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Updated: Jun 6, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Published on: April 6, 2012

MicroRNA miR-125b causes leukemia.

Marina Bousquet¹, Marian H Harris, Beiyan Zhou

¹Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.

Proceedings of the National Academy of Sciences of the United States of America

|December 2, 2010

Summary

MicroRNA miR-125b overexpression accelerates leukemia development. This study demonstrates miR-125b

Area of Science:

Molecular Biology
Hematology
Oncology

Background:

MicroRNA miR-125b is implicated in various leukemias.
Chromosomal translocations like t(2;11) and t(11;14) lead to miR-125b overexpression in myelodysplasia, acute myeloid leukemia, and B-cell acute lymphoblastic leukemia.
The precise oncogenic role of miR-125b in hematopoiesis requires further investigation.

Purpose of the Study:

To investigate the oncogenic mechanism of miR-125b in hematopoiesis and leukemia development.
To determine if miR-125b overexpression is sufficient to induce leukemia independently.
To assess the impact of miR-125b on BCR-ABL-induced leukemia.

Main Methods:

Transplantation experiments in mice using fetal liver cells.
Ectopic expression of miR-125b in transplanted cells.

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Coexpression of miR-125b with the BCR-ABL fusion gene.

Main Results:

Ectopic miR-125b expression increased white blood cell counts (neutrophils, monocytes) and caused macrocytic anemia.
Half of the mice developed B-cell acute lymphoblastic leukemia, T-cell acute lymphoblastic leukemia, or myeloproliferative neoplasm.
Coexpression with BCR-ABL accelerated leukemia development, indicating a proliferative advantage conferred by miR-125b.

Conclusions:

Overexpression of miR-125b is sufficient to induce leukemia independently in a mouse model.
miR-125b plays a significant role in early hematopoiesis.
miR-125b shortens the latency of BCR-ABL-induced leukemia.