Differential radiation response between normal astrocytes and glioma cells revealed by comparative transcriptome analysis
Normal astrocytes are more resistant to radiation than glioma cells. Radiation-resistant glioma cells and normal astrocytes usuallly share similar mechanisms of radioresistance. Investigation of the underlying mechanisms of differential radiation response between normal astrocytes and glioma cells i...
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| Veröffentlicht in: | OncoTargets and therapy 2017-01, Vol.10, p.5755-5764 |
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| creator | Gong, Liang Gu, Jiacheng Ge, Jianwei Wu, Xiang Zhang, Chao Yang, Chun Weng, Weiji Gao, Guoyi Feng, Junfeng Mao, Qing |
| description | Normal astrocytes are more resistant to radiation than glioma cells. Radiation-resistant glioma cells and normal astrocytes usuallly share similar mechanisms of radioresistance. Investigation of the underlying mechanisms of differential radiation response between normal astrocytes and glioma cells is thus significant for improvement of glioma treatment. Here, we report on the differential radiation responses between normal astrocytes and glioma cells at the transcriptome level. Human astrocytes (HA) and U251 glioma cell lines were used as in vitro models. The transcriptome profiles of radiation-treated and nontreated HA and U251 cells were generated by next-generation sequencing. In total, 296 mRNAs and 224 lncRNAs in HA and 201 mRNAs and 107 lncRNAs in U251 were found to be differentially expressed after radiation treatment. Bioinformatics analyses indicated that radiation causes similar alterations in HA and U251 cells, while several key pathways involved in cancer development and radiation resistance, including P53, TGF-β, VEGF, Hippo and serotonergic synapse pathways, were oppositely regulated by radiation treatment, suggesting their important role in this process. Furthermore, we showed the critical role of Hippo/YAP signaling in radiation resistance of glioma cells. In summary, our findings revealed novel insights about differential responses between normal astrocytes and glioma cells. Our work suggested that YAP inhibitor could not be used in combination with radiation for glioma treatment. |
| doi_str_mv | 10.2147/OTT.S144002 |
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Radiation-resistant glioma cells and normal astrocytes usuallly share similar mechanisms of radioresistance. Investigation of the underlying mechanisms of differential radiation response between normal astrocytes and glioma cells is thus significant for improvement of glioma treatment. Here, we report on the differential radiation responses between normal astrocytes and glioma cells at the transcriptome level. Human astrocytes (HA) and U251 glioma cell lines were used as in vitro models. The transcriptome profiles of radiation-treated and nontreated HA and U251 cells were generated by next-generation sequencing. In total, 296 mRNAs and 224 lncRNAs in HA and 201 mRNAs and 107 lncRNAs in U251 were found to be differentially expressed after radiation treatment. Bioinformatics analyses indicated that radiation causes similar alterations in HA and U251 cells, while several key pathways involved in cancer development and radiation resistance, including P53, TGF-β, VEGF, Hippo and serotonergic synapse pathways, were oppositely regulated by radiation treatment, suggesting their important role in this process. Furthermore, we showed the critical role of Hippo/YAP signaling in radiation resistance of glioma cells. In summary, our findings revealed novel insights about differential responses between normal astrocytes and glioma cells. Our work suggested that YAP inhibitor could not be used in combination with radiation for glioma treatment.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S144002</identifier><identifier>PMID: 29270020</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>Angiogenesis ; Astrocytes ; Brain cancer ; Cancer therapies ; Care and treatment ; Cell cycle ; Cyclin-dependent kinases ; Deoxyribonucleic acid ; Diagnosis ; DNA ; Genomes ; Glioma ; Gliomas ; Hypoxia ; Kinases ; Neurosurgery ; Original Research ; Radiation therapy ; Radiotherapy ; Signal transduction ; Stem cells ; Synapses</subject><ispartof>OncoTargets and therapy, 2017-01, Vol.10, p.5755-5764</ispartof><rights>COPYRIGHT 2017 Dove Medical Press Limited</rights><rights>2017. