Kristell Oizel, Chendong Yang, Ophelie Renoult, Fabien Gautier, Quyen N Do, Noemie Joalland, Xiaofei Gao, Bookyung Ko, François Vallette, Woo-Ping Ge, François Paris, Ralph J DeBerardinis, Claire Pecqueur
{"title":"人间质胶质母细胞瘤对谷氨酰胺的摄取和利用（正位小鼠模型）。","authors":"Kristell Oizel, Chendong Yang, Ophelie Renoult, Fabien Gautier, Quyen N Do, Noemie Joalland, Xiaofei Gao, Bookyung Ko, François Vallette, Woo-Ping Ge, François Paris, Ralph J DeBerardinis, Claire Pecqueur","doi":"10.1186/s40170-020-00215-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) are highly heterogeneous on the cellular and molecular basis. It has been proposed that glutamine metabolism of primary cells established from human tumors discriminates aggressive mesenchymal GBM subtype to other subtypes.</p><p><strong>Methods: </strong>To study glutamine metabolism in vivo, we used a human orthotopic mouse model for GBM. Tumors evolving from the implanted primary GBM cells expressing different molecular signatures were analyzed using mass spectrometry for their metabolite pools and enrichment in carbon 13 (<sup>13</sup>C) after <sup>13</sup>C-glutamine infusion.</p><p><strong>Results: </strong>Our results showed that mesenchymal GBM tumors displayed increased glutamine uptake and utilization compared to both control brain tissue and other GBM subtypes. Furthermore, both glutamine synthetase and transglutaminase-2 were expressed accordingly to GBM metabolic phenotypes.</p><p><strong>Conclusion: </strong>Thus, our results outline the specific enhanced glutamine flux in vivo of the aggressive mesenchymal GBM subtype.</p>","PeriodicalId":9418,"journal":{"name":"Cancer & Metabolism","volume":"8 ","pages":"9"},"PeriodicalIF":6.0000,"publicationDate":"2020-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416393/pdf/","citationCount":"0","resultStr":"{\"title\":\"Glutamine uptake and utilization of human mesenchymal glioblastoma in orthotopic mouse model.\",\"authors\":\"Kristell Oizel, Chendong Yang, Ophelie Renoult, Fabien Gautier, Quyen N Do, Noemie Joalland, Xiaofei Gao, Bookyung Ko, François Vallette, Woo-Ping Ge, François Paris, Ralph J DeBerardinis, Claire Pecqueur\",\"doi\":\"10.1186/s40170-020-00215-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Glioblastoma (GBM) are highly heterogeneous on the cellular and molecular basis. It has been proposed that glutamine metabolism of primary cells established from human tumors discriminates aggressive mesenchymal GBM subtype to other subtypes.</p><p><strong>Methods: </strong>To study glutamine metabolism in vivo, we used a human orthotopic mouse model for GBM. Tumors evolving from the implanted primary GBM cells expressing different molecular signatures were analyzed using mass spectrometry for their metabolite pools and enrichment in carbon 13 (<sup>13</sup>C) after <sup>13</sup>C-glutamine infusion.</p><p><strong>Results: </strong>Our results showed that mesenchymal GBM tumors displayed increased glutamine uptake and utilization compared to both control brain tissue and other GBM subtypes. Furthermore, both glutamine synthetase and transglutaminase-2 were expressed accordingly to GBM metabolic phenotypes.</p><p><strong>Conclusion: </strong>Thus, our results outline the specific enhanced glutamine flux in vivo of the aggressive mesenchymal GBM subtype.</p>\",\"PeriodicalId\":9418,\"journal\":{\"name\":\"Cancer & Metabolism\",\"volume\":\"8 \",\"pages\":\"9\"},\"PeriodicalIF\":6.0000,\"publicationDate\":\"2020-08-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416393/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer & Metabolism\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s40170-020-00215-8\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer & Metabolism","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s40170-020-00215-8","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Glutamine uptake and utilization of human mesenchymal glioblastoma in orthotopic mouse model.
Background: Glioblastoma (GBM) are highly heterogeneous on the cellular and molecular basis. It has been proposed that glutamine metabolism of primary cells established from human tumors discriminates aggressive mesenchymal GBM subtype to other subtypes.
Methods: To study glutamine metabolism in vivo, we used a human orthotopic mouse model for GBM. Tumors evolving from the implanted primary GBM cells expressing different molecular signatures were analyzed using mass spectrometry for their metabolite pools and enrichment in carbon 13 (13C) after 13C-glutamine infusion.
Results: Our results showed that mesenchymal GBM tumors displayed increased glutamine uptake and utilization compared to both control brain tissue and other GBM subtypes. Furthermore, both glutamine synthetase and transglutaminase-2 were expressed accordingly to GBM metabolic phenotypes.
Conclusion: Thus, our results outline the specific enhanced glutamine flux in vivo of the aggressive mesenchymal GBM subtype.
期刊介绍：
Cancer & Metabolism welcomes studies on all aspects of the relationship between cancer and metabolism, including: -Molecular biology and genetics of cancer metabolism -Whole-body metabolism, including diabetes and obesity, in relation to cancer -Metabolomics in relation to cancer; -Metabolism-based imaging -Preclinical and clinical studies of metabolism-related cancer therapies.
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