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Caspase-related apoptosis genes in gliomas by RNA-seq and bioinformatics analysis
1Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China.
Abstract:
Gliomas are the most common malignant tumors of the brain. The aim of this study is to identify caspase-dependent apoptotic genes and uncover their potential regulatory mechanism in glioma progression. Human glioma cell line U251 was used. Three experiment groups were set as control group, H2O2 group (treated with H2O2) and caspase inhibitor group (treated with caspase inhibitor). For samples in each group, RNA-sequencing was performed on Illumina platform and differentially expressed genes (DEGs) between any two of the three groups were selected using NOISeq package. By overlapping analysis, the caspase inhibitor-related DEGs were further screened out, followed by enrichment analyses. Drugs associating with these genes were selected by WebGestalt. Protein-protein interaction (PPI) network analysis was conducted based on SRINIG database. A set of 105 caspase inhibitor-related DEGs were identified, which were significantly enriched in cellular components related functions (for example, TUBB2A, RPSA and RPL5); and metabolism related pathways (for example, PSMC3, KHSRP, RPL5 and RPSA). In addition, KHSRP and TUBB2A were significantly associated with several drugs such as cefotaxime, cefacetrile and netilmicin. Besides, PSMC3 and RPL5 were identified as crucial nodes in the PPI network. Several crucial genes in gliomas cells such as TUBB2A, RPSA, RPL5, PSMC3 and KHSRP were identified, which might play significant roles in apoptosis in a caspase-dependent manner. These genes might also involve in the regulation of metabolism related functions and pathways. KHSRP and TUBB2A might be novel targets of three drugs, cefotaxime, cefacetrile and netilmicin.
Insights
This study identifies 105 caspase-dependent genes involved in glioma progression, revealing potential drug targets like KHSRP and TUBB2A for brain tumor treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gliomas represent the most prevalent malignant brain tumors.
- Understanding the molecular mechanisms driving glioma progression is crucial for developing effective therapies.
Purpose of the Study:
- To identify genes involved in caspase-dependent apoptosis during glioma progression.
- To elucidate the regulatory mechanisms of these genes and their potential as therapeutic targets.
Main Methods:
- RNA-sequencing was performed on the U251 human glioma cell line across control, H2O2-treated, and caspase inhibitor-treated groups.
- Differentially expressed genes (DEGs) were identified using NOISeq, followed by enrichment and drug association analyses (WebGestalt).
- Protein-protein interaction (PPI) network analysis was conducted using the SRINIG database.
Main Results:
- 105 caspase inhibitor-related DEGs were identified, enriched in cellular component functions and metabolism pathways.
- Genes such as TUBB2A, RPSA, RPL5, PSMC3, and KHSRP were highlighted for their roles in apoptosis and metabolism.
- KHSRP and TUBB2A showed significant associations with cefotaxime, cefacetrile, and netilmicin, suggesting potential drug targeting.
Conclusions:
- Several key genes (TUBB2A, RPSA, RPL5, PSMC3, KHSRP) play significant roles in caspase-dependent apoptosis in glioma cells.
- These genes are implicated in regulating cellular metabolism, offering insights into glioma progression.
- KHSRP and TUBB2A emerge as potential novel therapeutic targets for specific drug interventions in glioma treatment.
