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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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Autores principales: Cai, Changcheng, Chen, Xingyu, He, Jimin, Xiang, Chengwei, Liu, Yinggang, Wu, Ke, Luo, Ke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635750/
https://www.ncbi.nlm.nih.gov/pubmed/37954131
http://dx.doi.org/10.1155/2023/1543620
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author Cai, Changcheng
Chen, Xingyu
He, Jimin
Xiang, Chengwei
Liu, Yinggang
Wu, Ke
Luo, Ke
author_facet Cai, Changcheng
Chen, Xingyu
He, Jimin
Xiang, Chengwei
Liu, Yinggang
Wu, Ke
Luo, Ke
author_sort Cai, Changcheng
collection PubMed
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.
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spelling pubmed-106357502023-11-10 Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms Cai, Changcheng Chen, Xingyu He, Jimin Xiang, Chengwei Liu, Yinggang Wu, Ke Luo, Ke Int J Genomics Research Article 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. Hindawi 2023-11-02 /pmc/articles/PMC10635750/ /pubmed/37954131 http://dx.doi.org/10.1155/2023/1543620 Text en Copyright © 2023 Changcheng Cai et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Cai, Changcheng
Chen, Xingyu
He, Jimin
Xiang, Chengwei
Liu, Yinggang
Wu, Ke
Luo, Ke
Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms
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
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635750/
https://www.ncbi.nlm.nih.gov/pubmed/37954131
http://dx.doi.org/10.1155/2023/1543620
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