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Article: A combined proteomics and metabolomics profiling of gastric cardia cancer reveals characteristic dysregulations in glucose metabolism

TitleA combined proteomics and metabolomics profiling of gastric cardia cancer reveals characteristic dysregulations in glucose metabolism
Authors
Issue Date2010
Citation
Molecular and Cellular Proteomics, 2010, v. 9, n. 12, p. 2617-2628 How to Cite?
AbstractGastric cardia cancer (GCC), which occurs at the gastricesophageal boundary, is one of the most malignant tumors. Despite its high mortality and morbidity, the molecular mechanism of initiation and progression of this disease is largely unknown. In this study, using proteomics and metabolomics approaches, we found that the level of several enzymes and their related metabolic intermediates involved in glucose metabolism were deregulated in GCC. Among these enzymes, two subunits controlling pyruvic acid efflux, lactate dehydrogenase A (LDHA) and pyruvate dehydrogenase B (PDHB), were further analyzed in vitro. Either down-regulation of LDH subunit LDHA or overexpression of PDH subunit PDHB could force pyruvic acid into the Krebs cycle rather than the glycolysis process in AGS gastric cancer cells, which inhibited cell growth and cell migration. Our results reflect an important glucose metabolic signature, especially the dysregulation of pyruvic acid efflux in the development of GCC. Forced transition from glycolysis to the Krebs cycle had an inhibitory effect on GCC progression, providing potential therapeutic targets for this disease. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/342384
ISSN
2020 Impact Factor: 5.911
2023 SCImago Journal Rankings: 2.348
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCai, Zhen-
dc.contributor.authorZhao, Jiang Sha-
dc.contributor.authorLi, Jing Jing-
dc.contributor.authorPeng, Dan Ni-
dc.contributor.authorWang, Xiao Yan-
dc.contributor.authorChen, Tian Lu-
dc.contributor.authorQiu, Yun Ping-
dc.contributor.authorChen, Ping Ping-
dc.contributor.authorLi, Wen Jie-
dc.contributor.authorXu, Li Yan-
dc.contributor.authorLi, En Ming-
dc.contributor.authorTam, Jason P.M.-
dc.contributor.authorQi, Robert Z.-
dc.contributor.authorJia, Wei-
dc.contributor.authorXie, Dong-
dc.date.accessioned2024-04-17T07:03:26Z-
dc.date.available2024-04-17T07:03:26Z-
dc.date.issued2010-
dc.identifier.citationMolecular and Cellular Proteomics, 2010, v. 9, n. 12, p. 2617-2628-
dc.identifier.issn1535-9476-
dc.identifier.urihttp://hdl.handle.net/10722/342384-
dc.description.abstractGastric cardia cancer (GCC), which occurs at the gastricesophageal boundary, is one of the most malignant tumors. Despite its high mortality and morbidity, the molecular mechanism of initiation and progression of this disease is largely unknown. In this study, using proteomics and metabolomics approaches, we found that the level of several enzymes and their related metabolic intermediates involved in glucose metabolism were deregulated in GCC. Among these enzymes, two subunits controlling pyruvic acid efflux, lactate dehydrogenase A (LDHA) and pyruvate dehydrogenase B (PDHB), were further analyzed in vitro. Either down-regulation of LDH subunit LDHA or overexpression of PDH subunit PDHB could force pyruvic acid into the Krebs cycle rather than the glycolysis process in AGS gastric cancer cells, which inhibited cell growth and cell migration. Our results reflect an important glucose metabolic signature, especially the dysregulation of pyruvic acid efflux in the development of GCC. Forced transition from glycolysis to the Krebs cycle had an inhibitory effect on GCC progression, providing potential therapeutic targets for this disease. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.-
dc.languageeng-
dc.relation.ispartofMolecular and Cellular Proteomics-
dc.titleA combined proteomics and metabolomics profiling of gastric cardia cancer reveals characteristic dysregulations in glucose metabolism-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1074/mcp.M110.000661-
dc.identifier.pmid20699381-
dc.identifier.scopuseid_2-s2.0-78650138387-
dc.identifier.volume9-
dc.identifier.issue12-
dc.identifier.spage2617-
dc.identifier.epage2628-
dc.identifier.eissn1535-9484-
dc.identifier.isiWOS:000284882100004-

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