<p>microRNAs play a crucial role in the intricate process of muscle satellite cells proliferation and differentiation. Previous studies have demonstrated that miR-2400 can regulate bovine skeletal muscle satellite cell (MuSCs) proliferation, yet the underlying mechanism remains incompletely elucidated. In this study, we employed bioinformatics prediction and dual luciferase reporter assays to establish that miR-2400 directly targets the 3’ untranslated regions (UTRs) of melanoma antigen family D1 (MAGED1) mRNA, thereby suppressing its expression. To ascertain whether miR-2400 affects the proliferation of MuSCs through MAGED1, we constructed the MAGED1 interference vector using RNA interference technology (RNAi) and assessed changes in MuSCs proliferation subsequent to MAGED1 interference. The experimental data indicate that the cell viability and the rate of EdU-positive cells of MuSCs were increased after interference with MAGED1. The proportion of S-phase cells and the expression level of cell cycle-associated proteins CCND2 and CCNB1 increased. These findings align with miR-2400’s role in promoting cell proliferation and suggest that miR-2400 exerts its effects by directly targeting MAGED1.</p>

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miR-2400 promotes proliferation of bovine skeletal muscle-derived satellite cells by regulating MAGED1 genes expression

  • Li Yang,
  • Hai-Jing Luo,
  • Zhi-An Gong,
  • Wen-Tian Zhang,
  • Jing-Xuan Cui,
  • Xue-Peng Fu,
  • Wei-Wei Zhang

摘要

microRNAs play a crucial role in the intricate process of muscle satellite cells proliferation and differentiation. Previous studies have demonstrated that miR-2400 can regulate bovine skeletal muscle satellite cell (MuSCs) proliferation, yet the underlying mechanism remains incompletely elucidated. In this study, we employed bioinformatics prediction and dual luciferase reporter assays to establish that miR-2400 directly targets the 3’ untranslated regions (UTRs) of melanoma antigen family D1 (MAGED1) mRNA, thereby suppressing its expression. To ascertain whether miR-2400 affects the proliferation of MuSCs through MAGED1, we constructed the MAGED1 interference vector using RNA interference technology (RNAi) and assessed changes in MuSCs proliferation subsequent to MAGED1 interference. The experimental data indicate that the cell viability and the rate of EdU-positive cells of MuSCs were increased after interference with MAGED1. The proportion of S-phase cells and the expression level of cell cycle-associated proteins CCND2 and CCNB1 increased. These findings align with miR-2400’s role in promoting cell proliferation and suggest that miR-2400 exerts its effects by directly targeting MAGED1.