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Updated: Jan 23, 2026

In Ovo Xenografting of Patient-Derived Acute Lymphoblastic Leukemia (ALL) Cells (PDX-ALL)
Published on: August 1, 2025
MiR-137 inhibits cell proliferation in acute lymphoblastic leukemia by targeting JARID1B
Yiqun Huang1, Yong Zou1, Ruiji Zheng1
1Department of Hematology, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian, China.
Aim:
This study aimed to investigate the possible functions of interaction between JARID1B and miR-137 in ALL.
Methods:
The levels of H3K4me3 and H3K4me2 and the expression of JARID1B and miR-137 were analyzed in six ALL cell lines and 30 ALL patients. The effects of miR-137 and JARID1B on cell proliferation and apoptosis were investigated by silencing or promoting the respective genes. The interaction between miR-137 and JARID1B was confirmed by double-luciferase report assay.
Results:
The histone H3K4 expressions and miR-137 expression were lower in 30 ALL patients and in six ALL cell lines, while the expression of JARID1B was elevated. A negative correlation was observed between JARID1B and miR-137. Over-expression of miR-137 led to decreasing cell proliferation and increasing apoptosis in MOLT-4 and BALL-1 cells. MiR-137 inhibitor up-regulated JARID1B in these two cell lines, while promoted proliferation in BALL-1 cells only. Dual-luciferase report assay suggested that JARID1B was a direct target of miR-137 in ALL cell lines.
Conclusions:
The expression of miR-137 was declined in ALL, and JARID1B was directly repressed by miR-137. Aberrant JARID1B expression could result in abnormal histone methylation, which might be one cause of ALL.
Insights
MicroRNA-137 (miR-137) is downregulated in acute lymphoblastic leukemia (ALL), and JARID1B directly represses it. Aberrant JARID1B expression may cause ALL through abnormal histone methylation.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Acute lymphoblastic leukemia (ALL) is a hematological malignancy with complex molecular underpinnings.
- JARID1B is a histone demethylase implicated in various cancers.
- MicroRNAs (miRNAs) play crucial roles in gene regulation and are often dysregulated in leukemia.
Purpose of the Study:
- To investigate the functional interaction between JARID1B and miR-137 in ALL.
- To determine the impact of this interaction on leukemia cell behavior.
Main Methods:
- Analysis of H3K4me3, H3K4me2, JARID1B, and miR-137 expression in ALL cell lines and patient samples.
- Gene silencing and overexpression experiments to assess effects on cell proliferation and apoptosis.
- Dual-luciferase reporter assay to confirm direct interaction between JARID1B and miR-137.
Main Results:
- Lower levels of H3K4 methylation and miR-137, with elevated JARID1B, were observed in ALL.
- miR-137 overexpression reduced proliferation and increased apoptosis in ALL cells.
- JARID1B was identified as a direct target of miR-137, with a negative correlation between their expressions.
Conclusions:
- miR-137 is downregulated in ALL and directly represses JARID1B.
- Dysregulated JARID1B expression due to miR-137 downregulation may contribute to ALL pathogenesis via aberrant histone methylation.
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