Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma

Abstract Background: Diffuse intrinsic pontine glioma (DIPG) is the main cause of pediatric brain tumor death. This study was designed to identify key genes associated with DIPG. Methods: The gene expression profile GSE50021, which consisted of 35 pediatric DIPG samples and 10 normal brain samples...

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Autores principales: Wei,Li, He,Fei, Zhang,Wen, Chen,Wenhua, Yu,Bo
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2018
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100222
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spelling oai:scielo:S0716-976020180001002222018-09-05Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine gliomaWei,LiHe,FeiZhang,WenChen,WenhuaYu,Bo Diffuse intrinsic pontine glioma Differentially-expressed genes Neuroactive ligand-receptor interaction Protein-protein interaction network Transcription factor-microRNA-target gene network Abstract Background: Diffuse intrinsic pontine glioma (DIPG) is the main cause of pediatric brain tumor death. This study was designed to identify key genes associated with DIPG. Methods: The gene expression profile GSE50021, which consisted of 35 pediatric DIPG samples and 10 normal brain samples, was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified by limma package. Functional and pathway enrichment analyses were performed by the DAVID tool. Protein-protein interaction (PPI) network, and transcription factor (TF)-microRNA (miRNA)-target gene network were constructed using Cytoscape. Moreover, the expression levels of several genes were validated in human glioma cell line U251 and normal glia HEB cells through real-time polymerase chain reaction (PCR). Results: A total of 378 DEGs were screened (74 up-regulated and 304 down-regulated genes). In the PPI network, GRM1, HTR2A, GRM7 and GRM2 had higher degrees. Besides, GRM1 and HTR2A were significantly enriched in the neuroactive ligand-receptor interaction pathway, and calcium signaling pathway. In addition, TFAP2C was a significant down-regulated functional gene and hsa-miR-26b-5p had a higher degree in the TF-miRNA-target gene network. PCR analysis revealed that GRM7 and HTR2A were significantly downregulated while TFAP2C was upregulated in U251 cells compared with that in HEB cells (p < 0.001). GRM2 was not detected in cells. Conclusions: GRM1 and HTR2A might function in DIPG through the neuroactive ligand-receptor interaction pathway and the calcium signaling pathway. Furthermore, the TFAP2C and hsa-miR-26b-5p might play important roles in the development and progression mechanisms of DIPG.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.51 20182018-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100222en10.1186/s40659-018-0175-6
institution Scielo Chile
collection Scielo Chile
language English
topic Diffuse intrinsic pontine glioma
Differentially-expressed genes
Neuroactive ligand-receptor interaction
Protein-protein interaction network
Transcription factor-microRNA-target gene network
spellingShingle Diffuse intrinsic pontine glioma
Differentially-expressed genes
Neuroactive ligand-receptor interaction
Protein-protein interaction network
Transcription factor-microRNA-target gene network
Wei,Li
He,Fei
Zhang,Wen
Chen,Wenhua
Yu,Bo
Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
description Abstract Background: Diffuse intrinsic pontine glioma (DIPG) is the main cause of pediatric brain tumor death. This study was designed to identify key genes associated with DIPG. Methods: The gene expression profile GSE50021, which consisted of 35 pediatric DIPG samples and 10 normal brain samples, was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified by limma package. Functional and pathway enrichment analyses were performed by the DAVID tool. Protein-protein interaction (PPI) network, and transcription factor (TF)-microRNA (miRNA)-target gene network were constructed using Cytoscape. Moreover, the expression levels of several genes were validated in human glioma cell line U251 and normal glia HEB cells through real-time polymerase chain reaction (PCR). Results: A total of 378 DEGs were screened (74 up-regulated and 304 down-regulated genes). In the PPI network, GRM1, HTR2A, GRM7 and GRM2 had higher degrees. Besides, GRM1 and HTR2A were significantly enriched in the neuroactive ligand-receptor interaction pathway, and calcium signaling pathway. In addition, TFAP2C was a significant down-regulated functional gene and hsa-miR-26b-5p had a higher degree in the TF-miRNA-target gene network. PCR analysis revealed that GRM7 and HTR2A were significantly downregulated while TFAP2C was upregulated in U251 cells compared with that in HEB cells (p < 0.001). GRM2 was not detected in cells. Conclusions: GRM1 and HTR2A might function in DIPG through the neuroactive ligand-receptor interaction pathway and the calcium signaling pathway. Furthermore, the TFAP2C and hsa-miR-26b-5p might play important roles in the development and progression mechanisms of DIPG.
author Wei,Li
He,Fei
Zhang,Wen
Chen,Wenhua
Yu,Bo
author_facet Wei,Li
He,Fei
Zhang,Wen
Chen,Wenhua
Yu,Bo
author_sort Wei,Li
title Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
title_short Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
title_full Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
title_fullStr Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
title_full_unstemmed Bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
title_sort bioinformatics analysis of microarray data to reveal the pathogenesis of diffuse intrinsic pontine glioma
publisher Sociedad de Biología de Chile
publishDate 2018
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100222
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