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Updated: Mar 16, 2026
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
[Expression of miR-181a in Acute Myeloid Leukaemia and Its Effect on Cell Proliferation]
Yue Ma1, Mu-Xia Yan2, Zi-Yan Luo2
1Out-patient Department of Pediatrics,Guangzhou Women and Children's Medical Center, Guangzhou 510623, Guangdong Province, China.
Objective:
To investigate the expression of miR-181a in AML cell lines and explore its effect on cell proliferation.
Methods:
The expression of miR-181a in AML cell lines (NB4,HL-60,K562 and MV-4-11) was detected by quantiative polymerase chain reation(qPCR). Moreover, the cell proliferation and cell cycle were evaluated in several cell lines (HL60, NB4 and K562) by using CCK-8 and flow cytometry after the imitative transfection with miR-181a.
Results:
The miR-181a expression was significantly increased in most AML cell lines, including NB4,HL-60 and MV-4-11, but decreased in a few AML cell lines(K562), as compared with that in control(P<0.05). Overexpressed miR-181a in the cell lines significantly enhanced the cell proliferation, as well as the cell ratio of S-to and G2-phase by miR-181a imitative transfection in vitro.
Conclusion:
Overexpression of miR-181a can promote AML cell proliferation. MiR-181a may play an oncogene role in AML, studying the MiR-181a may provide a new method for treatment of AML.
Insights
MicroRNA-181a (miR-181a) is upregulated in most acute myeloid leukemia (AML) cell lines and promotes cancer cell proliferation. Further study of miR-181a may offer novel AML treatment strategies.
Area of Science:
- Molecular Biology
- Cancer Research
- Hematology
Background:
- Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy.
- MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
- The specific role of miR-181a in AML pathogenesis requires further elucidation.
Purpose of the Study:
- To determine the expression levels of miR-181a in various AML cell lines.
- To investigate the functional impact of miR-181a on AML cell proliferation and cell cycle progression.
Main Methods:
- Quantitative polymerase chain reaction (qPCR) was employed to measure miR-181a expression in NB4, HL-60, K562, and MV-4-11 cell lines.
- Cell proliferation was assessed using the CCK-8 assay.
- Cell cycle distribution was analyzed by flow cytometry following miR-181a mimic transfection in HL-60, NB4, and K562 cells.
Main Results:
- miR-181a expression was significantly elevated in NB4, HL-60, and MV-4-11 cell lines compared to controls (P<0.05).
- Conversely, miR-181a expression was decreased in the K562 cell line.
- Overexpression of miR-181a via transfection led to enhanced proliferation and an increased proportion of cells in the S and G2 phases of the cell cycle.
Conclusions:
- Upregulation of miR-181a promotes proliferation in AML cell lines.
- miR-181a exhibits oncogenic properties in AML.
- Targeting miR-181a may represent a potential therapeutic strategy for AML treatment.
