Abstract
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.
Highlights
Glioma is the widely occurring deadly neoplasm induced by glial cell canceration in the central nervous system, including the brain and spinal cord
The Protein-protein interaction (PPI) network mainly included AP1S3, Filamin A (FLNA), CALU, ACTN1, microtubule-associated protein Tau (MAPT), HSPA4, UBQLN4, RPN2, P4HB, MSN, AURKA, QGAP1, AURKA, and PGK1. These genes might be used for the identification of key biomarkers, and AP1S3 had a higher degree
Glioma, accompanied by a wide range of clinical behaviors, is the widely deadly neoplasm induced by glial cell canceration [16]
Summary
Glioma is the widely occurring deadly neoplasm induced by glial cell canceration in the central nervous system, including the brain and spinal cord. Based on TCGA database, differentially expressed genes were obtained. Protein-protein interaction (PPI) network analysis is performed by STRING. 215 key genes were screened by protein-protein interaction (PPI) analysis; AP1S3 had a higher degree. The KaplanMeier 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. Our data demonstrated that the reduction of AP1S3 in glioma cells could result in the inhibition of cell proliferation, invasion, and migration. Our results implied that AP1S3 was a promising biomarker of glioma diagnosis and displayed as an oncogene in glioma. To explore novel biomarkers and therapeutic targets for glioma patients is yet urgent, even though the existing strategies could certainly prolong many patients’ lifespan [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Computational and mathematical methods in medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
