Linked Life Data

11330838

Source:http://linkedlifedata.com/resource/pubmed/id/11330838

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2001-5-1
pubmed:abstractText
The CRE (cyclic AMP response element)-transcription factor complex plays a critical role in response to hormonal signals for cell proliferation, differentiation, and apoptosis. We have reported previously that the CRE-transcription factor decoy oligonucleotide specifically slows tumor cell proliferation and inhibits CRE- and Ap-1-directed transcription in vivo (Park et al., 1999). We have investigated the effect of inhibiting CRE-directed transcription on ovarian cancer cell growth. Here, we report that CRE-decoy oligonucleotide treatment results in the inhibition of cell growth and a marked reduction in the expression of the regulatory and catalytic subunits of protein kinase A and the type I and type II protein kinase A holoenzymes. Growth inhibition was accompanied by changes in cell morphology, appearance of apoptotic nuclei, and DNA fragmentation. In addition, MMP-9 (matrix methalloproteinase-9) activity was markedly reduced in CRE-decoy treated cells. Indirect immunofluorescence revealed that CRE-decoy oligonucleotide treatment promoted export of the CRE-binding protein, CREB, from the nucleus to the cytoplasm, while importing the catalytic subunit of protein kinase A from the cytoplasm to the nucleus. The results indicate that the decoy oligonucleotide, by binding specifically to CRE-transcription factors, interferes with CRE-directed transcription in vivo. These results show a critical role for CRE-directed transcription in ovarian cancer cell growth. Thus, the CRE-decoy oligonucleotide may provide a powerful means to combat ovarian cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
218
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
55-63
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11330838-Apoptosis, pubmed-meshheading:11330838-Blotting, Western, pubmed-meshheading:11330838-Cell Division, pubmed-meshheading:11330838-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:11330838-Cyclic AMP-Dependent Protein Kinase Type II, pubmed-meshheading:11330838-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:11330838-Dose-Response Relationship, Drug, pubmed-meshheading:11330838-Down-Regulation, pubmed-meshheading:11330838-Female, pubmed-meshheading:11330838-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11330838-Humans, pubmed-meshheading:11330838-Immunohistochemistry, pubmed-meshheading:11330838-Isoenzymes, pubmed-meshheading:11330838-Matrix Metalloproteinase 2, pubmed-meshheading:11330838-Matrix Metalloproteinase 9, pubmed-meshheading:11330838-Ovarian Neoplasms, pubmed-meshheading:11330838-Transcription Factor AP-1, pubmed-meshheading:11330838-Tumor Cells, Cultured
pubmed:year
2001
pubmed:articleTitle
Apoptosis, growth arrest and suppression of invasiveness by CRE-decoy oligonucleotide in ovarian cancer cells: protein kinase A downregulation and cytoplasmic export of CRE-binding proteins.
pubmed:affiliation
Cellular Biochemistry Section, Experimental Oncology Section, Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, MD 20892-1750, USA.
pubmed:publicationType
Journal Article, Comparative Study