Document Detail


Plumbagin treatment leads to apoptosis in human K562 leukemia cells through increased ROS and elevated TRAIL receptor expression.
MedLine Citation:
PMID:  21741707     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study examined the ability of plumbagin to induce apoptosis in chronic myelogenous leukemia (CML). Plumbagin exposure led to a significant reduction in cell viability and the induction of apoptosis. Mechanistically, plumbagin treatment led to elevated levels of ROS. Plumbagin-induced apoptosis was inhibited by N-acetyl L-cysteine (NAC) and PEG-catalase. Furthermore, plumbagin exposure led to elevated expression of DR4 and DR5 and increased killing through soluble TRAIL. The plumbagin-induced increase in DR4 and DR5 was inhibited by treatment with NAC. Together, this study suggests that plumbagin may be an effective treatment of CML through increased sensitivity to TRAIL-mediated killing.
Authors:
Jingping Sun; Robert J McKallip
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Publication Detail:
Type:  Journal Article     Date:  2011-07-08
Journal Detail:
Title:  Leukemia research     Volume:  35     ISSN:  1873-5835     ISO Abbreviation:  Leuk. Res.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-08-29     Completed Date:  2011-11-23     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  7706787     Medline TA:  Leuk Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  1402-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
Affiliation:
Division of Basic Medical Sciences, Mercer University School of Medicine, 1550 College St., Macon, GA 31207, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology
Apoptosis / drug effects*
Blotting, Western
Catalase / metabolism,  pharmacology
Cell Survival / drug effects
Flow Cytometry
Gene Expression / drug effects*
Humans
In Situ Nick-End Labeling
K562 Cells
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy,  metabolism*,  pathology
Naphthoquinones* / pharmacology
Oxidation-Reduction / drug effects
Oxidative Stress / drug effects
Polyethylene Glycols / metabolism,  pharmacology
Reactive Oxygen Species / metabolism
Receptors, TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors,  genetics,  metabolism*
Signal Transduction / drug effects*
Grant Support
ID/Acronym/Agency:
K22 CA109334-01A2/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Naphthoquinones; 0/Polyethylene Glycols; 0/Reactive Oxygen Species; 0/Receptors, TNF-Related Apoptosis-Inducing Ligand; 0/TNFRSF10A protein, human; 0/catalase-polyethylene glycol; 616-91-1/Acetylcysteine; EC 1.11.1.6/Catalase; YAS4TBQ4OQ/plumbagin
Comments/Corrections

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