Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms
Background. Glioblastoma (GBM) is an aggressive form of brain tumor characterized by limited treatment options and a bleak prognosis. Although the role of Like-Sm 1 (LSM1), a component of the mRNA splicing machinery, has been studied in various cancers, its significance in GBM remains unclear. The p...
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| Format: | Article |
| Language: | English |
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Wiley
2023-01-01
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| Series: | International Journal of Genomics |
| Online Access: | http://dx.doi.org/10.1155/2023/1543620 |
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| author | Changcheng Cai Xingyu Chen Jimin He Chengwei Xiang Yinggang Liu Ke Wu Ke Luo |
| author_facet | Changcheng Cai Xingyu Chen Jimin He Chengwei Xiang Yinggang Liu Ke Wu Ke Luo |
| author_sort | Changcheng Cai |
| collection | DOAJ |
| description | Background. Glioblastoma (GBM) is an aggressive form of brain tumor characterized by limited treatment options and a bleak prognosis. Although the role of Like-Sm 1 (LSM1), a component of the mRNA splicing machinery, has been studied in various cancers, its significance in GBM remains unclear. The purpose of this research was to investigate the expression of LSM1 and its role in driving GBM progression. Methods. We analyzed gene expression data obtained from TCGA and GTEx databases to compare the levels of LSM1 expression between GBM and normal brain tissues. To assess the impact of LSM1, we conducted experiments using U87 GBM cells, wherein we manipulated LSM1 expression through overexpression and knockdown techniques. These experiments allowed us to evaluate cellular behaviors such as proliferation and invasion. Additionally, we explored the correlation between LSM1 expression and immune cell infiltration in GBM. Results. Our analysis of TCGA and GTEx datasets revealed a significant upregulation of LSM1 expression in GBM compared to normal brain tissues. In our in vitro experiments using U87 cells, we observed that LSM1 overexpression promoted cell proliferation and invasion, while LSM1 knockdown exerted the opposite effects. Moreover, we discovered correlations between LSM1 expression and immune cell infiltration in GBM, specifically involving TFH cells, CD56bright cells, macrophages, and Th2 cells. Conclusions. The findings of this study demonstrate the upregulation of LSM1 in GBM and its contribution to tumor progression by enhancing cell proliferation, invasion, and influencing immune cell infiltration. Our research sheds light on the potential oncogenic role of LSM1 in GBM and suggests its viability as a therapeutic target for this aggressive brain tumor. |
| format | Article |
| id | doaj-art-c8d528ae2d3d407e8a776103fb65d031 |
| institution | DOAJ |
| issn | 2314-4378 |
| language | English |
| publishDate | 2023-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Genomics |
| spelling | doaj-art-c8d528ae2d3d407e8a776103fb65d0312025-08-20T03:05:10ZengWileyInternational Journal of Genomics2314-43782023-01-01202310.1155/2023/1543620Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional MechanismsChangcheng Cai0Xingyu Chen1Jimin He2Chengwei Xiang3Yinggang Liu4Ke Wu5Ke Luo6Department of NeurosurgeryDepartment of NeurosurgeryDepartment of NeurosurgeryDepartment of NeurosurgeryDepartment of NeurosurgeryDepartment of NeurosurgeryDepartment of NeurosurgeryBackground. Glioblastoma (GBM) is an aggressive form of brain tumor characterized by limited treatment options and a bleak prognosis. Although the role of Like-Sm 1 (LSM1), a component of the mRNA splicing machinery, has been studied in various cancers, its significance in GBM remains unclear. The purpose of this research was to investigate the expression of LSM1 and its role in driving GBM progression. Methods. We analyzed gene expression data obtained from TCGA and GTEx databases to compare the levels of LSM1 expression between GBM and normal brain tissues. To assess the impact of LSM1, we conducted experiments using U87 GBM cells, wherein we manipulated LSM1 expression through overexpression and knockdown techniques. These experiments allowed us to evaluate cellular behaviors such as proliferation and invasion. Additionally, we explored the correlation between LSM1 expression and immune cell infiltration in GBM. Results. Our analysis of TCGA and GTEx datasets revealed a significant upregulation of LSM1 expression in GBM compared to normal brain tissues. In our in vitro experiments using U87 cells, we observed that LSM1 overexpression promoted cell proliferation and invasion, while LSM1 knockdown exerted the opposite effects. Moreover, we discovered correlations between LSM1 expression and immune cell infiltration in GBM, specifically involving TFH cells, CD56bright cells, macrophages, and Th2 cells. Conclusions. The findings of this study demonstrate the upregulation of LSM1 in GBM and its contribution to tumor progression by enhancing cell proliferation, invasion, and influencing immune cell infiltration. Our research sheds light on the potential oncogenic role of LSM1 in GBM and suggests its viability as a therapeutic target for this aggressive brain tumor.http://dx.doi.org/10.1155/2023/1543620 |
| spellingShingle | Changcheng Cai Xingyu Chen Jimin He Chengwei Xiang Yinggang Liu Ke Wu Ke Luo Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms International Journal of Genomics |
| title | Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms |
| title_full | Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms |
| title_fullStr | Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms |
| title_full_unstemmed | Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms |
| title_short | Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms |
| title_sort | correlation between lsm1 expression and clinical outcomes in glioblastoma and functional mechanisms |
| url | http://dx.doi.org/10.1155/2023/1543620 |
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