The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM
Background: Glioblastoma (GBM) is widely known as a classical kind of malignant tumor originating in the brain with high morbidity and mortality. Targeted therapy has shown great promise in treating glioblastoma, but more promising targets, including effective therapeutic targets, remain to be ident...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2022-04-01
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Series: | Frontiers in Genetics |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fgene.2022.858882/full |
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author | Lei-Bo Wang Xue-Bin Zhang Jun Liu Qing-Jun Liu |
author_facet | Lei-Bo Wang Xue-Bin Zhang Jun Liu Qing-Jun Liu |
author_sort | Lei-Bo Wang |
collection | DOAJ |
description | Background: Glioblastoma (GBM) is widely known as a classical kind of malignant tumor originating in the brain with high morbidity and mortality. Targeted therapy has shown great promise in treating glioblastoma, but more promising targets, including effective therapeutic targets, remain to be identified. 18A (KIF18A) is a microtubule-based motor protein that is dysregulated and involved in the progression of multiple human cancers. However, the possible effects of KIF18A on GBM progression are still unclear.Methods: We performed DEG analysis, medical data analysis, and network analysis to identify critical genes affecting glioma progression. We also performed immunohistochemical analysis of the KIF18A levels in 94 patients with glioblastoma and the associated surrounding tissues. Patients were divided into two groups according to the high and low expression. Using a clinical analysis, we showed the potential associations between KIF18A expression and clinical characteristics of 94 GBM patients. We then investigated the effects of KIF18A on GBM cell proliferation by colony establishment, MTT, and immune blogging. The possible effect of KIF18A on GBM tumor growth was determined in mice.Results: We identified KIF18A as a potential gene affecting GBM progression. We further demonstrated that GBM tissues expressed KIF18A much higher, and its presentation was associated with recurrence in glioblastoma patients. We believe KIF18A promotes GBM cell proliferation.Conclusion: We demonstrated that KIF18A could be a promising target in treating GBM. |
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id | doaj.art-6a9c7def57d042bdbd62f510072da4ba |
institution | Directory Open Access Journal |
issn | 1664-8021 |
language | English |
last_indexed | 2024-12-13T23:07:15Z |
publishDate | 2022-04-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Genetics |
spelling | doaj.art-6a9c7def57d042bdbd62f510072da4ba2022-12-21T23:28:15ZengFrontiers Media S.A.Frontiers in Genetics1664-80212022-04-011310.3389/fgene.2022.858882858882The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBMLei-Bo Wang0Xue-Bin Zhang1Jun Liu2Qing-Jun Liu3Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, ChinaDepartment of Pathology, Tianjin Huanhu Hospital, Tianjin, ChinaDepartment of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, ChinaDepartment of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, ChinaBackground: Glioblastoma (GBM) is widely known as a classical kind of malignant tumor originating in the brain with high morbidity and mortality. Targeted therapy has shown great promise in treating glioblastoma, but more promising targets, including effective therapeutic targets, remain to be identified. 18A (KIF18A) is a microtubule-based motor protein that is dysregulated and involved in the progression of multiple human cancers. However, the possible effects of KIF18A on GBM progression are still unclear.Methods: We performed DEG analysis, medical data analysis, and network analysis to identify critical genes affecting glioma progression. We also performed immunohistochemical analysis of the KIF18A levels in 94 patients with glioblastoma and the associated surrounding tissues. Patients were divided into two groups according to the high and low expression. Using a clinical analysis, we showed the potential associations between KIF18A expression and clinical characteristics of 94 GBM patients. We then investigated the effects of KIF18A on GBM cell proliferation by colony establishment, MTT, and immune blogging. The possible effect of KIF18A on GBM tumor growth was determined in mice.Results: We identified KIF18A as a potential gene affecting GBM progression. We further demonstrated that GBM tissues expressed KIF18A much higher, and its presentation was associated with recurrence in glioblastoma patients. We believe KIF18A promotes GBM cell proliferation.Conclusion: We demonstrated that KIF18A could be a promising target in treating GBM.https://www.frontiersin.org/articles/10.3389/fgene.2022.858882/fullglioblastomakinesin family member 18Atherapeutic targetproliferationmedical data analysis |
spellingShingle | Lei-Bo Wang Xue-Bin Zhang Jun Liu Qing-Jun Liu The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM Frontiers in Genetics glioblastoma kinesin family member 18A therapeutic target proliferation medical data analysis |
title | The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM |
title_full | The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM |
title_fullStr | The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM |
title_full_unstemmed | The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM |
title_short | The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM |
title_sort | proliferation of glioblastoma is contributed to kinesin family member 18a and medical data analysis of gbm |
topic | glioblastoma kinesin family member 18A therapeutic target proliferation medical data analysis |
url | https://www.frontiersin.org/articles/10.3389/fgene.2022.858882/full |
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