Identification of common hub genes and pathways in systemic lupus erythematosus and cervical cancer using bioinformatics approach.

Systemic lupus erythematosus (SLE) is a complex autoimmune condition characterized by multifactorial pathogenesis involving dysregulated immune responses. It has been associated with an elevated risk of various cancers, notably cervical cancer (CC), one of the most common cancers in women globally. Despite this association, the molecular mechanisms linking SLE and CC remain incompletely defined. To investigate this intersection, we employed integrative bioinformatics approaches to analyze transcriptomic datasets relevant to both SLE and CC, including GSE112087, GSE154851, GSE46907, GSE49454, GSE50772, GSE63514, GSE64217, GSE63678, GSE7803, and GSE9750 . We performed differential gene expression analysis, constructed Protein-Protein Interaction (PPI) networks, and carried out functional annotation to pinpoint pivotal hub genes and signaling pathways implicated in both diseases. Our analysis revealed significant differentially expressed genes (DEGs) in SLE, predominantly associated with cytokine and interferon alpha/beta signaling pathways, as well as the innate immune response. Notable hub genes included MX1, ISG15, and STAT1. In CC, DEGs were chiefly enriched in the mitotic cell cycle and cytokine signaling processes, with CDK1 and DLGAP5 standing out as key hub genes. The cross-disease analysis identified shared DEGs between SLE and CC, particularly in the interferon-alpha/beta and cytokine signaling pathways. This suggests a shared molecular architecture that underlies both autoimmune and cancer pathogenesis. Our study underscores the common molecular pathways between SLE and CC, highlighting the significance of interferon and cytokine signaling in the pathogenesis of both diseases. These insights set the stage for future research into potential therapeutic targets for the treatment of both SLE and CC.