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Updated: Nov 7, 2025

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy
Hui-Min Liu1, Chun-Ling Guo2, Yao-Fang Zhang1
1Department of Hematology, The Second Hospital of Shanxi Medical University, Taiyuan, China.
Leonurine effectively inhibits chronic myeloid leukemia (CML) by downregulating miR-18a-5p and upregulating SOCS5, suppressing the JAK2/STAT3 pathway. This natural compound shows significant anti-leukemia effects in vitro and in vivo.
Area of Science:
- Pharmacology
- Molecular Biology
- Oncology
Background:
- Leonurine, a natural alkaloid from Herba leonuri, shows anticancer potential in solid tumors.
- Chronic myeloid leukemia (CML) is a malignancy requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the efficacy of leonurine against chronic myeloid leukemia (CML).
- To elucidate the molecular mechanisms underlying leonurine's anti-leukemic effects.
Main Methods:
- Cell proliferation, migration, colony formation, and apoptosis assays were performed on CML cells.
- In vivo studies using CML xenografts were conducted.
- Quantitative real-time PCR, Western blotting, and siRNA were used to analyze gene and protein expression and regulatory pathways (miR-18a-5p, SOCS5, JAK2/STAT3).
Main Results:
- Leonurine inhibited CML cell proliferation, migration, and colony formation while promoting apoptosis.
- Leonurine reduced CML xenograft growth in vivo.
- Leonurine upregulated SOCS5 expression and suppressed JAK2/STAT3 signaling, an effect mediated by SOCS5.
- Leonurine decreased miR-18a-5p expression, which targets SOCS5, thereby relieving SOCS5 repression.
Conclusions:
- Leonurine demonstrates significant anti-leukemic activity against CML.
- The anti-leukemic effect of leonurine is mediated through the miR-18a-5p/SOCS5/JAK2/STAT3 signaling pathway.
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