Identification of PTPRC as a potential serum biomarker in rheumatoid arthritis using bioinformatics analysis and molecular docking.

Background: Rheumatoid arthritis (RA) is a multifactorial autoimmune disease affecting joints. Early and accurate diagnosis is important for initiating the correct treatment and preventing long-term complications.

Methods: Microarray expression data of synovial tissues from people with osteoarthritis and healthy populations were downloaded from the Gene Expression Omnibus (GEO) database. Extracellular protein-differentially expressed genes (EP-DEGs) were screened using protein annotation databases. GO and KEGG were used to analyze the function and pathway of EP-DEGs. STRING, Cytoscape, and CytoHubba were used to construct a protein-protein interaction (PPI) network and screen key EP-DEGs. Serum PTPRC levels were measured by ELISA. Molecular docking was used to explore the affinity of drugs for PTPRC.

Results: A total of 135 potential target genes of EP-DEGs in RA were identified using Venn analysis. The EP-DEGs were enriched in the B cell receptor signaling pathway, humoral immune response, cytokine-cytokine receptor interaction, chemokine signaling pathway and PI3K-Akt signaling pathway. PTPRC was identified as a hub gene and its expression in RA was high. The ROC curve of PTPRC concentration in RA was plotted to obtain an AUC of 0.9191, a cutoff value of 39.38 pg/mL, and a sensitivity and specificity of 77.05 % and 73.33 %, respectively. Molecular docking analysis showed that prednisone, methotrexate, dexamethasone and cyclophosphamide bound to PTPRC with Vina scores of -9.2, -8.7, -10.1, and - 5.1, respectively.

Conclusion: PTPRC may be a potential marker for the diagnosis and a potential target for the treatment of RA and the mechanism of PTPRC involvement in RA may regulate immune function through PI3K-Akt signaling pathway.