Tumor-suppressing effects of miR-381-3p in pediatric acute myeloid leukemia via ROCK1 downregulation

Ye, Qidong; Ying, Qianqian; Dai, Qiaoyan; Li, Cong; Xiao, Gang

doi:10.1007/s10142-022-00950-9

Funct Integr Genomics

2023

DOI: 10.1007/s10142-022-00950-9

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Tumor-suppressing effects of miR-381-3p in pediatric acute myeloid leukemia via ROCK1 downregulation

Qidong Ye

Qianqian Ying

Qiaoyan Dai

et al.

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Cited by 4 publications

References 36 publications

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Exosome‐Shuttled METTL14 From AML‐Derived Mesenchymal Stem Cells Promotes the Proliferation and Radioresistance in AML Cells by Stabilizing ROCK1 Expression via an m6A‐IGF2BP3‐Dependent Mechanism

Wang,

Song,

Yuan

et al. 2024

Drug Development Research

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Acute myelogenous leukemia (AML)‐derived mesenchymal stem cells (MSCs) (AML‐MSCs) have been identified to play a significant role in AML progression. The functions of MSCs mainly depend on their paracrine action. Here, we investigated whether AML‐MSCs functioned in AML cells by transferring METTL14 (Methyltransferase 14) into AML cells via exosomes. Functional analyses were conducted using MTT assay, 5‐ethynyl‐2‐deoxyuridine assay and flow cytometry. qRT‐PCR and western blot analyses detected levels of mRNAs and proteins. Exosomes (exo) were isolated from AML‐MSCs by ultracentrifugation. The m6A modification profile was determined by methylated RNA immunoprecipitation (MeRIP) assay. The interaction between Insulin‐like growth factor 2 mRNA‐binding protein 3 (IGF2BP3) and Rho Kinase 1 (ROCK1) was validated using RIP assay. AML‐MSCs incubation promoted the proliferation and radioresistance in AML cells. Moreover, AML‐MSCs incubation led to increases in m6A levels and METTL14 levels in AML cells. METTL14 was transferred into AML cells by packaging into exosomes of AML‐MSCs. The knockdown of METTL14 in AML‐MSCs exosomes could reduce the proliferation and radioresistance in AML cells. Mechanistically, METTL14 induced ROCK1 m6A modification and stabilized its expression by an m6A‐IGF2BP3‐dependent mechanism. Rescue assay showed that ROCK1 overexpression reversed the inhibitory effects of METTL14 silencing in AML‐MSCs exosomes on AML cell proliferation and radioresistance. Exosome‐shuttled METTL14 from AML‐MSCs promoted proliferation and conferred radioresistance in AML cells by stabilizing ROCK1 expression via an m6A‐IGF2BP3‐dependent mechanism.

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Exosome‐Shuttled METTL14 From AML‐Derived Mesenchymal Stem Cells Promotes the Proliferation and Radioresistance in AML Cells by Stabilizing ROCK1 Expression via an m6A‐IGF2BP3‐Dependent Mechanism

Wang,

Song,

Yuan

et al. 2024

Drug Development Research

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MiR-455-3p mediates PPARα through UBN2 to promote apoptosis and autophagy in acute myeloid leukemia cells

Xie,

Tan,

et al. 2023

Experimental Hematology

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Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia

Wang

Tong

Xun

et al. 2023

Fundamental Research

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Tumor-suppressing effects of miR-381-3p in pediatric acute myeloid leukemia via ROCK1 downregulation

Cited by 4 publications

References 36 publications

Exosome‐Shuttled METTL14 From AML‐Derived Mesenchymal Stem Cells Promotes the Proliferation and Radioresistance in AML Cells by Stabilizing ROCK1 Expression via an m6A‐IGF2BP3‐Dependent Mechanism

Exosome‐Shuttled METTL14 From AML‐Derived Mesenchymal Stem Cells Promotes the Proliferation and Radioresistance in AML Cells by Stabilizing ROCK1 Expression via an m6A‐IGF2BP3‐Dependent Mechanism

MiR-455-3p mediates PPARα through UBN2 to promote apoptosis and autophagy in acute myeloid leukemia cells

Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia

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