长链非编码RNA核内小RNA宿主基因14/microRNA-183-5p通路在神经元细胞自噬中的作用研究OA

Objective To investigate the roles of long non-coding RNA(lncRNA)small nucleolar RNA host gene 14(SNHG14)and mircoRNA(miR)-183-5p in neuronal autophagy.Methods Dual-luciferase reporter assay was utilized to confirm the direct targeting interaction between SNHG14 and miR-183-5p in the mouse neuronal cell line HT-22.Quantitative real-time PCR was performed to determine the expression level of miR-183-5p following SNHG14 knockdown.For autophagy-related analyses,HT-22 cells were assigned to three groups:autophagy inducer-treated group,SNHG14 knockdown plus autophagy inducer-treated group,and miR-183-5p overexpression plus autophagy inducer-treated group.Western blotting analysis was then conducted to evaluate the expression changes of LC3 and p62,two key proteins involved in autophagy,across the three experimental groups.Results Dual-luciferase reporter assay confirmed that SNHG14 could directly target miR-183-5p.SNHG14 knockdown significantly upregulated miR-183-5p expression(P<0.05).After autophagy inducer treatment,the level of LC3-Ⅱ was increased,the level of p62 was decreased(all P<0.05),and the expression of miR-183-5p was downregulated(P<0.05)in neuronal cells.SNHG14 knockdown or miR-183-5p overexpression combined with autophagy inducer treatment could reverse the effect of the autophagy inducer.Conclusion SNHG14 can directly bind to miR-183-5p and inhibit its expression in neuronal cells,and regulates autophagy through the SNHG14/miR-183-5p pathway.