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Published on: February 21, 2018
miR-342-3p Inhibits Acute Myeloid Leukemia Progression by Targeting SOX12
Ying Wang1, Xiaonan Guo1, Lihua Wang1
1Department of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei, China.
Background:
It is well known that microRNAs (miRNAs) interfere with the progression of various human malignancies. This article is aimed at exploring the regulating role of miR-342-3p in acute myeloid leukemia (AML) and its mechanism.
Methods:
We used the Gene Expression Omnibus (GEO) database to determine miR-342-3p differential expression patterns in AML patients' plasma and cells as well as healthy individuals' plasma and T cells. Quantitative real-time PCR and Western blotting were performed for plasma and cell miR-342-3p and SRY-related high-mobility-group box (SOX12) expression quantification, and cell counting kit-8 assay and flow cytometry were used for the determination of AML cell growth, cycle, and apoptosis. A dual-luciferase reporter gene assay was further carried out to identify the targeted association between miR-342-3p and SOX12 mRNA 3'UTR after prediction by a bioinformatics website. Pearson's correlation analysis was performed to analyze the connection between miR-342-3p and SOX12 expressions. The LinkedOmics database was utilized to explore the downstream pathways in which SOX12 was enriched.
Results:
Evidently downregulated plasma miR-342-3p and markedly elevated SOX12 were observed in AML patients versus healthy individuals. miR-342-3p mimics suppressed AML cell growth, enhanced apoptosis, and induced G0/G1 phase arrest; conversely, enhanced capacity of AML cells to proliferate, suppressed apoptosis, and accelerated cell cycle were observed after treatment with miR-342-3p inhibitors. SOX12 was confirmed as miR-342-3p's target gene. Overexpressing or knocking down SOX12 reversed miR-342-3p's impacts on AML cell growth, apoptosis, and cycle. Upregulated SOX12 was positively related to DNA replication and RNA polymerase signaling pathways.
Conclusion:
miR-342-3p affects apoptosis of AML cells and their ability to proliferate via targeted regulation of SOX12.
Insights
MicroRNA miR-342-3p is downregulated in acute myeloid leukemia (AML). It regulates AML cell proliferation and apoptosis by targeting SOX12, offering potential therapeutic insights.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are known regulators of various human malignancies.
- This study investigates the specific role of miR-342-3p in acute myeloid leukemia (AML).
Purpose of the Study:
- To explore the regulatory function of miR-342-3p in AML.
- To elucidate the underlying molecular mechanism of miR-342-3p in AML progression.
Main Methods:
- Differential expression analysis using the GEO database.
- Quantitative real-time PCR and Western blotting for gene and protein expression.
- Functional assays including cell counting kit-8, flow cytometry, and dual-luciferase reporter assay.
Main Results:
- miR-342-3p was significantly downregulated in AML patients, while SOX12 was upregulated.
- miR-342-3p mimics inhibited AML cell growth and promoted apoptosis.
- SOX12 was identified as a direct target of miR-342-3p, mediating its effects on AML cells.
Conclusions:
- miR-342-3p plays a crucial role in regulating AML cell proliferation and apoptosis.
- Targeted regulation of SOX12 by miR-342-3p is a key mechanism in AML.
- These findings suggest miR-342-3p as a potential therapeutic target for AML.
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