MiR-206 Suppresses Triacylglycerol Accumulation via Fatty Acid Elongase 6 in Dairy Cow Mammary Epithelial Cells

MicroRNAs (miRNAs) can regulate the expression of target genes and modulate various biological processes, including lipid metabolism. Specifically, miR-206 impaired lipid accumulation in nonruminant hepatocytes. However, the effect and regulatory mechanisms of miR-206 on lipid metabolism in bovine mammary cells remains unclear. In the present study, we investigated the effects of miR-206 and its target gene on lipid metabolism in bovine mammary epithelial cells (BMECs). The results revealed that miR-206 overexpression significantly decreased the triacylglycerol (TAG) concentration and the abundance of acetyl-coenzyme A carboxylase alpha (ACACA), fatty acid synthase (FASN), sterol regulatory element binding transcription factor 1 (SREBF1), diacylglycerol acyltransferase 1 (DGAT1), 1-acylglycerol-3-phosphate O-acyltransferase 6 (AGPAT6), lipin 1 (LPIN1), and fatty acid elongase 6 (ELOVL6) coupled with an increase in patatin-like-phospholipase domain containing 2 (PNPLA2). Inhibition of miR-206 resulted in promotion of milk fat metabolism in vitro. Using a dual luciferase reporter assay, we demonstrated that ELOVL6 is a target of miR-206. Furthermore, intervention of ELOVL6 significantly downregulated the TAG level and elongation index of C16:0 and C16:1n-7 in BMECs. Finally, ELOVL6 siRNA partially alleviated the increased TAG accumulation caused by miR-206 inhibition. In summary, miR-206 inhibits milk fatty acid synthesis and lipid accumulation by targeting ELOVL6 in BMECs.