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MCM5 is an oncogenic driver in glioma progression through regulating cell cycle
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Abstract
Background: Minichromosome maintenance protein 5 (MCM5) has been found to be a new oncogene in many cancers. However, its role in glioma remains unclear. Therefore, we mainly plan to investigate the potential mechanism of MCM5 in glioma.
Methods: Bioinformatics tools were employed to evaluate the expression of MCM5 in glioma and its relationship with clinicopathological characteristics. GEPIA database was applied to assess the prognostic value of MCM5 in glioma, and functional enrichment analysis of MCM5 was also performed. Subsequently, we further investigated the effects of MCM5 on cell functions through cell experiments like scratch, Transwell, and flow cytometry experiments.
Results: MCM5 was overexpressed in glioma, and its expression level significantly affected the disease-free survival and overall survival of glioma patients. Besides, the expression level of MCM5 was positively correlated with Th2 cell, aCD and other immune cells. Gene enrichment analysis suggested that MCM5 might be involved in tumorigenesis by regulating DNA replication process. In vitro experiments showed that MCM5 promoted the cell proliferation, migration, and cell cycle in glioma.
Conclusion: By bioinformatics analysis and cell experiments, MCM5 is found to promote the progression of glioma by accelerating cell cycle, and it could be an independent factor for prognostic prediction in glioma. These findings will provide new clues for the mechanism exploration and prognostic prediction of glioma.
Title: MCM5 is an oncogenic driver in glioma progression through regulating cell cycle
Description:
Abstract
Background: Minichromosome maintenance protein 5 (MCM5) has been found to be a new oncogene in many cancers.
However, its role in glioma remains unclear.
Therefore, we mainly plan to investigate the potential mechanism of MCM5 in glioma.
Methods: Bioinformatics tools were employed to evaluate the expression of MCM5 in glioma and its relationship with clinicopathological characteristics.
GEPIA database was applied to assess the prognostic value of MCM5 in glioma, and functional enrichment analysis of MCM5 was also performed.
Subsequently, we further investigated the effects of MCM5 on cell functions through cell experiments like scratch, Transwell, and flow cytometry experiments.
Results: MCM5 was overexpressed in glioma, and its expression level significantly affected the disease-free survival and overall survival of glioma patients.
Besides, the expression level of MCM5 was positively correlated with Th2 cell, aCD and other immune cells.
Gene enrichment analysis suggested that MCM5 might be involved in tumorigenesis by regulating DNA replication process.
In vitro experiments showed that MCM5 promoted the cell proliferation, migration, and cell cycle in glioma.
Conclusion: By bioinformatics analysis and cell experiments, MCM5 is found to promote the progression of glioma by accelerating cell cycle, and it could be an independent factor for prognostic prediction in glioma.
These findings will provide new clues for the mechanism exploration and prognostic prediction of glioma.
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