Document Detail


Involvement of ERK, Bcl-2 family and caspase 3 in recombinant human activin A-induced apoptosis in A549.
MedLine Citation:
PMID:  19428937     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Activins are members of the transforming growth factor-beta (TGF-beta) superfamily. Previous studies have shown that activin A may have a central role in regulating both apoptosis and proliferation. However, direct studies of recombination human activin A on human NSCLC A549 cells have not yet been reported. The purpose of this study was to investigate whether activin A could induce apoptosis in A549 cells and the possible mechanisms via which it worked. METHODS: Cellular apoptosis induced by activin A was detected by TUNEL assay and the levels of protein expression were detected by western blot. RESULTS: Recombination human activin A induced apoptosis in human NSCLC A549 cells in a concentrate-dependent manner. Activin A-induced A549 apoptosis was accompanied by the up-regulation of Bax, Bad and Bcl-Xs and down-regulation of Bcl-2. Moreover, activin A treatment increased the expression of its typeII receptors, activated ERK and caspase 3 in A549. These results clearly demonstrate that the induction of apoptosis by activin-A involves multiple cellular/molecular pathways and strongly suggest that pro- and anti-apoptotic Bcl-2 family proteins and caspase 3 participate in activin A-induced apoptotic process in A549 cells. On the other hand, activin A treatment had little effect on primary human small airway epithelial cells (SAECs). CONCLUSION: Recombination human activin A induced apoptosis in A549 cells, at least partially, through ERK and mitochondrial pathway. The result that activin A did not affect the normal SAEC revealed activin A might be considered as a potential anticancer agent and worthy of further studies.
Authors:
Baiding Wang; Yuling Feng; Xingbo Song; Qingqing Liu; Yunye Ning; Xuemei Ou; Jie Yang; Xiaohong Zhang; Fuqiang Wen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-02-04
Journal Detail:
Title:  Toxicology     Volume:  258     ISSN:  0300-483X     ISO Abbreviation:  Toxicology     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-05-11     Completed Date:  2009-06-01     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0361055     Medline TA:  Toxicology     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  176-83     Citation Subset:  IM    
Affiliation:
Division of Pulmonary Disease, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Activins / genetics,  pharmacology*
Apoptosis / drug effects*
Blotting, Western
Carcinoma, Non-Small-Cell Lung / genetics,  metabolism
Caspase 3 / metabolism
Cell Line, Tumor
Dose-Response Relationship, Drug
Extracellular Signal-Regulated MAP Kinases / genetics,  metabolism
Humans
In Situ Nick-End Labeling
Lung Neoplasms / genetics,  metabolism
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Recombinant Proteins / pharmacology
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-bcl-2; 0/Recombinant Proteins; 0/activin A; 104625-48-1/Activins; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.-/Caspase 3

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


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