ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/051/SRR13954551/SRR13954551_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/047/SRR13954547/SRR13954547_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/047/SRR13954547/SRR13954547_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/049/SRR13954549/SRR13954549_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/051/SRR13954551/SRR13954551_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/048/SRR13954548/SRR13954548_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/054/SRR13954554/SRR13954554_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/053/SRR13954553/SRR13954553_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/050/SRR13954550/SRR13954550_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/052/SRR13954552/SRR13954552_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/054/SRR13954554/SRR13954554_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/046/SRR13954546/SRR13954546_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/050/SRR13954550/SRR13954550_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/046/SRR13954546/SRR13954546_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/053/SRR13954553/SRR13954553_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/052/SRR13954552/SRR13954552_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/048/SRR13954548/SRR13954548_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/049/SRR13954549/SRR13954549_2.fastq.gzprimaryOK200GenomicsNutrition and Food Hygiene, Harbin Medical Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA714101Mus musculusxref:PubMed:34261739Long-term high-fat diet feeding increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on β-cells, but the underlying molecular mechanisms have not been fully elucidated. Here, we evaluated the role of lncRNA TCONS_00077866 (lncRNA-866) in SA-induced β-cell inflammation. lncRNA-866 was selected for study because it demonstrated the largest fold-difference in expression of five lncRNAs that were affected by SA treatment using lncRNA High-throughput Sequencing analysis. Knockdown of lncRNA-866 by virus-mediated shRNA expression in mice or Smart Silencer in β-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and β-cell inflammation. lncRNA-866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3), according to lncRNA-miRNA-mRNA co-expression network analysis and luciferase reporter assay. Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in β-TC6 cells and mouse islets. In conclusion, lncRNA-866 silencing ameliorates SA-induced β-cell inflammation by targeting the miR-297b-5p/SAA3 axis. lncRNA-866 inhibition may represent a new strategy to protect β-cells against the effects of SA during the development of type 2 diabetes. Overall design: LncRNA profiles of nine samples from β-TC6 cells (three control, three stearic acid-treated, and three palmitic acid-treated samplesENAfalseInhibition of lncRNA TCONS_00077866 ameliorates the high stearic acid diet-induced mouse pancreatic β-cell inflammatory response by increasing miR-297b-5p to downregulate SAA3 expressionInhibition of lncRNA TCONS_00077866 ameliorates the high stearic acid diet-induced mouse pancreatic β-cell inflammatory response by increasing miR-297b-5p to downregulate SAA3 expression2025-09-242022-04-01PRJNA714101GSE1688251009034261739