rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
12
|
pubmed:dateCreated |
1998-7-13
|
pubmed:abstractText |
The potent mitogenic activity of insulin-like growth factor I (IGF-I) on breast epithelium is inhibited by retinoic acid in oestrogen receptor-positive (ER+) breast cancer cell lines. We studied and compared the effects of N-(4-hydroxyphenyl)-retinamide (4-HPR) in terms of growth inhibition and modulation of the IGF-I system in ER+ (MCF-7) and oestrogen receptor-negative (ER-) (MDA-MB231) breast cancer cell lines. Treatment with 1-10 microM 4-HPR for up to 96 h induced a dose- and time-dependent inhibition of proliferation in both breast cancer cell lines. Induction of apoptosis was much more evident in MCF-7 than in MDA-MB231 cells (30-40% compared with 0-5% respectively at 5 microM for 48 h). Exogenous human recombinant IGF-I (hr-IGF-I)-stimulated cell proliferation was abolished by 1 microM 4-HPR in MCF-7 cells. Immunoreactive IGF-I-like protein concentration in conditioned medium was reduced by 38% in MCF-7 and by 90% in MDA-MB231 cell lines following treatment for 48 h with 5 microM 4-HPR. Western ligand blot analysis showed a reduction of IGF-binding protein 4 (BP4) and BP5 by 67% and 87%, respectively, in MCF-7, whereas IGF-BP4 and -BP1 were reduced by approximately 20% in MDA-MB231 cells. Exposure to 5 microM 4-HPR for 48 h inhibited [125I]IGF-I binding and Scatchard analysis revealed a decrease of more than 50% in maximum binding capacity (Bmax) and a reduced receptor number/cell in both cancer cell lines. Steady-state type I IGF-receptor mRNA levels were reduced by approximately 30% in both tumour cell lines. We conclude that 4-HPR induces a significant down-regulation of the IGF-I system in both ER+ (MCF-7) and ER- (MDA-MB231) breast cancer cell lines. These findings suggest that, in our model, interference with the ER signalling pathway is not the only mechanism of breast cancer growth inhibition by 4-HPR.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9649125-1281161,
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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 |
Jun
|
pubmed:issn |
0007-0920
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
77
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
|
pubmed:pagination |
2138-47
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9649125-Antineoplastic Agents,
pubmed-meshheading:9649125-Breast Neoplasms,
pubmed-meshheading:9649125-Cell Division,
pubmed-meshheading:9649125-DNA, Neoplasm,
pubmed-meshheading:9649125-Drug Interactions,
pubmed-meshheading:9649125-Fenretinide,
pubmed-meshheading:9649125-Humans,
pubmed-meshheading:9649125-Insulin-Like Growth Factor I,
pubmed-meshheading:9649125-Receptors, Estrogen,
pubmed-meshheading:9649125-Receptors, Somatomedin,
pubmed-meshheading:9649125-Tumor Cells, Cultured
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pubmed:year |
1998
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pubmed:articleTitle |
Modulation of the insulin-like growth factor-I system by N-(4-hydroxyphenyl)-retinamide in human breast cancer cell lines.
|
pubmed:affiliation |
Department of Preclinical Oncology, National Institute for Cancer Research and Advanced Biotechnology Center, Genoa, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|