Document Detail


STAT-1-independent upregulation of FADD and procaspase-3 and -8 in cancer cells treated with cytotoxic drugs.
MedLine Citation:
PMID:  10080945     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously shown that treatment by anticancer drugs sensitized tumor cells to Fas (APO-1/CD95)-mediated cell death. The present study demonstrates that the cytotoxic drugs cisplatin, doxorubicin and mitomycin C induce the accumulation of the Fas receptor, the FADD adaptor molecule, the procaspases-8, -3 and -2L and the proapoptotic molecule Bax in several human colon cancer cells. This upregulation is also observed in U3A myeloblastoma cells that do not express STAT-1, a transcription factor involved in the constitutive expression of procaspases. We conclude that anticancer drugs sensitize tumor cells to Fas-mediated cell death by a STAT-1-independent upregulation of molecules involved in this apoptotic pathway.
Authors:
O Micheau; A Hammann; E Solary; M T Dimanche-Boitrel
Related Documents :
10404075 - Expression of fas ligand in human hepatoma cell lines: role of hepatitis-b virus x (hbx...
12953805 - Recent advances in understanding the pathogenesis of anemia in multiple myeloma.
7692265 - Hypersensitivity to oxygen is a uniform and secondary defect in fanconi anemia cells.
16611765 - Diffusion tensor imaging of tract involvement in children with pontine tumors.
6407845 - Treatment of metastatic lewis lung carcinoma with dl-alpha-difluoromethylornithine.
1424185 - Expression of the neuroendocrine cell marker 7b2 in human acth secreting tumours.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  256     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  1999 Mar 
Date Detail:
Created Date:  1999-04-19     Completed Date:  1999-04-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  603-7     Citation Subset:  IM    
Copyright Information:
Copyright 1999 Academic Press.
Affiliation:
Department of Biology and Therapy of Cancer (JE 515), Faculty of Medicine and Pharmacy, 7 boulevard Jeanne d'Arc, Dijon Cédex, 21033, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing*
Antigens, CD95
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects
Carrier Proteins / genetics,  metabolism*
Caspase 2
Caspase 3
Caspase 8
Caspase 9
Caspases / metabolism*
Cisplatin / pharmacology
Colonic Neoplasms / drug therapy,  enzymology,  genetics,  metabolism*
DNA-Binding Proteins / genetics,  physiology*
Dactinomycin / pharmacology
Doxorubicin / pharmacology
Enzyme Precursors / metabolism*
Fas-Associated Death Domain Protein
Gene Expression Regulation, Neoplastic / drug effects
Humans
Isoenzymes / metabolism
Mitomycin / pharmacology
Poly(ADP-ribose) Polymerases / metabolism
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-bcl-2*
RNA, Messenger / metabolism
Receptors, Tumor Necrosis Factor / physiology
STAT1 Transcription Factor
Trans-Activators / genetics,  physiology*
Transcription, Genetic
Tumor Cells, Cultured
Up-Regulation / drug effects*
bcl-2-Associated X Protein
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Antigens, CD95; 0/Antineoplastic Agents; 0/BAX protein, human; 0/Carrier Proteins; 0/DNA-Binding Proteins; 0/Enzyme Precursors; 0/FADD protein, human; 0/Fas-Associated Death Domain Protein; 0/Isoenzymes; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/RNA, Messenger; 0/Receptors, Tumor Necrosis Factor; 0/STAT1 Transcription Factor; 0/STAT1 protein, human; 0/Trans-Activators; 0/bcl-2-Associated X Protein; 15663-27-1/Cisplatin; 23214-92-8/Doxorubicin; 50-07-7/Mitomycin; 50-76-0/Dactinomycin; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; 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 2; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases

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


Previous Document:  A role for leptin in brain development.
Next Document:  The immediate early gene products of human cytomegalovirus increase vascular smooth muscle cell migr...