pubmed-article:11149423 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C1458155 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C0027627 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C2699153 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C1269955 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:11149423 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:11149423 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11149423 | pubmed:dateCreated | 2001-1-8 | lld:pubmed |
pubmed-article:11149423 | pubmed:abstractText | Several studies have correlated escape from TGF-beta-mediated cell cycle arrest with the tumorigenic phenotype. Most often, this escape from growth control has been linked to dysfunctional TGF-beta receptors or defects in the TGF-beta-mediated SMAD signaling pathway. In this report, we found that highly metastatic 4T1 mammary carcinoma cells express functional TGF-beta receptors capable of initiating SMAD-mediated transcription, yet are not growth inhibited by TGF-beta1. We further observed that TGF-beta directly contributes to the metastatic behavior of this cell line. Exposure to TGF-beta caused 4T1 cells to undergo morphological changes associated with the metastatic phenotype and invade more readily through collagen coated matrices. Furthermore, expression of a dominant negative truncated type II receptor diminished TGF-beta signaling and significantly restricted the ability of 4T1 cells to establish distant metastases. Our results suggest that regardless of 4T1 resistance to TGF-beta-mediated growth inhibition, TGF-beta signaling is required for tumor invasion and metastases formation. | lld:pubmed |
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pubmed-article:11149423 | pubmed:language | eng | lld:pubmed |
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pubmed-article:11149423 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11149423 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11149423 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11149423 | pubmed:issn | 0020-7136 | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:WuR SRS | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:HendrixM JMJ | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:DumontNN | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:ArteagaC LCL | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:AkporiayeE... | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:KatsanisEE | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:MachSS | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:SeftorEE | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:BesselsenDD | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:Meade-TollinL... | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:McEarchernJ... | lld:pubmed |
pubmed-article:11149423 | pubmed:author | pubmed-author:KobieJ JJJ | lld:pubmed |
pubmed-article:11149423 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11149423 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11149423 | pubmed:volume | 91 | lld:pubmed |
pubmed-article:11149423 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11149423 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11149423 | pubmed:pagination | 76-82 | lld:pubmed |
pubmed-article:11149423 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11149423 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11149423 | pubmed:articleTitle | Invasion and metastasis of a mammary tumor involves TGF-beta signaling. | lld:pubmed |
pubmed-article:11149423 | pubmed:affiliation | Department of Microbiology and Immunology, University of Arizona, Tucson 85724, USA. | lld:pubmed |
pubmed-article:11149423 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11149423 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11149423 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:11149423 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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