Linked Life Data

8647631

Source:http://linkedlifedata.com/resource/pubmed/id/8647631

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-7-22
pubmed:abstractText
Numerous established human tumor lines co-express platelet-derived growth factor (PDGF) and cognate receptors, suggesting that an autocrine and/or paracrine growth mechanism may be a causal or contributing mechanism to their transformed phenotype. Indeed, it is known that a PDGF-autocrine system is functional in several established tumor lines, especially in human gliomas, and a model for a functional paracrine mechanism has been established in a human melanoma line. However, at least 168 human cell lines representing 26 different human tumor types have been reported to continuously express PDGF-A and/or -B chains, and 55 of these also express PDGF receptors. For the majority of these cases, the significance of co-expression and the relative roles of autocrine and paracrine mechanisms in transformation remains unclear. Here, we show that human glioblastoma T98G cells co-express PDGF-B/c-sis and moderate levels of the cognate beta-type PDGF receptor (PR-beta) but are not tumorigenic in athymic mice. In contrast, human breast carcinoma MCF-7 cells do not express PR-beta and are tumorigenic. Clonal lines of each cell type with greatly increased secretion of p16w(T98Gsis and MCF-7sis cells) were characterized. T98Gsis cells are 85% tumorigenic and occasionally develop pulmonary metastases, showing that endogenous PR-beta can mediate complete transformation upon sufficient stimulation. In contrast, MCF-7sis cells exhibit some growth slowing in vitro and an exactly proportional decrease in tumor growth rate. We conclude that a PDGF-autocrine, and not a paracrine, mechanism best accounts for the acquired tumorigenicity of T98Gsis cells, thereby emphasizing the potential significance of expression of even moderate levels of PR-beta by human tumor cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
669-77
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:8647631-Animals, pubmed-meshheading:8647631-Antibodies, Neoplasm, pubmed-meshheading:8647631-Antibody Specificity, pubmed-meshheading:8647631-Breast Neoplasms, pubmed-meshheading:8647631-Cell Division, pubmed-meshheading:8647631-Cell Transformation, Neoplastic, pubmed-meshheading:8647631-Female, pubmed-meshheading:8647631-Glioblastoma, pubmed-meshheading:8647631-Humans, pubmed-meshheading:8647631-Mice, pubmed-meshheading:8647631-Mice, Inbred BALB C, pubmed-meshheading:8647631-Mice, Nude, pubmed-meshheading:8647631-Phenotype, pubmed-meshheading:8647631-Platelet-Derived Growth Factor, pubmed-meshheading:8647631-Precipitin Tests, pubmed-meshheading:8647631-Proto-Oncogene Proteins, pubmed-meshheading:8647631-Proto-Oncogene Proteins c-sis, pubmed-meshheading:8647631-Receptors, Platelet-Derived Growth Factor, pubmed-meshheading:8647631-Transfection, pubmed-meshheading:8647631-Tumor Cells, Cultured
pubmed:year
1996
pubmed:articleTitle
Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism.
pubmed:affiliation
The Sidney Kimmel Cancer Center, San Diego, CA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't