Literature DB >> 27746145

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

Wen-Lian Chen1, Yue-Ying Wang2, Aihua Zhao3, Li Xia2, Guoxiang Xie4, Mingming Su4, Linjing Zhao5, Jiajian Liu3, Chun Qu3, Runmin Wei5, Cynthia Rajani5, Yan Ni4, Zhen Cheng6, Zhu Chen2, Sai-Juan Chen7, Wei Jia8.   

Abstract

Rapidly 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.
Copyright © 2016 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  GLUT5; SLC2A5; acute myeloid leukemia; fructose utilization

Mesh：

Substances：

Year:  2016        PMID： 27746145      PMCID： PMC5496656          DOI： 10.1016/j.ccell.2016.09.006

Source DB:  PubMed          Journal:  Cancer Cell        ISSN： 1535-6108            Impact factor:   31.743


  35 in total

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