Linked Life Data

15254403

Source:http://linkedlifedata.com/resource/pubmed/id/15254403

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-10-19
pubmed:abstractText
Recent findings showed that type I interferons (IFN-alpha/beta) induce the transcription of tumor suppressor p53 and sensitize primary mouse embryonic fibroblasts (MEFs) to p53-mediated apoptosis by oncolytic viruses. However, the ability of RNA viruses to induce a p53-mediated apoptotic response may differ between primary and tumor cells and may be dependent upon the virus type. We have investigated this hypothesis by analyzing the apoptotic effects of various oncolytic viruses on the human colon carcinoma HCT116 cells and their derivatives lacking either p53 or bax gene. We show that HCT116 cells are resistant to the apoptotic effects of vesicular stomatitis virus, reovirus or poliovirus but activate the p53/Bax apoptotic pathway after infection with Sendai virus. These data substantiate the role of p53 in virus-mediated apoptosis and show that, unlike primary cells, tumor cells may be more selective in the activation of p53 pathway in response to the infection with specific types of viruses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1043-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Induction of p53-dependent apoptosis in HCT116 tumor cells by RNA viruses and possible implications in virus-mediated oncolysis.
pubmed:affiliation
Lady Davis Institute for Medical Research, McGill University, Jewish General Hospital, Montreal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't