Source:http://linkedlifedata.com/resource/pubmed/id/10750020
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2000-5-8
|
| pubmed:abstractText |
Insulin-like growth factor-I (IGF-I), transforming growth factor alpha (TGFalpha) and epidermal growth factor (EGF) induced cathepsin D gene expression and reporter gene activity in MCF-7 human breast cancer cells transiently transfected with a construct (pCD1) containing a -2576 to -124 cathepsin D gene promoter insert. In contrast, IGF-I, but not TGFalpha or EGF, induced reporter gene activity in cells cotransfected with wild-type estrogen receptor (ER) expression plasmid and a construct (pCD2) containing estrogen-responsive downstream elements from -208 to -101. Promoter deletion and mutational analysis experiments identified four GC-rich sites and an imperfect palindromic estrogen responsive element required for IGF-I activation of the ER (ligand-independent). Subsequent studies with the mitogen-activated protein kinase (MAPK) inhibitor, PD98059, and a serine(118(-ER mutant confirmed the role of the MAPK pathway for IGF-I activation of the ER in MCF-7 cells. Thus, growth factor activation of ER can mediate transactivation vs ER/Sp1 binding to GC-rich sites and represents a novel pathway for ligand-independent ER action. The divergent pathways for IGF-I and TGFalpha/EGF activation of the ER observed in MCF-7 cells contrast with previous data indicating that pathways for growth factor activation of the ER are dependent on the gene and/or gene promoter and on cell context.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cathepsin D,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0952-5041
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
24
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
193-202
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:10750020-Base Sequence,
pubmed-meshheading:10750020-Breast Neoplasms,
pubmed-meshheading:10750020-Cathepsin D,
pubmed-meshheading:10750020-Cell Division,
pubmed-meshheading:10750020-Epidermal Growth Factor,
pubmed-meshheading:10750020-Female,
pubmed-meshheading:10750020-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:10750020-Genes, Reporter,
pubmed-meshheading:10750020-Growth Substances,
pubmed-meshheading:10750020-Humans,
pubmed-meshheading:10750020-Insulin-Like Growth Factor I,
pubmed-meshheading:10750020-Molecular Sequence Data,
pubmed-meshheading:10750020-Plasmids,
pubmed-meshheading:10750020-Promoter Regions, Genetic,
pubmed-meshheading:10750020-Receptors, Estrogen,
pubmed-meshheading:10750020-Sequence Deletion,
pubmed-meshheading:10750020-Transcriptional Activation,
pubmed-meshheading:10750020-Transfection,
pubmed-meshheading:10750020-Transforming Growth Factor alpha,
pubmed-meshheading:10750020-Tumor Cells, Cultured
|
| pubmed:year |
2000
|
| pubmed:articleTitle |
Transcriptional activation of cathepsin D gene expression by growth factors.
|
| pubmed:affiliation |
Department of Veterinary Physiology, Texas A & M University, College Station, Texas 77843-4466, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|