AUTHOR=Song Jie , Hao Linlin , Zeng Xiangfang , Yang Rui , Qiao Shiyan , Wang Chunli , Yu Hao , Wang Siyao , Jiao Yingying , Jia Hongyao , Liu Songcai , Zhang Ying TITLE=A Novel miRNA Y-56 Targeting IGF-1R Mediates the Proliferation of Porcine Skeletal Muscle Satellite Cells Through AKT and ERK Pathways JOURNAL=Frontiers in Veterinary Science VOLUME=Volume 9 - 2022 YEAR=2022 URL=https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2022.754435 DOI=10.3389/fvets.2022.754435 ISSN=2297-1769 ABSTRACT=

As a key regulator of gene transcription and post-transcriptional modification, miRNAs play a wide range of roles in skeletal muscle development. Skeletal muscle satellite cells contribute to postnatal growing muscle fibers. Thus, the goal of this study was to explore the effects of novel miRNA Y-56 on porcine skeletal muscle satellite cells (PSCs). We found that Y-56 was highly expressed in porcine muscle tissues, and its expression was higher in Bama Xiang pigs than in Landrace pigs. The EdU assay, cell counting kit-8, and flow cytometry results showed that Y-56 overexpression suppressed cell proliferation and cell cycle, whereas Y-56 inhibition resulted in the opposite consequences. The results of qRT-PCR and Western blot showed that Y-56 remarkably inhibited the expression levels of cyclin-dependent kinase 4 (CDK4), proliferating cell nuclear antigen (PCNA), and cyclin D1. We identified that IGF-1R was a direct target of Y-56 by dual-luciferase reporter assay. Moreover, IGF-1R overexpression promoted the proliferation and cell cycle process of PSCs and upregulated the expression of CDK4, PCNA, and cyclin D1. Conversely, IGF-1R knockdown had the opposite effect. Furthermore, IGF-1R overexpression partially reversed the inhibition of the cell proliferation and cell cycle process of PSCs and the downregulation of the expression of CDK4, PCNA, and Cyclin D1 caused by Y-56 overexpression. Finally, Y-56 inhibited the protein expression levels of p-AKT and p-ERK. Collectively, our findings suggested that Y-56 represses the proliferation and cell cycle process of PSCs by targeting IGF-1R-mediated AKT and ERK pathways.