Document Detail


Mechanism of Fas-mediated cell death and its enhancement by TNF-alpha in human salivary gland adenocarcinoma cell line HSG.
MedLine Citation:
PMID:  15279653     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fas-mediated cell death in a human salivary gland adenocarcinoma cell line (HSG) was induced by treatment of the cells with agonistic anti-Fas antibody (CH-11), and this cell death was enhanced by pretreatment with tumor necrosis factor alpha (TNF-alpha). The mode of cell death was apoptosis, because it was accompanied by caspase activation and the cleavage of poly(ADP-ribose) polymerase. The TNF-alpha treatment of the cells increased the expression of Fas, which was accompanied by the activation of nuclear factor kappaB (NFkappaB). These results suggest that the enhancement of the apoptosis caused by TNF-alpha resulted from increased sensitivity of the HSG cells to CH-11-mediated apoptosis due to induction of Fas protein by TNF-alpha via the activation of NFkappaB. In order to elucidate the apoptosis signaling pathway, we examined the effect of various caspase inhibitors on the apoptosis induced by CH-11. Fas-mediated apoptosis of HSG cells was slightly inhibited by the caspase-9 inhibitor although it was mainly inhibited by that for caspase-8. Based on this finding, we consider CH-11-induced apoptosis in HSG cells to be mainly mediated by the type I death signaling pathway that is caused by a caspase cascade initiated by the activation of caspase-8 at the death-inducing signaling complex (DISC).
Authors:
Naoyuki Chosa; Seiko Kyakumoto; Noriko Kito; Masaharu Kamo; Nobuko Sato
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of oral sciences     Volume:  112     ISSN:  0909-8836     ISO Abbreviation:  Eur. J. Oral Sci.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-28     Completed Date:  2004-10-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9504563     Medline TA:  Eur J Oral Sci     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  338-46     Citation Subset:  D; IM    
Affiliation:
Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate, Japan. nchose@iwate-med.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma
Antibodies / pharmacology
Antigens, CD95 / pharmacology*
Apoptosis / drug effects,  genetics,  physiology*
Blotting, Western
Caspases / antagonists & inhibitors,  metabolism
Cell Line, Tumor
Death Domain Receptor Signaling Adaptor Proteins
Humans
NF-kappa B / metabolism
Proteins / metabolism*
RNA, Messenger / analysis
Receptors, Tumor Necrosis Factor / metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Salivary Gland Neoplasms
Tumor Necrosis Factor-alpha / pharmacology
Up-Regulation
Chemical
Reg. No./Substance:
0/Antibodies; 0/Antigens, CD95; 0/CH-11 anti-fas antibody, human; 0/Death Domain Receptor Signaling Adaptor Proteins; 0/FAS protein, human; 0/NF-kappa B; 0/Proteins; 0/RNA, Messenger; 0/Receptors, Tumor Necrosis Factor; 0/Tumor Necrosis Factor-alpha; EC 3.4.22.-/Caspases

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