miR-103-3p Regulates the Proliferation and Differentiation of C2C12 Myoblasts by Targeting BTG2

• Published in: International journal of molecular sciences Vol. 24; no. 20; p. 15318
• Main Authors: He, Yulin, Yang, Peiyu, Yuan, Tiantian, Zhang, Lin, Yang, Gongshe, Jin, Jianjun, Yu, Taiyong
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 18.10.2023; MDPI
• Subjects: Atrophy; BTG2; Cell cycle; Cell growth; differentiation; Genes; MicroRNAs; miR-103-3p; Musculoskeletal system; myoblasts; Myogenesis; proliferation; Protein expression; Proteins; Senescence
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms242015318

Skeletal muscle, a vital and intricate organ, plays a pivotal role in maintaining overall body metabolism, facilitating movement, and supporting normal daily activities. An accumulating body of evidence suggests that microRNA (miRNA) holds a crucial role in orchestrating skeletal muscle growth. Therefore, the primary aim of this study was to investigate the influence of miR-103-3p on myogenesis. In our study, the overexpression of miR-103-3p was found to stimulate proliferation while suppressing differentiation in C2C12 myoblasts. Conversely, the inhibition of miR-103-3p expression yielded contrasting effects. Through bioinformatics analysis, potential binding sites of miR-103-3p with the 3’UTR region of BTG anti-proliferative factor 2 (BTG2) were predicted. Subsequently, dual luciferase assays conclusively demonstrated BTG2 as the direct target gene of miR-103-3p. Further investigation into the role of BTG2 in C2C12 myoblasts unveiled that its overexpression impeded proliferation and encouraged differentiation in these cells. Notably, co-transfection experiments showcased that the overexpression of BTG2 could counteract the effects induced by miR-103-3p. In summary, our findings elucidate that miR-103-3p promotes proliferation while inhibiting differentiation in C2C12 myoblasts by targeting BTG2.