Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway
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 <i>FKBP1A</i> plays an important role in tumor progression and may be therap...
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MDPI AG
2022-11-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/23/14935 |
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| author | Shaoyi Cai Zhiyou Chen Heng Tang Siyan Meng Liang Tao Qin Wang |
| author_facet | Shaoyi Cai Zhiyou Chen Heng Tang Siyan Meng Liang Tao Qin Wang |
| author_sort | Shaoyi Cai |
| collection | DOAJ |
| description | 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 <i>FKBP1A</i> plays an important role in tumor progression and may be therapeutically useful. However, the role of <i>FKBP1A</i> in glioblastoma and the underlying biologic mechanism remain unclear. The purpose of this study was to identify the role of <i>FKBP1A</i> in GBM and its molecular mechanism. We demonstrated that <i>FKBP1A</i> 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 <i>FKBP1A</i> protein could promote GBM cell death by CCK-8 assays in U87MG and t98g GBM cell lines. We further demonstrated two key pathways of <i>FKBP1A</i> 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 <i>FKBP1A</i> could inhibit GBM growth via the apoptosis pathway. Together, these findings may contribute to future GBM treatment. |
| first_indexed | 2024-03-09T17:45:52Z |
| format | Article |
| id | doaj.art-cc9750b90f494d24877b75f8840e7e88 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T17:45:52Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-cc9750b90f494d24877b75f8840e7e882023-11-24T11:10:37ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-11-0123231493510.3390/ijms232314935Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis PathwayShaoyi Cai0Zhiyou Chen1Heng Tang2Siyan Meng3Liang Tao4Qin Wang5Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaGlioblastoma (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 <i>FKBP1A</i> plays an important role in tumor progression and may be therapeutically useful. However, the role of <i>FKBP1A</i> in glioblastoma and the underlying biologic mechanism remain unclear. The purpose of this study was to identify the role of <i>FKBP1A</i> in GBM and its molecular mechanism. We demonstrated that <i>FKBP1A</i> 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 <i>FKBP1A</i> protein could promote GBM cell death by CCK-8 assays in U87MG and t98g GBM cell lines. We further demonstrated two key pathways of <i>FKBP1A</i> 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 <i>FKBP1A</i> could inhibit GBM growth via the apoptosis pathway. Together, these findings may contribute to future GBM treatment.https://www.mdpi.com/1422-0067/23/23/14935<i>FKBP1A</i>GBMbulk RNA-seqscRNA-seqpathway enrichmentWGCNA |
| spellingShingle | Shaoyi Cai Zhiyou Chen Heng Tang Siyan Meng Liang Tao Qin Wang Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway International Journal of Molecular Sciences <i>FKBP1A</i> GBM bulk RNA-seq scRNA-seq pathway enrichment WGCNA |
| title | Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway |
| title_full | Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway |
| title_fullStr | Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway |
| title_full_unstemmed | Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway |
| title_short | Upregulated <i>FKBP1A</i> Suppresses Glioblastoma Cell Growth via Apoptosis Pathway |
| title_sort | upregulated i fkbp1a i suppresses glioblastoma cell growth via apoptosis pathway |
| topic | <i>FKBP1A</i> GBM bulk RNA-seq scRNA-seq pathway enrichment WGCNA |
| url | https://www.mdpi.com/1422-0067/23/23/14935 |
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