Glioblastoma (GBM), the most deadly primary brain tumor, presents a major medical difficulty. The need for better therapeutic targets in GBM is therefore urgent. A growing body of evidence suggests that the gene FKBP1A plays an important role in tumor progression and may be therapeutically useful. However, the role of FKBP1A in glioblastoma and the underlying biologic mechanism remain unclear. The purpose of this study was to identify the role of FKBP1A in GBM and its molecular mechanism. We demonstrated that FKBP1A was the hub gene in GBM via a weighted correlation network analysis (WGCNA) and differentially expressed genes (DEGs) analysis based on the bulk RNA-seq data from TCGA and GTEx. Afterwards, we proved that the upregulated FKBP1A protein could promote GBM cell death by CCK-8 assays in U87MG and t98g GBM cell lines. We further demonstrated two key pathways of FKBP1A in GBM by bioinformatics methods: 'Apoptosis' and 'mTOR signaling pathway'. Subsequently, the key pathways were verified by flow cytometry and Western blot. We identified that upregulated FKBP1A could inhibit GBM growth via the apoptosis pathway. Together, these findings may contribute to future GBM treatment.
Keywords: FKBP1A; GBM; WGCNA; bulk RNA-seq; pathway enrichment; scRNA-seq.