MiR-26a Inhibits Porcine Adipogenesis by Regulating ACADM and ACSL1 Genes and Cell Cycle Progression

MicroRNAs play essential roles in biological processes by regulating gene expression at the post-transcriptional level. Our previous studies suggested the role of miR-26a in porcine fat accumulation. Here, through gain- and loss-of-function analyses, we first showed that miR-26a increased the proliferation of porcine preadipocytes by promoting cell division and that miR-26a inhibited the preadipocyte differentiation. Next, acyl-CoA dehydrogenase, medium chain (ACADM) was revealed to promote the proliferation and differentiation of preadipocytes for the first time. Then, it was revealed that miR-26a regulates adipogenesis by directly binding to the 3' untranslated region of ACADM and the long-chain acyl-Co A synthetase 1 (ACSL1) gene, a previously known regulator of adipogenesis. Finally, RNA-sequencing, performed on preadipocytes overexpressing miR-26a, identified 337 differentially expressed genes in the early stage of adipogenesis; among them, nine genes were characterized as potential targets of miR-26a. The 337 genes were mainly involved in Gene Ontology terms related to cell division, indicating that cell cycle progression was also a major event regulated by miR-26a during adipogenesis. We provide novel data for understanding the molecular mechanisms underlying adipogenesis, which will contribute to controlling fat accumulation in animals.