Upregulated FKBP1A Suppresses Glioblastoma Cell Growth via Apoptosis Pathway

• Published in: International journal of molecular sciences Vol. 23; no. 23; p. 14935
• Main Authors: Cai, Shaoyi, Chen, Zhiyou, Tang, Heng, Meng, Siyan, Tao, Liang, Wang, Qin
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 29.11.2022; MDPI
• Subjects: Apoptosis; Bioinformatics; Brain cancer; Brain Neoplasms - metabolism; Brain tumors; bulk RNA-seq; Cancer therapies; Cell cycle; Cell death; Cell growth; Cell Proliferation - genetics; Chemotherapy; Cholecystokinin; Computational Biology; FKBP1A; Flow cytometry; GBM; Gene expression; Gene Expression Regulation, Neoplastic; Glioblastoma; Glioblastoma - metabolism; Humans; Kinases; Medical prognosis; Network analysis; pathway enrichment; Proteins; scRNA-seq; Signal transduction; Tacrolimus Binding Proteins - genetics; Tacrolimus Binding Proteins - metabolism; Therapeutic targets; TOR protein; Tumors; WGCNA; FKBP1A; pathway enrichment; scRNA-seq; GBM; bulk RNA-seq; WGCNA
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms232314935

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 plays an important role in tumor progression and may be therapeutically useful. However, the role of in glioblastoma and the underlying biologic mechanism remain unclear. The purpose of this study was to identify the role of in GBM and its molecular mechanism. We demonstrated that 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 protein could promote GBM cell death by CCK-8 assays in U87MG and t98g GBM cell lines. We further demonstrated two key pathways of 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 could inhibit GBM growth via the apoptosis pathway. Together, these findings may contribute to future GBM treatment.