Linked Life Data

15164982

Source:http://linkedlifedata.com/resource/pubmed/id/15164982

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-5-28
pubmed:abstractText
Interferon (IFN)-beta is known to exert cytostatic or cytocidal effects in human glioma cells and is widely used in the treatment for gliomas. However, precise mechanisms of cell death induced by IFN-beta are not well understood. In this study, the authors investigated the intracellular signal transduction of IFN-beta in human glioma cells. The cell death process observed in susceptible cells SK-MG-1 was accompanied by characteristic morphological changes of apoptosis, processing of caspases, and DNA fragmentation. Use of caspase inhibitors confirmed the activation of caspases, however activated executioner caspase was caspase-7 rather than caspases-3 or -6. Activation of DNA endonuclease, DNase-gamma was also observed. Observation of other IFN-beta relatively resistant glioma cells (U251SP, T98G, U251MG, U87MG, SK-AO2) revealed two different mechanisms of apoptosis resistance. In contrast to T98G, U87MG, and SK-AO2 which showed no activation of caspases, surprisingly, all the apoptosis process except DNase-gamma activation was observed in U251SP and U251MG cells. Collectively, these findings indicate that IFN-beta induced apoptosis in human glioma cells through activation of caspase-7 and activation of DNase-gamma. The similar activations of caspases were found also in some of the apoptosis resistant cells. These findings may help to improve the IFN-beta therapy in near future.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0167-594X
pubmed:author
pubmed:issnType
Print
pubmed:volume
67
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
273-80
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Two different mechanisms of apoptosis resistance observed in interferon-beta induced apoptosis of human glioma cells.
pubmed:affiliation
Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
pubmed:publicationType
Journal Article