| Summary: | Introduction. Glioma is the widely occurring deadly neoplasm induced by glial cell canceration in the central nervous system, including the brain and spinal cord. The function of AP1S3 is special in numerous diseases, but its exact role in glioma remains unknown. Methods. Bioinformatics analysis was performed at the beginning. Based on TCGA database, differentially expressed genes were obtained. Protein-protein interaction (PPI) network analysis is performed by STRING. The annotation, visualization, and synthesis (DAVID) discovery database program was used for gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The Kaplan-Meier curve was plotted to determine the prognostic value of AP1S3 Also, in vitro experiments were conducted in our research. Results. 4370 differentially expressed genes were identified. 215 key genes were screened by protein-protein interaction (PPI) analysis; AP1S3 had a higher degree. The top five enriched pathways related to AP1S3 contain protein processing in the endoplasmic reticulum (ER), extracellular matrix receptor (ECM receptor) interaction, focal adhesion, advanced glycation end product (AGE) receptor for AGE (RAGE) signaling pathway in diabetic complications, and mRNA surveillance pathway. Additionally, the AP1S3 level was dramatically upregulated in glioblastoma (GBM) samples, but greatly reduced in low-grade glioma (LGG) samples when compared to that in normal tissues. The Kaplan-Meier curve data showed that AP1S3 was closely related to the disease-free survival (DFS) of glioma. Our data suggested that the expression of AP1S3 was increased in glioma in comparison with normal tissues, in line with the data of clinical samples. What was more, our data demonstrated that the reduction of AP1S3 in glioma cells could result in the inhibition of cell proliferation, invasion, and migration. Conclusion. Collectively, our results implied that AP1S3 was a promising biomarker of glioma diagnosis and displayed as an oncogene in glioma.
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