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Gong et al. This work is published and licensed by Dove Medical Press Limited 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-d70dc5726f793cb8e050b4b7f46dc00cace2415569244b56a573c1cedeb169663</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5720034/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5720034/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,3862,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29270020$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gong, Liang</creatorcontrib><creatorcontrib>Gu, Jiacheng</creatorcontrib><creatorcontrib>Ge, Jianwei</creatorcontrib><creatorcontrib>Wu, Xiang</creatorcontrib><creatorcontrib>Zhang, Chao</creatorcontrib><creatorcontrib>Yang, Chun</creatorcontrib><creatorcontrib>Weng, Weiji</creatorcontrib><creatorcontrib>Gao, Guoyi</creatorcontrib><creatorcontrib>Feng, Junfeng</creatorcontrib><creatorcontrib>Mao, Qing</creatorcontrib><title>Differential radiation response between normal astrocytes and glioma cells revealed by comparative transcriptome analysis</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>Normal astrocytes are more resistant to radiation than glioma cells. Radiation-resistant glioma cells and normal astrocytes usuallly share similar mechanisms of radioresistance. Investigation of the underlying mechanisms of differential radiation response between normal astrocytes and glioma cells is thus significant for improvement of glioma treatment. Here, we report on the differential radiation responses between normal astrocytes and glioma cells at the transcriptome level. Human astrocytes (HA) and U251 glioma cell lines were used as in vitro models. The transcriptome profiles of radiation-treated and nontreated HA and U251 cells were generated by next-generation sequencing. In total, 296 mRNAs and 224 lncRNAs in HA and 201 mRNAs and 107 lncRNAs in U251 were found to be differentially expressed after radiation treatment. Bioinformatics analyses indicated that radiation causes similar alterations in HA and U251 cells, while several key pathways involved in cancer development and radiation resistance, including P53, TGF-β, VEGF, Hippo and serotonergic synapse pathways, were oppositely regulated by radiation treatment, suggesting their important role in this process. Furthermore, we showed the critical role of Hippo/YAP signaling in radiation resistance of glioma cells. In summary, our findings revealed novel insights about differential responses between normal astrocytes and glioma cells. Our work suggested that YAP inhibitor could not be used in combination with radiation for glioma treatment.</description><subject>Angiogenesis</subject><subject>Astrocytes</subject><subject>Brain cancer</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cyclin-dependent kinases</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnosis</subject><subject>DNA</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Gliomas</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Neurosurgery</subject><subject>Original Research</subject><subject>Radiation therapy</subject><subject>Radiotherapy</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Synapses</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkkuL2zAUhU1p6TzaVfdFUCgDJenVw1K8GRimTxiYRdO1kOXrRIMtuZKd4n9fhUmHpBQtJKTvnMu9OkXxhsKSUaE-3q_Xyx9UCAD2rDinVK0WsuLw_Oh8Vlyk9AAg5YqJl8UZq5jKOJwX8yfXthjRj850JJrGmdEFTyKmIfiEpMbxN6InPsQ-EyaNMdh5xESMb8imc6E3xGLXpazZoemwIfVMbOgHE7PXDskYjU82umEMPWaZ6ebk0qviRWu6hK8P-2Xx88vn9e23xd391--3N3cLW4IaF42CxpaKyVZV3NYrhBJqUatWyMYCWGORCVqWsmJC1KU0peKWWmywprKSkl8W14--w1T32NjcajSdHqLrTZx1ME6fvni31Zuw07koABfZ4OpgEMOvCdOoe5f2HRuPYUqaVqqqJOewyui7f9CHMMXccNKMCVZSCfyI2uRpaefbkOvavam-KblgoICrTC3_Q-XVYO9s8Ni6fH8ieH8k2OavGLcpdNP-P9Mp-OERtDGkFLF9GgYFvY-UzpHSh0hl-u3x_J7YvxnifwBoAse9</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Gong, Liang</creator><creator>Gu, Jiacheng</creator><creator>Ge, Jianwei</creator><creator>Wu, Xiang</creator><creator>Zhang, Chao</creator><creator>Yang, Chun</creator><creator>Weng, Weiji</creator><creator>Gao, Guoyi</creator><creator>Feng, Junfeng</creator><creator>Mao, Qing</creator><general>Dove