DNA methylation profiling identifies potentially significant epigenetically-regulated genes in glioblastoma multiforme
Glioblastoma multiforme (GBM) is one of the most lethal and damaging types of human cancer. The current study was conducted to identify differentially methylated genes (DMGs) between GBM and normal controls, and to improve our understanding of GBM at the epigenetic level. The DNA methylation profile...
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Veröffentlicht in: | Oncology letters 2019-08, Vol.18 (2), p.1679-1688 |
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description | Glioblastoma multiforme (GBM) is one of the most lethal and damaging types of human cancer. The current study was conducted to identify differentially methylated genes (DMGs) between GBM and normal controls, and to improve our understanding of GBM at the epigenetic level. The DNA methylation profile of GBM was downloaded from the Gene Expression Omnibus (GEO) database using the accession number GSE50923. The MethyAnalysis package was applied to identify DMGs between GBM and controls, which were then analyzed by functional enrichment analysis. Protein-protein interaction (PPI) networks were constructed using the hypermethylated and hypomethylated genes. Finally, transcription factors (TFs) that can regulate the hypermethylated and hypomethylated genes were predicted, followed by construction of transcriptional regulatory networks. Furthermore, another relevant dataset, GSE22867, was downloaded from the GEO database for data validation. A total of 476 hypermethylated and 850 hypomethylated genes were identified, which were mainly associated with the functions of 'G-protein-coupled receptors ligand binding', 'cytokine activity', 'cytokine-cytokine receptor interaction', and 'D-glutamine and D-glutamate metabolism'. The hypermethylated gene neuropeptide Y (
) and the hypomethylated gene tumor necrosis factor (
) demonstrated high degrees in the PPI network. Forkhead box protein A1 (
), potassium voltage-gated channel subfamily C member 3 (
) and caspase-8 (
) exhibited high degrees in the transcriptional regulatory networks. In addition, the methylation profiles of
and
were confirmed by another dataset. In summary, the present study systematically analyzed the DNA methylation profile of GBM using bioinformatics approaches and identified several abnormally methylated genes, providing insight into the molecular mechanism underlying GBM. |
doi_str_mv | 10.3892/ol.2019.10512 |
format | Article |
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) and the hypomethylated gene tumor necrosis factor (
) demonstrated high degrees in the PPI network. Forkhead box protein A1 (
), potassium voltage-gated channel subfamily C member 3 (
) and caspase-8 (
) exhibited high degrees in the transcriptional regulatory networks. In addition, the methylation profiles of
and
were confirmed by another dataset. In summary, the present study systematically analyzed the DNA methylation profile of GBM using bioinformatics approaches and identified several abnormally methylated genes, providing insight into the molecular mechanism underlying GBM.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2019.10512</identifier><identifier>PMID: 31423235</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Biochemistry ; Bioinformatics ; Biomarkers ; Brain cancer ; Cancer ; Cancer therapies ; Computational biology ; Cytokines ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA binding proteins ; DNA methylation ; Encyclopedias ; Epigenetic inheritance ; Epigenetics ; Gene expression ; Genes ; Genetic aspects ; Genomes ; Glioblastomas ; Gliomas ; Glutamate ; Glutamine ; Ligands ; Medical prognosis ; Metabolism ; Methylation ; Necrosis ; Neuropeptide Y ; Neuropeptides ; Physiological aspects ; Protein binding ; Protein-protein interactions ; Proteins ; Studies ; Transcription (Genetics) ; Transcription factors ; Tumors</subject><ispartof>Oncology letters, 2019-08, Vol.18 (2), p.1679-1688</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Kan