Document Detail


Induction of apoptosis by trichostatin A, a histone deacetylase inhibitor, is associated with inhibition of cyclooxygenase-2 activity in human non-small cell lung cancer cells.
MedLine Citation:
PMID:  16010430     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although histone deacetylase (HDAC) inhibitors are emerging as a promising new treatment strategy in malignancy, how they exert their effect on human non-small cell lung cancer cells is as yet unclear. This study was undertaken to investigate the underlying mechanism of an HDAC inhibitor, Trichostatin A (TSA), -induced apoptosis in a human lung carcinoma cell line A549. The effects of this compound were also tested on cyclooxygenase (COX) activity. Treatment of A549 cells to TSA resulted in the inhibition of viability and the induction of apoptosis in a concentration-dependent manner, which could be proved by trypan blue counts, DAPI staining, agarose gel electrophoresis and flow cytometry analysis. Apoptosis of A549 cells by TSA was associated with a down-regulation of anti-apoptotic Bcl-2 protein and an up-regulation of pro-apoptotic Bax protein. TSA treatment induced the proteolytic activation of caspase-3 and caspase-9, and a concomitant degradation of poly(ADP-ribose)-polymerase protein. Furthermore, TSA decreased the levels of COX-2 mRNA and protein expression without significant changes in the levels of COX-1, which was correlated with an inhibition in prostaglandin E2 synthesis. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of TSA.
Authors:
Yung Hyun Choi
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  27     ISSN:  1019-6439     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-12     Completed Date:  2005-12-23     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  473-9     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Dongeui University College of Oriental Medicine, Busan 614-052, South Korea. choiyh@deu.ac.kr
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Blotting, Western
Carcinoma, Non-Small-Cell Lung / enzymology,  pathology
Caspase 3
Caspase 9
Caspases / metabolism
Cell Line, Tumor
Cell Survival / drug effects
DNA Fragmentation / drug effects
Dinoprostone / metabolism
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology*
Flow Cytometry
Gene Expression Regulation, Enzymologic / drug effects
Histone Deacetylase Inhibitors*
Histone Deacetylases / metabolism
Humans
Hydroxamic Acids / pharmacology*
Lung Neoplasms / enzymology,  pathology
Poly(ADP-ribose) Polymerases / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Histone Deacetylase Inhibitors; 0/Hydroxamic Acids; 0/Proto-Oncogene Proteins c-bcl-2; 363-24-6/Dinoprostone; 58880-19-6/trichostatin A; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases; EC 3.5.1.98/Histone Deacetylases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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