| pubmed-article:12140283 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0030297 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0053574 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0694891 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:12140283 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12140283 | pubmed:issue | 39 | lld:pubmed |
| pubmed-article:12140283 | pubmed:dateCreated | 2002-9-23 | lld:pubmed |
| pubmed-article:12140283 | pubmed:abstractText | Overexpression of the small leucine-rich proteoglycan biglycan (BGN) in fibrosis and desmoplasia results from enhanced activity of transforming growth factor-beta (TGF-beta). In pancreatic adenocarcinoma, the tumor cells themselves may contribute to BGN synthesis in vivo, since 8 of 18 different pancreatic carcinoma cell lines constitutively expressed BGN mRNA, as shown by reverse transcription-PCR analysis. In PANC-1 cells, TGF-beta1 dramatically stimulated BGN mRNA accumulation through a BGN transcription-independent, cycloheximide-sensitive mechanism and strongly increased the synthesis and release of the proteoglycan form of BGN. The ability of TGF-beta1 to induce BGN mRNA was critically dependent on Smad signaling, since 1) the up-regulation of BGN mRNA was preceded by a marked increase in Smad2 phosphorylation in TGF-beta1-treated PANC-1 cells, 2) TGF-beta1 was unable to induce BGN mRNA in pancreatic carcinoma cell lines that carry homozygous deletions of the Smad4/DPC4 gene, 3) inhibition of the Smad pathway in PANC-1 cells by transfection with a dominant negative Smad4/DPC4 mutant significantly reduced TGF-beta1-induced BGN mRNA expression, 4) stable reintroduction of wild type Smad4/DPC4 into Smad4-null CFPAC-1 cells restored the TGF-beta1 effect, and 5) overexpression of Smad2 and Smad3 in PANC-1 cells augmented TGF-beta1 induction of BGN mRNA, whereas forced expression of Smad7, an inhibitory Smad, effectively blocked it. These results clearly show that a functional Smad pathway is crucial for TGF-beta regulation of BGN mRNA expression. Since BGN has been shown to inhibit growth of pancreatic cancer cells, the Smad4/DPC4 mediation of the TGF-beta effect may represent a novel tumor suppressor function for Smad4/DPC4: antiproliferation via expression of autoinhibitory BGN. | lld:pubmed |
| pubmed-article:12140283 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12140283 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12140283 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12140283 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12140283 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:FischerJens... | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:KalthoffHolge... | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:ChenWen-BinWB | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:LenschowWolfg... | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:TiedeKarenK | lld:pubmed |
| pubmed-article:12140283 | pubmed:author | pubmed-author:UngefrorenHen... | lld:pubmed |
| pubmed-article:12140283 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12140283 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:12140283 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:12140283 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12140283 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12140283 | pubmed:pagination | 36118-28 | lld:pubmed |
| pubmed-article:12140283 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:12140283 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12140283 | pubmed:articleTitle | Smad4/DPC4-dependent regulation of biglycan gene expression by transforming growth factor-beta in pancreatic tumor cells. | lld:pubmed |
| pubmed-article:12140283 | pubmed:affiliation | Research Unit Molecular Oncology, Clinic for General Surgery and Thoracic Surgery, Christian-Albrechts-University, D-24105 Kiel, Germany. | lld:pubmed |
| pubmed-article:12140283 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12140283 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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