NDLI: Targeting aberrant glutathione metabolism to eradicate human acute myelogenous leukemia cells.

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Targeting aberrant glutathione metabolism to eradicate human acute myelogenous leukemia cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Benes, Cyril Li, Zheng Crooks, Peter A. Settleman, Jeffrey Hagen, Fred K. Callahan, Kevin P. Corbett, Cheryl Balys, Marlene Ashton, John M. Jordan, Craig T. Lagadinou, Eleni D. Neering, Sarah J. O'dwyer, Kristen M. Pei, Shanshan Minhajuddin, Mohammad Ye, Haobin Shi, Lei Greninger, Patricia Liesveld, Jane L. Munger, Joshua Becker, Michael W.
Description	Author Affiliation: Pei S ( From the Departments of Biomedical Genetics.)
Abstract	The development of strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challenge to the leukemia research field. In particular, primitive leukemia cells, often termed leukemia stem cells, are typically refractory to many forms of therapy. To investigate improved strategies for targeting of human AML cells we compared the molecular mechanisms regulating oxidative state in primitive (CD34(+)) leukemic versus normal specimens. Our data indicate that CD34(+) AML cells have elevated expression of multiple glutathione pathway regulatory proteins, presumably as a mechanism to compensate for increased oxidative stress in leukemic cells. Consistent with this observation, CD34(+) AML cells have lower levels of reduced glutathione and increased levels of oxidized glutathione compared with normal CD34(+) cells. These findings led us to hypothesize that AML cells will be hypersensitive to inhibition of glutathione metabolism. To test this premise, we identified compounds such as parthenolide (PTL) or piperlongumine that induce almost complete glutathione depletion and severe cell death in CD34(+) AML cells. Importantly, these compounds only induce limited and transient glutathione depletion as well as significantly less toxicity in normal CD34(+) cells. We further determined that PTL perturbs glutathione homeostasis by a multifactorial mechanism, which includes inhibiting key glutathione metabolic enzymes (GCLC and GPX1), as well as direct depletion of glutathione. These findings demonstrate that primitive leukemia cells are uniquely sensitive to agents that target aberrant glutathione metabolism, an intrinsic property of primary human AML cells.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	47
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-11-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Anti-Inflammatory Agents, Non-Steroidal Pharmacology Dioxolanes Glutathione Metabolism Leukemia, Myeloid, Acute Drug Therapy Oxidative Stress Drug Effects Sesquiterpenes Antigens, CD34 Glutamate-Cysteine Ligase Antagonists & Inhibitors Glutathione Peroxidase Pathology Oxidation-Reduction Tumor Cells, Cultured Clinical Trial Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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