Medical Press Limited</general><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170101</creationdate><title>Differential radiation response between normal astrocytes and glioma cells revealed by comparative transcriptome analysis</title><author>Gong, Liang ; Gu, Jiacheng ; Ge, Jianwei ; Wu, Xiang ; Zhang, Chao ; Yang, Chun ; Weng, Weiji ; Gao, Guoyi ; Feng, Junfeng ; Mao, Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-d70dc5726f793cb8e050b4b7f46dc00cace2415569244b56a573c1cedeb169663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis</topic><topic>Astrocytes</topic><topic>Brain cancer</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cyclin-dependent kinases</topic><topic>Deoxyribonucleic acid</topic><topic>Diagnosis</topic><topic>DNA</topic><topic>Genomes</topic><topic>Glioma</topic><topic>Gliomas</topic><topic>Hypoxia</topic><topic>Kinases</topic><topic>Neurosurgery</topic><topic>Original Research</topic><topic>Radiation therapy</topic><topic>Radiotherapy</topic><topic>Signal transduction</topic><topic>Stem cells</topic><topic>Synapses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gong, Liang</creatorcontrib><creatorcontrib>Gu, Jiacheng</creatorcontrib><creatorcontrib>Ge, Jianwei</creatorcontrib><creatorcontrib>Wu, Xiang</creatorcontrib><creatorcontrib>Zhang, Chao</creatorcontrib><creatorcontrib>Yang, Chun</creatorcontrib><creatorcontrib>Weng, Weiji</creatorcontrib><creatorcontrib>Gao, Guoyi</creatorcontrib><creatorcontrib>Feng, Junfeng</creatorcontrib><creatorcontrib>Mao, Qing</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gong, Liang</au><au>Gu, Jiacheng</au><au>Ge, Jianwei</au><au>Wu, Xiang</au><au>Zhang, Chao</au><au>Yang, Chun</au><au>Weng, Weiji</au><au>Gao, Guoyi</au><au>Feng, Junfeng</au><au>Mao, Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential radiation response between normal astrocytes and glioma cells revealed by comparative transcriptome analysis</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>10</volume><spage>5755</spage><epage>5764</epage><pages>5755-5764</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>Normal astrocytes are more resistant to radiation than glioma cells. Radiation-resistant glioma cells and normal astrocytes usuallly share similar mechanisms of radioresistance. Investigation of the underlying mechanisms of differential radiation response between normal astrocytes and glioma cells is thus significant for improvement of glioma treatment. Here, we report on the differential radiation responses between normal astrocytes and glioma cells at the transcriptome level. Human astrocytes (HA) and U251 glioma cell lines were used as in vitro models. The transcriptome profiles of radiation-treated and nontreated HA and U251 cells were generated by next-generation sequencing. In total, 296 mRNAs and 224 lncRNAs in HA and 201 mRNAs and 107 lncRNAs in U251 were found to be differentially expressed after radiation treatment. Bioinformatics analyses indicated that radiation causes similar alterations in HA and U251 cells, while several key pathways involved in cancer development and radiation resistance, including P53, TGF-β, VEGF, Hippo and serotonergic synapse pathways, were oppositely regulated by radiation treatment, suggesting their important role in this process. Furthermore, we showed the critical role of Hippo/YAP signaling in radiation resistance of glioma cells. In summary, our findings revealed novel insights about differential responses between normal astrocytes and glioma cells. Our work suggested that YAP inhibitor could not be used in combination with radiation for glioma treatment.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>29270020</pmid><doi>10.2147/OTT.S144002</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Astrocytes Brain cancer Cancer therapies Care and treatment Cell cycle Cyclin-dependent kinases Deoxyribonucleic acid Diagnosis DNA Genomes Glioma Gliomas Hypoxia Kinases Neurosurgery Original Research Radiation therapy Radiotherapy Signal transduction Stem cells Synapses |
| title | Differential radiation response between normal astrocytes and glioma cells revealed by comparative transcriptome analysis |
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