Linked Life Data

11719464

Source:http://linkedlifedata.com/resource/pubmed/id/11719464

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
2001-11-23
pubmed:abstractText
Transforming growth factor (TGF)-beta is growth inhibitory for normal epithelial cells and melanocytes but can stimulate mesenchymal cells. Resistance to its inhibitory effects is characteristic of human melanoma, the growth of which may instead be promoted by TGF-beta, because its production is increased with melanoma progression. Whether TGF-beta has an autocrine function for melanoma cells or is important for paracrine stimulation of the tumor stroma is not known. In this study, TGF-beta1 was expressed in melanoma cells via adenoviral gene transfer, and tumor growth was analyzed in vitro, in human skin grafts, and in mixtures with fibroblasts that were injected s.c. into immunodeficient mice. The TGF-beta1 produced by the melanoma cells activated the fibroblasts to produce matrix within and around the tumor mass, whereas control tumors showed less stroma and more cell death. High expression of collagen, fibronectin, tenascin, and alpha2 integrin was detected in the TGF-beta1-expressing tumors by immunohistochemistry. Number and size of lung metastases were significantly increased. cDNA expression array analysis of TGF-beta1-transduced fibroblasts embedded in type I collagen and of TGF-beta1-transduced melanoma cells demonstrated induction of types XV, XVIII, and VI collagens, tenascin, plasminogen activator inhibitor-I, vascular endothelial growth factor, cysteine-rich fibroblast growth factor receptor-1, and platelet-derived growth factor receptor-beta, which could be linked to promotion of growth and survival in melanoma. These data suggest that remodeling of the neighboring stroma, which provides a supporting scaffolding and a positive feedback stimulation of tumor growth, is an important function of TGF-beta1 in melanoma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8306-16
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11719464-Animals, pubmed-meshheading:11719464-Cell Communication, pubmed-meshheading:11719464-Cell Death, pubmed-meshheading:11719464-Cell Survival, pubmed-meshheading:11719464-Extracellular Matrix Proteins, pubmed-meshheading:11719464-Female, pubmed-meshheading:11719464-Fibroblasts, pubmed-meshheading:11719464-Gene Expression, pubmed-meshheading:11719464-Gene Expression Profiling, pubmed-meshheading:11719464-Humans, pubmed-meshheading:11719464-Immunohistochemistry, pubmed-meshheading:11719464-Male, pubmed-meshheading:11719464-Melanoma, pubmed-meshheading:11719464-Mice, pubmed-meshheading:11719464-Mice, SCID, pubmed-meshheading:11719464-Stromal Cells, pubmed-meshheading:11719464-Transduction, Genetic, pubmed-meshheading:11719464-Transforming Growth Factor beta, pubmed-meshheading:11719464-Transforming Growth Factor beta1
pubmed:year
2001
pubmed:articleTitle
Transforming growth factor-beta1 increases survival of human melanoma through stroma remodeling.
pubmed:affiliation
The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't