Source:http://linkedlifedata.com/resource/pubmed/id/16087702
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2006-1-18
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| pubmed:abstractText |
Gata-3 has been shown to specifically alter its expression patterns in different types of cancers. Recent evidence suggests that an interference of Gata-3 exists in the TGF-beta signaling pathway. To determine the role of Gata-3 in pancreatic cancer, pancreatic cancer samples were analyzed in comparison to normal pancreatic tissues. Furthermore, four different pancreatic cancer cell lines with different alterations of the TGF-beta pathway were studied. To evaluate if a potential relationship with TGF-beta signaling pathway exists, we correlated mRNA expression levels with the expression of TGF-betas, TGF-beta receptors, and Smad-3. Finally, we analyzed the influence of TGF-beta on Gata-3 expression in vitro. All pancreatic cancer samples demonstrated a marked overexpression of Gata-3 mRNA and protein. Immunohistochemical staining revealed strong and persistent cytoplasmic Gata-3 immunoreactivity in cancer cells. In an electrophoretic mobility shift assay, a disturbed nuclear translocation was confirmed. The expression of Gata-3 showed a significant correlation with the expression of TGF-betas, TGF-beta receptors, and Smad-3. TGF-beta responsive cell lines showed a downregulation of Gata-3 mRNA upon TGF-beta exposure, whereas in TGF-beta-unresponsive cell lines, Gata-3 mRNA expression persisted at high levels. Furthermore, strong specific upregulation of Gata-3 impaired nuclear translocation and its cooperative action with the TGF-beta pathway, suggesting that Gata-3 plays a central role in human pancreatic cancer.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0022-1554
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| pubmed:author |
pubmed-author:AutschbachFrankF,
pubmed-author:BüchlerMarkus WMW,
pubmed-author:BerberatPascal OPO,
pubmed-author:DambrauskasZilvinasZ,
pubmed-author:FriessHelmutH,
pubmed-author:GieseNathaliaN,
pubmed-author:GieseThomasT,
pubmed-author:GulbinasAntanasA,
pubmed-author:KleeffJoergJ,
pubmed-author:MeuerStefanS
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| pubmed:issnType |
Print
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| pubmed:volume |
54
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
161-9
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| pubmed:meshHeading |
pubmed-meshheading:16087702-Adult,
pubmed-meshheading:16087702-Aged,
pubmed-meshheading:16087702-Aged, 80 and over,
pubmed-meshheading:16087702-Cell Line, Tumor,
pubmed-meshheading:16087702-Cell Nucleus,
pubmed-meshheading:16087702-Cytoplasm,
pubmed-meshheading:16087702-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:16087702-Female,
pubmed-meshheading:16087702-GATA3 Transcription Factor,
pubmed-meshheading:16087702-Humans,
pubmed-meshheading:16087702-Immunohistochemistry,
pubmed-meshheading:16087702-Male,
pubmed-meshheading:16087702-Microscopy, Confocal,
pubmed-meshheading:16087702-Middle Aged,
pubmed-meshheading:16087702-Neoplasm Staging,
pubmed-meshheading:16087702-Pancreas,
pubmed-meshheading:16087702-Pancreatic Neoplasms,
pubmed-meshheading:16087702-Protein Transport,
pubmed-meshheading:16087702-RNA, Messenger,
pubmed-meshheading:16087702-Signal Transduction,
pubmed-meshheading:16087702-Transforming Growth Factor beta,
pubmed-meshheading:16087702-Up-Regulation
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| pubmed:year |
2006
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| pubmed:articleTitle |
Aberrant gata-3 expression in human pancreatic cancer.
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| pubmed:affiliation |
Department of General Surgery, University of Heidelberg, Im Neuenheimer Feld 110 69120, Heidelberg, Germany.
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| pubmed:publicationType |
Journal Article
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