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Background Rheumatoid arthritis (RA) is a common chronic autoimmune disease characterized by inflammation of the synovial membrane. However, the etiology and underlying molecular events of RA are unclear. Here, we applied bioinformatics analysis to identify the key genes involved in RA. Methods GSE77298 was downloaded from the Gene Expression Omnibus (GEO) database. We used the R software screen the differentially expressed genes (DEGs). Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway were analyzed by using the DAVID online tool. The STRING database was used to analyze the interaction of differentially encoded proteins. PPI interaction network was divided into subnetworks using MCODE algorithm and was analyzed using Cytoscape. Gene set enrichment analysis (GSEA) was performed to identify relevant biological functions. qRT-PCR analysis was also performed to verify the expression of identified hub DEGs. Results A total of 4062 differentially expressed genes were selected, including 1847 upregulated genes and 2215 downregulated genes. In the biological process, DEGs were mainly concentrated in the fields of muscle filament sliding, muscle contraction, intracellular signal transduction, cardiac muscle contraction, signal transduction, and skeletal muscle tissue development. In the cellular components, DEGs were mainly concentrated in the parts of cytosol, Z disk, membrane, extracellular exosome, mitochondrion, and M band. In molecular functions, DEGs were mainly concentrated in protein binding, structural constituent of muscle, actin binding, and actin filament binding. KEGG pathway analysis shows that DEGs mainly focuses on pathways about lysosome, Wnt/β-catenin signaling pathway, and NF-κB signaling pathway. CXCR3, GNB4, and CXCL16 were identified as the core genes that involved in the progression of RA. By qRT-PCR analysis, we found that CXCR3, GNB4, and CXCL16 were significantly upregulated in RA tissue as compared to healthy controls. Conclusion In conclusion, DEGs and hub genes identified in the present study help us understand the molecular mechanisms underlying the progression of RA, and provide candidate targets for diagnosis and treatment of RA.