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Identification of key genes and pathways in meningioma by bioinformatics analysis

Meningioma is the most frequently occurring type of brain tumor. The present study aimed to conduct a comprehensive bioinformatics analysis of key genes and relevant pathways involved in meningioma, and acquire further insight into the underlying molecular mechanisms. Initially, differentially expre...

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Autores principales: Dai, Junxi, Ma, Yanbin, Chu, Shenghua, Le, Nanyang, Cao, Jun, Wang, Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5950024/
https://www.ncbi.nlm.nih.gov/pubmed/29805558
http://dx.doi.org/10.3892/ol.2018.8376
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author Dai, Junxi
Ma, Yanbin
Chu, Shenghua
Le, Nanyang
Cao, Jun
Wang, Yang
author_facet Dai, Junxi
Ma, Yanbin
Chu, Shenghua
Le, Nanyang
Cao, Jun
Wang, Yang
author_sort Dai, Junxi
collection PubMed
description Meningioma is the most frequently occurring type of brain tumor. The present study aimed to conduct a comprehensive bioinformatics analysis of key genes and relevant pathways involved in meningioma, and acquire further insight into the underlying molecular mechanisms. Initially, differentially expressed genes (DEGs) in 47 meningioma samples as compared with 4 normal meninges were identified. Subsequently, these DEGs were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. In addition, a protein-protein interaction (PPI) network of the identified DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes and visualized using Cytoscape. In total, 1,683 DEGs were identified, including 66 upregulated and 1,617 downregulated genes. The GO analysis results revealed that the DEGs were significantly associated with the ‘protein binding’, ‘cytoplasm’, ‘extracellular matrix (ECM) organization’ and ‘cell adhesion’ terms. The KEGG analysis results demonstrated the significant pathways included ‘AGE-RAGE signaling pathway in diabetic complications’, ‘PI3K-Akt signaling pathway’, ‘ECM-receptor interaction’ and ‘cell adhesion molecules’. The top five hub genes obtained from the PPI network were JUN, PIK3R1, FOS, AGT and MYC, and the most enriched KEGG pathways associated with the four obtained modules were ‘chemokine signaling pathway’, ‘cytokine-cytokine receptor interaction’, ‘allograft rejection’, and ‘complement and coagulation cascades’. In conclusion, bioinformatics analysis identified a number of potential biomarkers and relevant pathways that may represent key mechanisms involved in the development and progression of meningioma. However, these findings require verification in future experimental studies.
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spelling pubmed-59500242018-05-27 Identification of key genes and pathways in meningioma by bioinformatics analysis Dai, Junxi Ma, Yanbin Chu, Shenghua Le, Nanyang Cao, Jun Wang, Yang Oncol Lett Articles Meningioma is the most frequently occurring type of brain tumor. The present study aimed to conduct a comprehensive bioinformatics analysis of key genes and relevant pathways involved in meningioma, and acquire further insight into the underlying molecular mechanisms. Initially, differentially expressed genes (DEGs) in 47 meningioma samples as compared with 4 normal meninges were identified. Subsequently, these DEGs were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. In addition, a protein-protein interaction (PPI) network of the identified DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes and visualized using Cytoscape. In total, 1,683 DEGs were identified, including 66 upregulated and 1,617 downregulated genes. The GO analysis results revealed that the DEGs were significantly associated with the ‘protein binding’, ‘cytoplasm’, ‘extracellular matrix (ECM) organization’ and ‘cell adhesion’ terms. The KEGG analysis results demonstrated the significant pathways included ‘AGE-RAGE signaling pathway in diabetic complications’, ‘PI3K-Akt signaling pathway’, ‘ECM-receptor interaction’ and ‘cell adhesion molecules’. The top five hub genes obtained from the PPI network were JUN, PIK3R1, FOS, AGT and MYC, and the most enriched KEGG pathways associated with the four obtained modules were ‘chemokine signaling pathway’, ‘cytokine-cytokine receptor interaction’, ‘allograft rejection’, and ‘complement and coagulation cascades’. In conclusion, bioinformatics analysis identified a number of potential biomarkers and relevant pathways that may represent key mechanisms involved in the development and progression of meningioma. However, these findings require verification in future experimental studies. D.A. Spandidos 2018-06 2018-03-29 /pmc/articles/PMC5950024/ /pubmed/29805558 http://dx.doi.org/10.3892/ol.2018.8376 Text en Copyright: © Dai et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Dai, Junxi
Ma, Yanbin
Chu, Shenghua
Le, Nanyang
Cao, Jun
Wang, Yang
Identification of key genes and pathways in meningioma by bioinformatics analysis
title Identification of key genes and pathways in meningioma by bioinformatics analysis
title_full Identification of key genes and pathways in meningioma by bioinformatics analysis
title_fullStr Identification of key genes and pathways in meningioma by bioinformatics analysis
title_full_unstemmed Identification of key genes and pathways in meningioma by bioinformatics analysis
title_short Identification of key genes and pathways in meningioma by bioinformatics analysis
title_sort identification of key genes and pathways in meningioma by bioinformatics analysis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5950024/
https://www.ncbi.nlm.nih.gov/pubmed/29805558
http://dx.doi.org/10.3892/ol.2018.8376
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