Document Detail

The decrease of mitochondrial NADH dehydrogenease and drug induced apoptosis in doxorubicin resistant A431 cells.
MedLine Citation:
PMID:  10954045     Owner:  NLM     Status:  MEDLINE    
Doxorubicin (DOX) resistant A10A cells derived from human squamous carcinoma A431 cells were found to exhibit a smaller degree of apoptosis after DOX treatment as compared to their parent cells. Induction of reactive oxygen species (ROS) formation and mitochondrial depolarization by DOX were more pronounced in the parent cells than in the A10A cells. The fact that catalase suppressed the DOX effect on ROS induction, mitochondrial depolarization and apoptosis in both cell lines suggests an involvement of ROS in the DOX-induced apoptosis. To investigate the underlying mechanisms for DOX resistance in A10A cells, RT-PCR based differential display was used. One of the clones, which was down-regulated in the A10A cells, had sequence homology with part of the mitochondrial NADH dehydrogenase III (ND3) gene. NADH dehydrogenase plays an important role in generating ROS during DOX treatment. The results indicate that down-regulation of ND3 may at least in part contribute to the mechanism for A10A cells resistant to DOX-induced apoptosis.
T W Wong; H Y Yu; S K Kong; K P Fung; T T Kwok
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Life sciences     Volume:  67     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2000  
Date Detail:
Created Date:  2000-09-06     Completed Date:  2000-09-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1111-8     Citation Subset:  IM    
Department of Biochemistry, The Chinese University of Hong Kong, Shatin.
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MeSH Terms
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects*,  physiology
Carcinoma, Squamous Cell / drug therapy,  enzymology*,  pathology
Catalase / metabolism
DNA Probes
DNA, Complementary / genetics
Dose-Response Relationship, Drug
Doxorubicin / pharmacology*
Drug Resistance, Neoplasm
Gene Expression Profiling
Isoenzymes / biosynthesis,  genetics,  metabolism
Mitochondria / drug effects,  enzymology*
NADH Dehydrogenase / biosynthesis,  genetics,  metabolism*
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Reg. No./Substance:
0/Antineoplastic Agents; 0/DNA Probes; 0/DNA, Complementary; 0/Isoenzymes; 0/Reactive Oxygen Species; 23214-92-8/Doxorubicin; EC; EC Dehydrogenase

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