|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
1
|
|
pubmed:dateCreated |
2001-1-8
|
|
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.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jan
|
|
pubmed:issn |
0020-7136
|
|
pubmed:author |
pubmed-author:AkporiayeE TET,
pubmed-author:ArteagaC LCL,
pubmed-author:BesselsenDD,
pubmed-author:DumontNN,
pubmed-author:HendrixM JMJ,
pubmed-author:KatsanisEE,
pubmed-author:KobieJ JJJ,
pubmed-author:MachSS,
pubmed-author:McEarchernJ AJA,
pubmed-author:Meade-TollinLL,
pubmed-author:SeftorEE,
pubmed-author:WuR SRS
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
91
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
76-82
|
|
pubmed:dateRevised |
2007-11-14
|
|
pubmed:meshHeading |
pubmed-meshheading:11149423-Animals,
pubmed-meshheading:11149423-Blotting, Northern,
pubmed-meshheading:11149423-Blotting, Western,
pubmed-meshheading:11149423-Cell Cycle,
pubmed-meshheading:11149423-Cell Division,
pubmed-meshheading:11149423-Cell Movement,
pubmed-meshheading:11149423-Collagen,
pubmed-meshheading:11149423-Cross-Linking Reagents,
pubmed-meshheading:11149423-DNA-Binding Proteins,
pubmed-meshheading:11149423-Dose-Response Relationship, Drug,
pubmed-meshheading:11149423-Female,
pubmed-meshheading:11149423-Flow Cytometry,
pubmed-meshheading:11149423-Genes, Dominant,
pubmed-meshheading:11149423-Mammary Neoplasms, Animal,
pubmed-meshheading:11149423-Mice,
pubmed-meshheading:11149423-Mice, SCID,
pubmed-meshheading:11149423-Microscopy, Confocal,
pubmed-meshheading:11149423-Neoplasm Invasiveness,
pubmed-meshheading:11149423-Phenotype,
pubmed-meshheading:11149423-Plasmids,
pubmed-meshheading:11149423-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:11149423-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11149423-Signal Transduction,
pubmed-meshheading:11149423-Transcription, Genetic,
pubmed-meshheading:11149423-Transforming Growth Factor beta,
pubmed-meshheading:11149423-Transforming Growth Factor beta1,
pubmed-meshheading:11149423-Tumor Cells, Cultured
|
|
pubmed:year |
2001
|
|
pubmed:articleTitle |
Invasion and metastasis of a mammary tumor involves TGF-beta signaling.
|
|
pubmed:affiliation |
Department of Microbiology and Immunology, University of Arizona, Tucson 85724, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|
