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Article: Enhanced Fructose Utilization Mediated by SLC2A5 Is a Unique Metabolic Feature of Acute Myeloid Leukemia with Therapeutic Potential

TitleEnhanced Fructose Utilization Mediated by SLC2A5 Is a Unique Metabolic Feature of Acute Myeloid Leukemia with Therapeutic Potential
Authors
Chen, Wen LianWang, Yue YingZhao, AihuaXia, LiXie, GuoxiangSu, MingmingZhao, LinjingLiu, JiajianQu, ChunWei, RunminRajani, CynthiaNi, YanCheng, ZhenChen, ZhuChen, Sai JuanJia, Wei
Keywordsacute myeloid leukemia
fructose utilization
GLUT5
SLC2A5
Issue Date2016
Citation
Cancer Cell, 2016, v. 30, n. 5, p. 779-791 How to Cite?
DOI: http://dx.doi.org/10.1016/j.ccell.2016.09.006
AbstractRapidly proliferating leukemic progenitor cells consume substantial glucose, which may lead to glucose insufficiency in bone marrow. We show that acute myeloid leukemia (AML) cells are prone to fructose utilization with an upregulated fructose transporter GLUT5, which compensates for glucose deficiency. Notably, AML patients with upregulated transcription of the GLUT5-encoding gene SLC2A5 or increased fructose utilization have poor outcomes. Pharmacological blockage of fructose uptake ameliorates leukemic phenotypes and potentiates the cytotoxicity of the antileukemic agent, Ara-C. In conclusion, this study highlights enhanced fructose utilization as a metabolic feature of AML and a potential therapeutic target.
Persistent Identifierhttp://hdl.handle.net/10722/342533
ISSN
1535-6108
2023 Impact Factor: 48.8
2023 SCImago Journal Rankings: 17.507
ISI Accession Number ID
WOS:000388064800016

 

DC FieldValueLanguage
dc.contributor.authorChen, Wen Lian-
dc.contributor.authorWang, Yue Ying-
dc.contributor.authorZhao, Aihua-
dc.contributor.authorXia, Li-
dc.contributor.authorXie, Guoxiang-
dc.contributor.authorSu, Mingming-
dc.contributor.authorZhao, Linjing-
dc.contributor.authorLiu, Jiajian-
dc.contributor.authorQu, Chun-
dc.contributor.authorWei, Runmin-
dc.contributor.authorRajani, Cynthia-
dc.contributor.authorNi, Yan-
dc.contributor.authorCheng, Zhen-
dc.contributor.authorChen, Zhu-
dc.contributor.authorChen, Sai Juan-
dc.contributor.authorJia, Wei-
dc.date.accessioned2024-04-17T07:04:30Z-
dc.date.available2024-04-17T07:04:30Z-
dc.date.issued2016-
dc.identifier.citationCancer Cell, 2016, v. 30, n. 5, p. 779-791-
dc.identifier.issn1535-6108-
dc.identifier.urihttp://hdl.handle.net/10722/342533-
dc.description.abstractRapidly proliferating leukemic progenitor cells consume substantial glucose, which may lead to glucose insufficiency in bone marrow. We show that acute myeloid leukemia (AML) cells are prone to fructose utilization with an upregulated fructose transporter GLUT5, which compensates for glucose deficiency. Notably, AML patients with upregulated transcription of the GLUT5-encoding gene SLC2A5 or increased fructose utilization have poor outcomes. Pharmacological blockage of fructose uptake ameliorates leukemic phenotypes and potentiates the cytotoxicity of the antileukemic agent, Ara-C. In conclusion, this study highlights enhanced fructose utilization as a metabolic feature of AML and a potential therapeutic target.-
dc.languageeng-
dc.relation.ispartofCancer Cell-
dc.subjectacute myeloid leukemia-
dc.subjectfructose utilization-
dc.subjectGLUT5-
dc.subjectSLC2A5-
dc.titleEnhanced Fructose Utilization Mediated by SLC2A5 Is a Unique Metabolic Feature of Acute Myeloid Leukemia with Therapeutic Potential-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ccell.2016.09.006-
dc.identifier.pmid27746145-
dc.identifier.scopuseid_2-s2.0-85006489776-
dc.identifier.volume30-
dc.identifier.issue5-
dc.identifier.spage779-
dc.identifier.epage791-
dc.identifier.eissn1878-3686-
dc.identifier.isiWOS:000388064800016-

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