et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-4d7f2300fc1509cfce5ced96d6529f089159af1e9b550adb92035d50b2b77e673</citedby><cites>FETCH-LOGICAL-c513t-4d7f2300fc1509cfce5ced96d6529f089159af1e9b550adb92035d50b2b77e673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614665/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614665/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31423235$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kan, Shifeng</creatorcontrib><creatorcontrib>Chai, Song</creatorcontrib><creatorcontrib>Chen, Wenhua</creatorcontrib><creatorcontrib>Yu, Bo</creatorcontrib><title>DNA methylation profiling identifies potentially significant epigenetically-regulated genes in glioblastoma multiforme</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Glioblastoma multiforme (GBM) is one of the most lethal and damaging types of human cancer. The current study was conducted to identify differentially methylated genes (DMGs) between GBM and normal controls, and to improve our understanding of GBM at the epigenetic level. The DNA methylation profile of GBM was downloaded from the Gene Expression Omnibus (GEO) database using the accession number GSE50923. The MethyAnalysis package was applied to identify DMGs between GBM and controls, which were then analyzed by functional enrichment analysis. Protein-protein interaction (PPI) networks were constructed using the hypermethylated and hypomethylated genes. Finally, transcription factors (TFs) that can regulate the hypermethylated and hypomethylated genes were predicted, followed by construction of transcriptional regulatory networks. Furthermore, another relevant dataset, GSE22867, was downloaded from the GEO database for data validation. A total of 476 hypermethylated and 850 hypomethylated genes were identified, which were mainly associated with the functions of 'G-protein-coupled receptors ligand binding', 'cytokine activity', 'cytokine-cytokine receptor interaction', and 'D-glutamine and D-glutamate metabolism'. The hypermethylated gene neuropeptide Y (
) and the hypomethylated gene tumor necrosis factor (
) demonstrated high degrees in the PPI network. Forkhead box protein A1 (
), potassium voltage-gated channel subfamily C member 3 (
) and caspase-8 (
) exhibited high degrees in the transcriptional regulatory networks. In addition, the methylation profiles of
and
were confirmed by another dataset. In summary, the present study systematically analyzed the DNA methylation profile of GBM using bioinformatics approaches and identified several abnormally methylated genes, providing insight into the molecular mechanism underlying GBM.</description><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomarkers</subject><subject>Brain cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Computational biology</subject><subject>Cytokines</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA binding proteins</subject><subject>DNA methylation</subject><subject>Encyclopedias</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glioblastomas</subject><subject>Gliomas</subject><subject>Glutamate</subject><subject>Glutamine</subject><subject>Ligands</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Methylation</subject><subject>Necrosis</subject><subject>Neuropeptide Y</subject><subject>Neuropeptides</subject><subject>Physiological aspects</subject><subject>Protein binding</subject><subject>Protein-protein interactions</subject><subject>Proteins</subject><subject>Studies</subject><subject>Transcription (Genetics)</subject><subject>Transcription factors</subject><subject>Tumors</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkstv1DAQhyMEolXpkSuyhIS4ZPEjduIL0qo8pQoucLYcZ5J15diL7VTa_74OLUsXYR9sz3z-jeZRVS8J3rBO0nfBbSgmckMwJ_RJdU5aSWuCO_r0eG-bs-oypRtcFhek68Tz6oyRhjLK-Hl1--HbFs2Qdwensw0e7WMYrbN-QnYAn-1oIaF9yOtdO3dAyU6-WI32GcHeTuAhl1dx1RGmpcjAgFZrQtajydnQO51ymDWaF1cEQ5zhRfVs1C7B5cN5Uf389PHH1Zf6-vvnr1fb69pwwnLdDO1IGcajIRxLMxrgBgYpBsGpHHEnCZd6JCB7zrEeekkx4wPHPe3bFkTLLqr397r7pZ9hMCWLqJ3aRzvreFBBW3Xq8XanpnCrhCCNELwIvH0QiOHXAimr2SYDzmkPYUmK0pbLhjdYFvT1P-hNWKIv6RWKcyJxy9lfatIOlPVjKHHNKqq2RUmIRrZr2M1_qLIHmK0JHkqP4PTDm0cfdqBd3qXglrWn6RSs70ETQ0oRxmMxCFbrUKng1DpU6vdQFf7V4woe6T8jxO4ASkDIsQ</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Kan, Shifeng</creator><creator>Chai, Song</creator><creator>Chen, Wenhua</creator><creator>Yu, Bo</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190801</creationdate><title>DNA methylation profiling identifies potentially significant epigenetically-regulated genes in glioblastoma multiforme</title><author>Kan, Shifeng ; Chai, Song ; Chen, Wenhua ; Yu, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-4d7f2300fc1509cfce5ced96d6529f089159af1e9b550adb92035d50b2b77e673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Biochemistry</topic><topic>Bioinformatics</topic><topic>Biomarkers</topic><topic>Brain cancer</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Computational biology</topic><topic>Cytokines</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>DNA binding proteins</topic><topic>DNA methylation</topic><topic>Encyclopedias</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Glioblastomas</topic><topic>Gliomas</topic><topic>Glutamate</topic><topic>Glutamine</topic><topic>Ligands</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Methylation</topic><topic>Necrosis</topic><topic>Neuropeptide Y</topic><topic>Neuropeptides</topic><topic>Physiological aspects</topic><topic>Protein binding</topic><topic>Protein-protein interactions</topic><topic>Proteins</topic><topic>Studies</topic><topic>Transcription (Genetics)</topic><topic>Transcription factors</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Kan, Shifeng</creatorcontrib><creatorcontrib>Chai, Song</creatorcontrib><creatorcontrib>Chen, Wenhua</creatorcontrib><creatorcontrib>Yu, Bo</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kan, Shifeng</au><au>Chai, Song</au><au>Chen, Wenhua</au><au>Yu, Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA methylation profiling identifies potentially significant epigenetically-regulated genes in glioblastoma multiforme</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>18</volume><issue>2</issue><spage>1679</spage><epage>1688</epage><pages>1679-1688</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>Glioblastoma multiforme (GBM) is one of the most lethal and damaging types of human cancer. The current study was conducted to identify differentially methylated genes (DMGs) between GBM and normal controls, and to improve our understanding of GBM at the epigenetic level. The DNA methylation profile of GBM was downloaded from the Gene Expression Omnibus (GEO) database using the accession number GSE50923. The MethyAnalysis package was applied to identify DMGs between GBM and controls, which were then analyzed by functional enrichment analysis. Protein-protein interaction (PPI) networks were constructed using the hypermethylated and hypomethylated genes. Finally, transcription factors (TFs) that can regulate the hypermethylated and hypomethylated genes were predicted, followed by construction of transcriptional regulatory networks. Furthermore, another relevant dataset, GSE22867, was downloaded from the GEO database for data validation. A total of 476 hypermethylated and 850 hypomethylated genes were identified, which were mainly associated with the functions of 'G-protein-coupled receptors ligand binding', 'cytokine activity', 'cytokine-cytokine receptor interaction', and 'D-glutamine and D-glutamate metabolism'. The hypermethylated gene neuropeptide Y (
) and the hypomethylated gene tumor necrosis factor (
) demonstrated high degrees in the PPI network. Forkhead box protein A1 (
), potassium voltage-gated channel subfamily C member 3 (
) and caspase-8 (
) exhibited high degrees in the transcriptional regulatory networks. In addition, the methylation profiles of
and
were confirmed by another dataset. In summary, the present study systematically analyzed the DNA methylation profile of GBM using bioinformatics approaches and identified several abnormally methylated genes, providing insight into the molecular mechanism underlying GBM.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31423235</pmid><doi>10.3892/ol.2019.10512</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biochemistry Bioinformatics Biomarkers Brain cancer Cancer Cancer therapies Computational biology Cytokines Deoxyribonucleic acid Development and progression DNA DNA binding proteins DNA methylation Encyclopedias Epigenetic inheritance Epigenetics Gene expression Genes Genetic aspects Genomes Glioblastomas Gliomas Glutamate Glutamine Ligands Medical prognosis Metabolism Methylation Necrosis Neuropeptide Y Neuropeptides Physiological aspects Protein binding Protein-protein interactions Proteins Studies Transcription (Genetics) Transcription factors Tumors |
title | DNA methylation profiling identifies potentially significant epigenetically-regulated genes in glioblastoma multiforme |
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