Long noncoding RNA Gm20319, acting as competing endogenous RNA, regulated GNE expression by sponging miR-7240-5p to involve in deoxynivalenol-induced liver damage in vitro.

Abstract The regulatory effects of competing endogenous RNA (ceRNA) network have been highlighted on the occurrence and development of diseases. However, the effect of ceRNA network in liver with subchronic deoxynivalenol (DON) exposure has remained unclear so far. Here, lncRNA Gm20319-miR-7240-5p-GNE (glucosamine UDP-N-acetyl-2-epimerase/N-acetylmannosamine kinase) network was identified in DON exposed-liver tissues after DON exposure for 90 days. Subchronic DON exposure induced the mild inflammation in liver tissues. In DON-treated liver tissues and Hepa 1–6 cell line, the expression of Gm20319 and GNE were both downregulated while miR-7240-5p expression was upregulated. The gain- and loss-of-function expression in vitro revealed there was a mutual repression between Gm20319 and miR-7240-5p, and they regulated GNE expression in an opposite direction. Dual luciferase reporter assays showed miR-7240-5p inhibited Gm20319 and GNE expression by directly binding. Co-transfection experiment in vitro revealed Gm20319 and miR-7240-5p could indirectly regulate sialic acid level by directly modulating GNE expression, thereby also influencing the expression of SOD1 and IL-1β. This study revealed Gm20319-miR-7240-5p-GNE network reduced sialic acid level to influence the expression of SOD1 and IL-1β in liver, which might involve in liver damage induced by DON. Gm20319 might be a potential research molecular target for DON-induced liver damage.