Linked Life Data

8542581

Source:http://linkedlifedata.com/resource/pubmed/id/8542581

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-2-13
pubmed:abstractText
Autocrine stimulation by platelet-derived growth factor-B (PDGF-B)-like factors has been widely implicated as an important mechanism in the cause and/or maintenance of a variety of human tumors. However, normal human cells appear to be resistant to transformation by PDGF-B-like molecules, and a direct demonstration of the tumor-promoting or tumor-maintaining property of a PDGF-B autocrine system is lacking. T98G human glioblastoma cells are nontumorigenic in athymic mice. We show that these cells express predominantly PDGF-beta type receptors and continuously secrete small amount of PDGF-B/c-sis. Addition of suramin or specific anti-PDGF-B/v-sis antibody inhibits proliferation in culture. Conversely, multiple clonal lines that stably overexpress PDGF-B/v-sis (T98Gsis cells) exhibit a striking 200-250% increased proliferation rate and an enhanced colony-forming frequency in soft agar. Clonal lines with stable expression of PDGF-B/v-sis (T98Gsis cells) reliably (80%) develop tumors in 4-6 weeks, whereas the empty-vector control cells are nontumorigenic. Moreover, in some cases, T98Gsis cells disseminate to form bilateral and multifocal pulmonary metastases. The results show that T98G cells contain functional PDGF receptors that, upon sufficient stimulation, can cause greatly increased mitogenic response, which may account for the development of the malignant phenotype. Metastatic tumor formation in athymic mice by PDGF stimulation has not been reported previously. The mechanism may depend on preexisting changes such as the lost p53 function of these cells. T98Gsis cells provide a model of growth factor-dependent tumorigenesis and metastases, which may be helpful in elucidating these relationships.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
280-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8542581-Animals, pubmed-meshheading:8542581-Antibodies, Neoplasm, pubmed-meshheading:8542581-Antibody Specificity, pubmed-meshheading:8542581-Cell Division, pubmed-meshheading:8542581-Cell Transformation, Neoplastic, pubmed-meshheading:8542581-Female, pubmed-meshheading:8542581-Glioblastoma, pubmed-meshheading:8542581-Humans, pubmed-meshheading:8542581-Lung Neoplasms, pubmed-meshheading:8542581-Male, pubmed-meshheading:8542581-Mice, pubmed-meshheading:8542581-Mice, Nude, pubmed-meshheading:8542581-Middle Aged, pubmed-meshheading:8542581-Oncogene Proteins v-sis, pubmed-meshheading:8542581-Phenotype, pubmed-meshheading:8542581-Platelet-Derived Growth Factor, pubmed-meshheading:8542581-Proto-Oncogene Proteins, pubmed-meshheading:8542581-Proto-Oncogene Proteins c-sis, pubmed-meshheading:8542581-Retroviridae Proteins, Oncogenic, pubmed-meshheading:8542581-Transfection, pubmed-meshheading:8542581-Tumor Cells, Cultured
pubmed:year
1996
pubmed:articleTitle
Platelet-derived growth factor-B/v-sis confers a tumorigenic and metastatic phenotype to human T98G glioblastoma cells.
pubmed:affiliation
Sidney Kimmel Cancer Center, San Diego, California 92121, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't