Document Detail


Hypoxia induces p53-dependent transactivation and Fas/CD95-dependent apoptosis.
MedLine Citation:
PMID:  16917513     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
p53 triggers apoptosis in response to cellular stress. We analyzed p53-dependent gene and protein expression in response to hypoxia using wild-type p53-carrying or p53 null HCT116 colon carcinoma cells. Hypoxia induced p53 protein levels and p53-dependent apoptosis in these cells. cDNA microarray analysis revealed that only a limited number of genes were regulated by p53 upon hypoxia. Most classical p53 target genes were not upregulated. However, we found that Fas/CD95 was significantly induced in response to hypoxia in a p53-dependent manner, along with several novel p53 target genes including ANXA1, DDIT3/GADD153 (CHOP), SEL1L and SMURF1. Disruption of Fas/CD95 signalling using anti-Fas-blocking antibody or a caspase 8 inhibitor abrogated p53-induced apoptosis in response to hypoxia. We conclude that hypoxia triggers a p53-dependent gene expression pattern distinct from that induced by other stress agents and that Fas/CD95 is a critical regulator of p53-dependent apoptosis upon hypoxia.
Authors:
T Liu; C Laurell; G Selivanova; J Lundeberg; P Nilsson; K G Wiman
Related Documents :
12138103 - Transcriptional regulation during p21waf1/cip1-induced apoptosis in human ovarian cance...
11485313 - Transcriptional activity of the promoter region of rat frizzled-related protein gene.
22303253 - Flower development.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-18
Journal Detail:
Title:  Cell death and differentiation     Volume:  14     ISSN:  1350-9047     ISO Abbreviation:  Cell Death Differ.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-02-15     Completed Date:  2007-06-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9437445     Medline TA:  Cell Death Differ     Country:  England    
Other Details:
Languages:  eng     Pagination:  411-21     Citation Subset:  IM    
Affiliation:
Department of Oncology-Pathology, Cancer Center Karolinska, Karolinska Institute, Stockholm, Sweden.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Antigens, CD95 / metabolism*,  physiology
Apoptosis*
Base Sequence
Binding Sites
Blotting, Northern
Blotting, Western
Cell Hypoxia*
Cell Line, Tumor
Humans
Molecular Sequence Data
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Transcription, Genetic
Transcriptional Activation*
Transfection
Tumor Suppressor Protein p53 / metabolism*,  physiology
Chemical
Reg. No./Substance:
0/Antigens, CD95; 0/Tumor Suppressor Protein p53

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


Previous Document:  MALT1 gene rearrangements and NF-kappaB activation involving p65 and p50 are absent or rare in prima...
Next Document:  Role of glutathione in the growth of Bradyrhizobium sp. (peanut microsymbiont) under different envir...