Document Detail


Caspase-3 mediated feedback activation of apical caspases in doxorubicin and TNF-alpha induced apoptosis.
MedLine Citation:
PMID:  17013758     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aberrant apoptosis has been associated with the development and therapeutic resistance of cancer. Recent studies suggest that caspase deficiency/downregulation is frequently detected in different cancers. We have previously shown that caspase-3 reconstitution significantly sensitized MCF-7 cells to doxorubicin and etoposide. In contrast to the well established role of caspase-3 as an effector caspase, the focus of this study is to delineate caspase-3 induced feedback activation of the apical caspases-2, -8, -9 and -10A in doxorubicin and TNF-alpha induced apoptosis. Using cell-free systems we show that caspases-9 and 2 are the most sensitive, caspase-8 is less sensitive and caspase-10A is the least sensitive to caspase-3 mediated-cleavage. When apoptosis is induced by doxorubicin or TNF-alpha in an intact cell model, cleavage of caspases-8 and -9, but not caspase-2, was markedly enhanced by caspase-3. Caspase-3 mediated-feedback and activation of caspase-8 and -9 in MCF-7/C3 cells is further supported by an increase in the cleavage of caspase-8 and 9 substrates and cytochrome c release. These data indicate that, in addition to its function as an effector caspase, caspase-3 plays an important role in maximizing the activation of apical caspases and crosstalk between the two major apoptotic pathways. The significant impact of caspase-3 on both effector and apical caspases suggests that modulation of caspase-3 activity would be a useful approach to overcome drug resistance in clinical oncology.
Authors:
Shihe Yang; Ann D Thor; Susan Edgerton; XiaoHe Yang
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  11     ISSN:  1360-8185     ISO Abbreviation:  Apoptosis     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-11-06     Completed Date:  2007-09-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1987-97     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
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MeSH Terms
Descriptor/Qualifier:
Antibiotics, Antineoplastic / pharmacology*
Apoptosis*
Caspase 10 / metabolism
Caspase 2 / metabolism
Caspase 3 / metabolism*
Caspase 8 / metabolism
Caspase 9 / metabolism
Cell Line, Tumor
Cysteine Endopeptidases / metabolism
Cytosol / enzymology
Doxorubicin / pharmacology*
Humans
Tumor Necrosis Factor-alpha / metabolism
Chemical
Reg. No./Substance:
0/Antibiotics, Antineoplastic; 0/CASP10 protein, human; 0/Tumor Necrosis Factor-alpha; 23214-92-8/Doxorubicin; EC 3.4.22.-/CASP2 protein, human; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Caspase 10; EC 3.4.22.-/Caspase 2; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Cysteine Endopeptidases

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


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