Identification of the potential regulatory interactions in rheumatoid arthritis through a comprehensive analysis of lncRNA-related ceRNA networks

Abstract

Abstract Objective This study aimed at constructing a network of competing endogenous RNA (ceRNA) in the synovial tissues of rheumatoid arthritis (RA). It seeks to discern potential biomarkers and explore the long non-coding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) axes that are intricately linked to the pathophysiological mechanisms underpinning RA, and providing a scientific basis for the pathogenesis and treatment of RA. Methods Microarray data pertaining to RA synovial tissue, GSE103578, GSE128813, and GSE83147, were acquired from the Gene Expression Omnibus (GEO) database (http://www.ncbi.nlm.nih.gov/geo). Conducted to discern both differentially expressed lncRNAs (DELncRNAs) and differentially expressed genes (DEGs). A ceRNA network was obtained through key lncRNAs, key miRNAs, and key genes. Further investigations involved co-expression analyses to uncover the lncRNA-miRNA-mRNA axes contributing to the pathogenesis of RA. To delineate the immune-relevant facets of this axis, we conducted an assessment of key genes, emphasizing those with the most substantial immunological correlations, employing the GeneCards database. Finally, gene set enrichment analysis (GSEA) was executed on the identified key lncRNAs to elucidate their functional implications in RA. Results The 2 key lncRNAs, 7 key miRNAs and 6 key genes related to the pathogenesis of RA were obtained, as well as 2 key lncRNA-miRNA-mRNA axes (KRTAP5-AS1-hsa-miR-30b-5p-PNN, XIST-hsa-miR-511-3p/hsa-miR-1277-5p-F2RL1). GSEA of two key lncRNAs obtained biological processes and signaling pathways related to RA synovial lesions. Conclusion The findings of this investigation hold promise in furnishing a foundational framework and guiding future research endeavors aimed at comprehending the etiology and therapeutic interventions for RA.