • miR-125b inhibits interferon regulatory factor 4 (IRF4) through distinct mechanisms for myeloid and B-cell leukemia.

Conclusions:

  • miR-125b induces myeloid leukemia by repressing IRF4 mRNA.
  • miR-125b induces B-cell leukemia via genetic deletion of the IRF4 gene.
  • miR-125b plays a critical role in the development of myeloid and B-cell leukemias through IRF4 inhibition.

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