Abstract
The aim of the present study was to identify the common molecular mechanisms of multiple glioma subtypes, including astrocytoma, glioblastoma and oligodendroglioma, in addition to the specific mechanisms of different types. The gene expression profile set GSE4290 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) from three types of glioma, relative to non-tumor tissue, were calculated by the t-test method with a linear regression model. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the DEGs was performed. GeneVenn online analysis software was used for the comparison of the DEGs between subtypes. A total of 795 DEGs, including 619 up and 176 downregulated DEGs were screened from the astrocytoma expression profiles; these were enriched in the KEGG pathways of ‘neuroactive ligand-receptor interaction’ (upregulated) and ‘Wnt signaling pathway’ (downregulated). Protein-protein interaction networks for astrocytoma, glioblastoma and oligodendroglioma were constructed with 1,617, 7,027 and 1,172 pairs, respectively. A total of 595 common DEGs were obtained between the three subtypes, which were enriched in pathways associated with neural signaling. Glioblastoma is a subtype of astrocytoma; there were 195 DEGs common between these subtypes that were not also associated with oligodendroglioma. DEGs unique to astrocytoma, glioblastoma and oligodendroglioma were associated with the development of the nervous system, the cell cycle and cell matrix components, respectively. The screened DEG p53 gene is likely to be critical for glioma development, including via the Wnt and p53 signaling pathways. Brain-derived neurotrophic factor and cyclin-dependent kinase 1 genes were also likely to be important in the mechanism of glioma development, and were associated with the cell cycle and p53 signaling pathways. Immune system-associated and cell matrix component pathways may be unique signaling pathways associated with astrocytoma and oligodendroglioma, respectively.
Published Version (Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.