Potential diagnostic and drug target markers in glioblastoma
Abstract Glioblastoma multiforme (GBM) IDH-wildtype is the most prevalent brain malignancy in adults. However, molecular mechanisms, which leads to GBM have not been completely elucidated. Granulocyte colony-stimulating factor (GCSF), Granulocyte colony-stimulating factor receptor GCSFR, and Signal...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2024-03-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-024-57752-1 |
| _version_ | 1797233637892030464 |
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| author | Hina Ahsan Muhammad Asghar Shaukat Iqbal Malik |
| author_facet | Hina Ahsan Muhammad Asghar Shaukat Iqbal Malik |
| author_sort | Hina Ahsan |
| collection | DOAJ |
| description | Abstract Glioblastoma multiforme (GBM) IDH-wildtype is the most prevalent brain malignancy in adults. However, molecular mechanisms, which leads to GBM have not been completely elucidated. Granulocyte colony-stimulating factor (GCSF), Granulocyte colony-stimulating factor receptor GCSFR, and Signal transducers and activators of transcription 3 (STAT3) have been involved in the occurrence and development of various cancers, but their role in GBM is little known. Herein, we have investigated the gene and protein expression of GCSF, GCSFR, and STAT3 in 21 tissue biopsy samples and also in tumor associated normal tissue (TANT) samples derived from glioblastoma patients, which revealed significantly differential expression of these genes. To validate our findings, we performed a comprehensive integrated analysis of transcriptomic and proteomic profiling of respective genes by retrieving GBM RNA-sequence data from Genome Atlas Databases. GO and KEGG analysis revealed enrichment in disease-related pathways, such as JAK/STAT pathway activation, which were associated with GBM progression. We further performed computational docking analysis of potential drug candidate Nisin against GCSF, and the results were validated in vitro through cytotoxic activity assay using a human glioblastoma cell line SF-767 in a dose-dependent manner. Our comprehensive analysis reveals that GCSF augments glioma progression, and its blockade with anticancer bacteriocin peptide Nisin can potentially inhibit the growth and metastasis of GBM. |
| first_indexed | 2024-04-24T16:19:21Z |
| format | Article |
| id | doaj.art-ff72723451174ad8b163e0913d43ac71 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-04-24T16:19:21Z |
| publishDate | 2024-03-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-ff72723451174ad8b163e0913d43ac712024-03-31T11:17:58ZengNature PortfolioScientific Reports2045-23222024-03-0114111910.1038/s41598-024-57752-1Potential diagnostic and drug target markers in glioblastomaHina Ahsan0Muhammad Asghar1Shaukat Iqbal Malik2Department of Bioinformatics and Biosciences, Faculty of Health and Life Sciences, Capital University of Science and Technology (CUST)Department of Biology, Lund UniversityDepartment of Bioinformatics and Biosciences, Faculty of Health and Life Sciences, Capital University of Science and Technology (CUST)Abstract Glioblastoma multiforme (GBM) IDH-wildtype is the most prevalent brain malignancy in adults. However, molecular mechanisms, which leads to GBM have not been completely elucidated. Granulocyte colony-stimulating factor (GCSF), Granulocyte colony-stimulating factor receptor GCSFR, and Signal transducers and activators of transcription 3 (STAT3) have been involved in the occurrence and development of various cancers, but their role in GBM is little known. Herein, we have investigated the gene and protein expression of GCSF, GCSFR, and STAT3 in 21 tissue biopsy samples and also in tumor associated normal tissue (TANT) samples derived from glioblastoma patients, which revealed significantly differential expression of these genes. To validate our findings, we performed a comprehensive integrated analysis of transcriptomic and proteomic profiling of respective genes by retrieving GBM RNA-sequence data from Genome Atlas Databases. GO and KEGG analysis revealed enrichment in disease-related pathways, such as JAK/STAT pathway activation, which were associated with GBM progression. We further performed computational docking analysis of potential drug candidate Nisin against GCSF, and the results were validated in vitro through cytotoxic activity assay using a human glioblastoma cell line SF-767 in a dose-dependent manner. Our comprehensive analysis reveals that GCSF augments glioma progression, and its blockade with anticancer bacteriocin peptide Nisin can potentially inhibit the growth and metastasis of GBM.https://doi.org/10.1038/s41598-024-57752-1GlioblastomaTranscriptomic profilingDifferential gene expressionAnti-cancer peptidesBiomarkers |
| spellingShingle | Hina Ahsan Muhammad Asghar Shaukat Iqbal Malik Potential diagnostic and drug target markers in glioblastoma Scientific Reports Glioblastoma Transcriptomic profiling Differential gene expression Anti-cancer peptides Biomarkers |
| title | Potential diagnostic and drug target markers in glioblastoma |
| title_full | Potential diagnostic and drug target markers in glioblastoma |
| title_fullStr | Potential diagnostic and drug target markers in glioblastoma |
| title_full_unstemmed | Potential diagnostic and drug target markers in glioblastoma |
| title_short | Potential diagnostic and drug target markers in glioblastoma |
| title_sort | potential diagnostic and drug target markers in glioblastoma |
| topic | Glioblastoma Transcriptomic profiling Differential gene expression Anti-cancer peptides Biomarkers |
| url | https://doi.org/10.1038/s41598-024-57752-1 |
| work_keys_str_mv | AT hinaahsan potentialdiagnosticanddrugtargetmarkersinglioblastoma AT muhammadasghar potentialdiagnosticanddrugtargetmarkersinglioblastoma AT shaukatiqbalmalik potentialdiagnosticanddrugtargetmarkersinglioblastoma |