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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-8
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pubmed:dateCreated |
1992-5-18
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pubmed:abstractText |
MCF-7 cells were grown in serum free medium (Dulbecco MEM without phenol red, supplemented with Costar SF-1 without insulin). Insulin was added as required and gave dose dependent growth stimulation at concentrations between 5 and 10,000 nM. Identical growth response curves were obtained for thymidine uptake and cell number. Oestradiol and insulin-like growth factor I (IGF-I) added individually both gave a dose dependent stimulation of cell growth in serum free medium containing 50 nM insulin. The growth stimulatory effect of oestradiol was to a large extent inhibited with suramine, a general inhibitor of growth factors, indicating that the effect of oestradiol was mediated through stimulating autocrine secretion of a growth factor. To investigate a possible link between the effects of oestradiol and IGF-I, a specific IGF-I receptor antibody (alpha IR-3), 10 micrograms/ml was used. These experiments were carried out with 2.5 nM insulin in the medium, a concentration at which insulin had no growth stimulatory effect. Stimulation was carried out for 18 h before assay of thymidine uptake. The effect of oestradiol was not significantly reduced by alpha IR-3, indicating that IGF-I was not an autocrine mediator of oestradiol stimulation of cell growth under these conditions, whereas alpha IR-3 extensively reduced growth stimulation by IGF-I. On long term stimulation (5 days) oestradiol had a marked stimulatory effect on cell number and alpha IR-3 almost totally abrogated this effect. When oestradiol (1 nM) and IGF-I (2.5 nM) were added together, the combined effect on thymidine incorporation and cell number was significantly greater than additive. This synergistic effect on the IGF-I growth response was totally abolished by the IGF-I receptor antibody. The results suggest a cooperative interaction of oestradiol and IGF-I. It is concluded that growth stimulation of MCF-7 cells by long term treatment with oestradiol may be mediated through autocrine secretion of IGF-I. the effect of short term stimulation of thymidine incorporation suggest that the growth response of oestradiol is more complex, and indicate that a cooperative interaction with IGF-I is involved, which is unrelated to stimulated autocrine secretion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0960-0760
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
41
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
537-40
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:1562524-Antibodies,
pubmed-meshheading:1562524-Breast Neoplasms,
pubmed-meshheading:1562524-Cell Division,
pubmed-meshheading:1562524-Cell Line,
pubmed-meshheading:1562524-DNA Replication,
pubmed-meshheading:1562524-Dose-Response Relationship, Drug,
pubmed-meshheading:1562524-Drug Synergism,
pubmed-meshheading:1562524-Estradiol,
pubmed-meshheading:1562524-Humans,
pubmed-meshheading:1562524-Insulin-Like Growth Factor I,
pubmed-meshheading:1562524-Kinetics
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pubmed:year |
1992
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pubmed:articleTitle |
Oestradiol treatment increases the sensitivity of MCF-7 cells for the growth stimulatory effect of IGF-I.
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pubmed:affiliation |
Department of Biochemical Endocrinology, University of Bergen, Norway.
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pubmed:publicationType |
Journal Article
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