Linked Life Data

10327065

Source:http://linkedlifedata.com/resource/pubmed/id/10327065

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1999-5-26
pubmed:abstractText
The CD95 (Fas/APO-1) system regulates a number of physiological and pathological processes of cell death. The ligand for CD95 induces apoptosis in sensitive target cells by interacting with a transmembrane cell surface CD95 receptor. We previously reported that the recombinant adenovirus-mediated transfer of the wild-type p53 gene caused apoptotic cell death in a variety of human cancer cells. To better understand the mechanism responsible for this cell death signaling, we have investigated the potential involvement of the CD95 receptor/ligand system in p53-mediated apoptosis. The transient expression of the wild-type p53 gene upregulated the CD95 ligand mRNA as well as protein expression in H1299 human lung cancer cells deficient for p53 and in DLD-1 and SW620 human colon cancer cells with mutated p53, all of which constitutively expressed CD95 receptor as shown by a flow cytometric analysis, and induced rapid apoptotic cell death as early as 24 h after gene transfer. However, the sensitivity to the cytolytic effect of agonistic anti-CD95 antibody (CH11) varied among these cell lines: CH11 induced apoptosis in H1299 cells, but not in DLD-1 and SW620 cells despite their abundant CD95 receptor expression, suggesting that the CD95 receptors on DLD-1 and SW620 cells might be inactivated. In addition, an antagonistic anti-CD95 ligand antibody (4H9) that interfered with the CD95-receptor-ligand interaction partially reduced the apoptosis induced by the wild-type p53 gene transfer in H1299 cells, whereas apoptosis of DLD-1 and SW620 cells occurred in the presence of 4H9. Taken together, these findings led us to conclude that the CD95 receptor/ligand system is differentially involved in p53-mediated apoptosis, suggesting that the restoration of the wild-type p53 function may mediate apoptosis through CD95 receptor/ligand interactions as well as an alternative pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2189-99
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10327065-Adenocarcinoma, pubmed-meshheading:10327065-Adenoviruses, Human, pubmed-meshheading:10327065-Antibody-Dependent Cell Cytotoxicity, pubmed-meshheading:10327065-Antigens, CD95, pubmed-meshheading:10327065-Apoptosis, pubmed-meshheading:10327065-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:10327065-Colonic Neoplasms, pubmed-meshheading:10327065-Cytomegalovirus, pubmed-meshheading:10327065-Fas Ligand Protein, pubmed-meshheading:10327065-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10327065-Genes, p53, pubmed-meshheading:10327065-Genetic Vectors, pubmed-meshheading:10327065-Humans, pubmed-meshheading:10327065-Lung Neoplasms, pubmed-meshheading:10327065-Membrane Glycoproteins, pubmed-meshheading:10327065-Neoplasm Proteins, pubmed-meshheading:10327065-Promoter Regions, Genetic, pubmed-meshheading:10327065-RNA, Messenger, pubmed-meshheading:10327065-RNA, Neoplasm, pubmed-meshheading:10327065-Signal Transduction, pubmed-meshheading:10327065-Transfection, pubmed-meshheading:10327065-Tumor Cells, Cultured, pubmed-meshheading:10327065-Tumor Suppressor Protein p53
pubmed:year
1999
pubmed:articleTitle
Differential involvement of the CD95 (Fas/APO-1) receptor/ligand system on apoptosis induced by the wild-type p53 gene transfer in human cancer cells.
pubmed:affiliation
First Department of Surgery, Okayama University Medical School, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't