The miR-6240 target gene Igf2bp3 promotes myoblast fusion by enhancing myomaker mRNA stability

文献类型： 外文期刊

第一作者： Huang, Yuxin

作者： Huang, Yuxin;Wang, Wei;Fan, Xinhao;Liu, Xiaoqin;Liu, Weiwei;Wang, Zishuai;Yang, Yalan;Tang, Zhonglin;Huang, Yuxin;Liu, Weiwei;Li, Yixing;Huang, Yuxin;Liu, Weiwei;Li, Yixing;Wang, Wei;Fan, Xinhao;Wang, Wei;Fan, Xinhao;Huang, Yuxin;Wang, Wei;Fan, Xinhao;Liu, Xiaoqin;Liu, Weiwei;Wang, Zishuai;Yang, Yalan;Tang, Zhonglin

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关键词： Igf2bp3; Myobalst fusion; Mymk; mRNA stability; miR-6240; Myogenesis

期刊名称：CELLULAR & MOLECULAR BIOLOGY LETTERS （ 影响因子：10.2； 五年影响因子：9.4 ）

ISSN： 1425-8153

年卷期： 2024 年 29 卷 1 期

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收录情况： SCI

摘要： BackgroundMyoblast fusion plays a crucial role in myogenesis. Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) functions as an RNA N6-methyladenosine reader and exerts important roles in various biological processes. While our prior study suggested Igf2bp3 contributes to myogenesis, its molecular regulatory mechanism is largely unclear.MethodsReal-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used for gene expression analysis. siRNA and CRISPRi technologies were conducted to knockdown the expression of Igf2bp3. CRISPR/Cas9 technology was performed to knockout Igf2bp3. The Igf2bp3 overexpression vector was designed using the pcDNA3.1(+) vector. Immunofluorescence detection was employed for subcellular localization and cell differentiation analysis. Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2 '-deoxyuridine (EdU) assays were conducted for cell proliferation and fusion detection. The dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were utilized for regulatory mechanism analysis of Igf2bp3.ResultsThe overexpression of Igf2bp3 enhances myoblast fusion while knockdown of Igf2bp3 blocks the formation of myotubes. miR-6240 promotes myoblast proliferation while preventing myoblast differentiation and fusion by targeting the 3 ' untranslated rgion (UTR) of Igf2bp3. Notably, the impacts of miR-6240 mimics on myoblast proliferation, differentiation, and fusion can be effectively counteracted by the overexpression of Igf2bp3. Moreover, our findings elucidate a direct interaction between Igf2bp3 and the myoblast fusion factor myomaker (Mymk). Igf2bp3 binds to Mymk to enhance its mRNA stability. This interaction results in increased expression of Mymk and heightened myoblast fusion.ConclusionsOur study unveils Igf2bp3 as a novel post-transcriptional regulator of myoblast fusion through the miR-6240/Mymk axis, significantly contributing to our understanding of skeletal muscle development.

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