Linked Life Data

15806297

Source:http://linkedlifedata.com/resource/pubmed/id/15806297

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-4-4
pubmed:abstractText
Malignant gliomas represent the most aggressive tumours of the central nervous system and are characterised by both extensive proliferation and invasive growth. Matrix degrading proteases called matrix metalloproteinases (MMPs), particularly MMP-9, play a crucial role in glioma infiltration. The activity of these enzymes is regulated at different levels. In this regard, the control of transcriptional activity by specific transcription factors is believed to be very important. In the present study, we examined whether rat C6 glioma cells express the Ets 1 transcription factor and whether inhibition of Ets 1 by a specific decoy strategy affects C6 glioma cell proliferation and mmp-9 expression. We found that C6 glioma cells express Ets 1 and can efficiently be transfected with an Ets 1-specific decoy oligodesoxynucleotide (ODN). This ODN significantly reduces cell proliferation and mmp-9 expression, the latter in a dose-dependent manner. We conclude that inhibition of transcription factors, which play a role for glioma development and progression such as Ets 1 by specific decoy approaches, might represent useful tools for experimental therapeutic strategies against malignant gliomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1107-3756
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
771-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Inactivation of Ets 1 transcription factor by a specific decoy strategy reduces rat C6 glioma cell proliferation and mmp-9 expression.
pubmed:affiliation
Institute of Pathology, University of Bonn, 53011 Bonn, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't