Document Detail


N,N-Dimethyl phytosphingosine sensitizes HL-60/MX2, a multidrug-resistant variant of HL-60 cells, to doxorubicin-induced cytotoxicity through ROS-mediated release of cytochrome c and AIF.
MedLine Citation:
PMID:  20512627     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Doxorubicin (Dox) is widely used to treat a variety of tumors. However, resistance to this drug is common, making successful treatment more difficult. Previously, we introduced a novel phytosphingosine derivative, N,N-dimethyl phytosphingosine (DMPS), as a potent anticancer therapeutic agent in human leukemia cells. This study was performed to investigate whether DMPS can sensitize HL-60/MX2, a multidrug-resistant variant of HL-60, to Dox-induced apoptosis. Low concentrations of DMPS sensitized HL-60/MX2 cells to Dox-induced apoptosis. Combined Dox + DMPS treatment-induced apoptosis was accompanied by the activation of caspase-8 and caspase-3 as well as PARP cleavage. Cytochrome c and AIF release were also observed in Dox + DMPS-treated HL60/MX2 cells. Pretreatment with z-VAD-fmk markedly prevented caspase-3 activation and moderately suppressed apoptosis, suggesting that Dox + DMPS-induced apoptosis is somewhat (not completely) dependent on caspase. Cytochrome c and AIF release were not affected by pretreatment with z-VAD-fmk. The ROS scavenger NAC efficiently suppressed not only ROS generation, but also caspase-3-mediated PARP cleavage, apoptosis, and release of cytochrome c and AIF, indicating a role of ROS in combined Dox + DMPS treatment-induced apoptotic death signaling. Taken together, these observations suggest that DMPS may be used as a therapeutic agent for overcoming drug-resistance in cancer cells by enhancing drug-induced apoptosis.
Authors:
Byeong Mo Kim; Yun Jung Choi; Yong Heon Lee; Young Ae Joe; Sung Hee Hong
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  15     ISSN:  1573-675X     ISO Abbreviation:  Apoptosis     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-15     Completed Date:  2010-10-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  982-93     Citation Subset:  IM    
Affiliation:
Korea Institute of Radiological and Medical Sciences, Nowon-Gu, Seoul, Republic of Korea.
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology
Amino Acid Chloromethyl Ketones / metabolism
Antibiotics, Antineoplastic / pharmacology
Antioxidants / pharmacology
Apoptosis Inducing Factor / metabolism*
Caspases / antagonists & inhibitors,  metabolism
Cell Survival
Cysteine Proteinase Inhibitors / metabolism
Cytochromes c / metabolism*
Doxorubicin / pharmacology*
Drug Resistance, Multiple / drug effects*
Enzyme Activation
Free Radical Scavengers / pharmacology
HL-60 Cells / drug effects*
Humans
Mitochondria / metabolism
Reactive Oxygen Species / metabolism*
Sphingosine / analogs & derivatives*,  pharmacology
Chemical
Reg. No./Substance:
0/Amino Acid Chloromethyl Ketones; 0/Antibiotics, Antineoplastic; 0/Antioxidants; 0/Apoptosis Inducing Factor; 0/Cysteine Proteinase Inhibitors; 0/Free Radical Scavengers; 0/Reactive Oxygen Species; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 123-78-4/Sphingosine; 23214-92-8/Doxorubicin; 554-62-1/phytosphingosine; 616-91-1/Acetylcysteine; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspases

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