Abstract

<b>Background:</b> Ovarian cancer (OC) is a leading cause of gynecological cancer-linked deaths worldwide. Exosomal <i>miR-1825</i> and its target gene C-type lectin domain family 5 member A (<i>CLEC5A</i>) are associated with tumorigenesis in cancers that was further probed. <b>Methods:</b> Exosomal <i>miR-1825</i> expression in exosomes and its impact on overall survival (OS) prediction were determined using Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data. Target genes of <i>miR-1825</i> were searched in five prediction databases and prognostically significant differentially expressed genes were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were carried out. The ability of <i>CLEC5A</i> to predict OS was evaluated using univariate and multivariate Cox regression analyses and Kaplan-Meier curves. The <i>CLEC5A</i> expression pattern in OC was validated using immunohistochemistry. The CIBERSORT algorithm was used to compare the immune cell landscape, and the results were validated in a GEO cohort. Finally, the predicted half maximal inhibitory concentration (IC50) values for five commonly used chemotherapy agents were also compared. <b>Results:</b> <i>MiR-1825</i> level was higher in exosomes derived from OC cells and served as a tumor suppressor. The <i>CLEC5A</i> gene was found to be a target of <i>miR-1825</i>, the upregulation of which was correlated with a poor prognosis. M2 macrophage infiltration was significantly enhanced in the <i>CLEC5A</i> high expression group, while T follicular helper cell infiltration was reduced in it. While the predicted IC50 for cisplatin and doxorubicin was higher in the <i>CLEC5A</i> high expression group, that of docetaxel, gemcitabine, and paclitaxel was lower. <b>Conclusion:</b> <i>MiR-1825</i>, a promising OC biomarker, may promote OC progression by increasing <i>CLEC5A</i> expression via exosome-mediated efflux from tumor cells.

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