Background. Gliomas are one of the most prevalent malignant brain tumors. Hence, identifying biological markers for glioma is imperative. TTC7B (Tetratricopeptide Repeat Domain 7B) is a gene whose role in cancer in currently identified. To this end, we examined the TTC7B expression as well as its prognostic significance, biological roles, and immune system impacts in patients with glioma. Methods. We evaluated the function of TTC7B in GBM and LGG through the published CGGA (Chinese Glioma Genome Atlas) and TCGA (The Cancer Genome Atlas) databases. CIBERSORT and TIMER were used to analyze the link between TTC7B and immune cells, while R was used for statistical analysis. In addition, Transwell analysis, including migration and invasion assays, was performed to identify the relationship between TTC7B and temozolomide. Results. Low expression of TTC7B was observed in GBM and LGG. 1p/19q codeletion, IDH mutation, chemotherapy, and grade were found to have a significant correlation with TTC7B. Besides, low TTC7B expression was linked with low overall survival (OS) in both GBM and LGG. In the Cox analysis, TTC7B was found to independently function as a risk element for OS of patients with glioma. Furthermore, CIBERSORT analysis demonstrated a positive link between TTC7B and multiple immune cells, especially activated NK cells. Transwell analysis, including migration and invasion assays, revealed that temozolomide reduced the migration and invasion capacity of glioma cells and increased the expression of TTC7B. Conclusion. In all, TTC7B could serve as a promising prognostic indicator of LGG and GBM, and is closely associated with immune infiltration and response to oxidative stress by temozolomide.

Several blood biomarkers are now considered increasingly important for stratifying risk, monitoring disease progression, and evaluating the response to therapy in ischemic stroke. The purpose of the present study was to identify the key genes associated with ischemic stroke progression and elucidate the potential therapeutic small molecules. Microarray datasets related to stroke for GSE58294, GSE22255, and GSE16561 were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were filtered using the Limma package. DAVID was then searched to perform gene ontology (GO) and pathway enrichment analyses. Based on the DEGs, a protein-protein interaction (PPI) network was developed using Cytoscape, and MCODE was applied to conduct module analysis. Finally, to identify the potential drugs for ischemic stroke, the connectivity map (CMap) database was used. Sixty DEGs were identified after analyzing the three datasets. The GO data analysis revealed that the DEGs were significantly associated with biological processes, including positive regulation of programmed cell death, protein localization in organelles, and positive regulation of apoptosis. KEGG analysis showed that the DEGs were particularly enriched in the Fc epsilon RI signaling pathway, MAPK signaling pathway, and Huntington’s disease. We selected five DEGs with high connectivity (CYBB, SYK, DUSP1, TNF, and SP1) that significantly predicted stroke progression. In addition, CMap prediction showed ten small molecules that could be used as adjuvants when treating ischemic stroke. The outcomes of the present study indicated that the five genes mentioned above can be considered potential targets for developing new medications that can modify the ischemic stroke process, and mycophenolic acid was the most promising small molecule to treat ischemic stroke.