Document Detail

Acetylcholinesterase expression mediated by c-Jun-NH2-terminal kinase pathway during anticancer drug-induced apoptosis.
MedLine Citation:
PMID:  16715131     Owner:  NLM     Status:  MEDLINE    
It has been shown that acetylcholinesterase (AChE) expression was induced during apoptosis and the anti-sense oligonucleotides and siRNA of AChE may prevent apoptosis in various cell types. However, the mechanisms underlying AChE upregulation remain elusive. We demonstrated here that c-Jun NH2-terminal kinase (JNK) could mediate AChE expression. In this study, both etoposide and excisanin A, two anticancer agents, induced apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP). The results showed that both the agents upregulated AChE in SW620 cells. In the meantime, JNK was also activated and the expression and phosphorylation of c-Jun increased in SW620 cells exposed to the two agents. The induced AChE mRNA and protein expression could be blocked by SP600125, a specific inhibitor of SAPK/JNK, and small interfering RNA directed against JNK1/2. Transfection with adenovirus-mediated dominant negative c-Jun also blocked the upregulation of AChE expression. Together, these results suggest that AChE expression may be mediated by the activation of JNK pathway during apoptosis through a c-Jun-dependent mechanism.
R Deng; W Li; Z Guan; J-M Zhou; Y Wang; Y-P Mei; M-T Li; G-K Feng; W Huang; Z-C Liu; Y Han; Y-X Zeng; X-F Zhu
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-22
Journal Detail:
Title:  Oncogene     Volume:  25     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-11-09     Completed Date:  2006-12-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  7070-7     Citation Subset:  IM    
State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-sen University, Guangzhou, China.
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MeSH Terms
Acetylcholinesterase / genetics,  metabolism*
Adenoviridae / genetics
Anthracenes / pharmacology
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects*
Caspase 3 / metabolism
Cell Line, Tumor
Cytoprotection / drug effects
Diterpenes / pharmacology*
Enzyme Activation / drug effects
Etoposide / pharmacology*
Gene Expression Regulation, Neoplastic
JNK Mitogen-Activated Protein Kinases / genetics,  metabolism*
Poly(ADP-ribose) Polymerases / metabolism
RNA, Small Interfering / genetics
Signal Transduction / drug effects*
Up-Regulation / drug effects
Reg. No./Substance:
0/Anthracenes; 0/Antineoplastic Agents; 0/Diterpenes; 0/RNA, Small Interfering; 0/anthra(1,9-cd)pyrazol-6(2H)-one; 33419-42-0/Etoposide; 78536-37-5/excisanin A; EC Polymerases; EC Mitogen-Activated Protein Kinases; EC; EC 3.4.22.-/Caspase 3

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

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