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rdf:type |
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lifeskim:mentions |
umls-concept:C0023688,
umls-concept:C0037083,
umls-concept:C0040690,
umls-concept:C0085862,
umls-concept:C0599946,
umls-concept:C0665341,
umls-concept:C1299583,
umls-concept:C1512505,
umls-concept:C1549571,
umls-concept:C1608386,
umls-concept:C1710082
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pubmed:issue |
2
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pubmed:dateCreated |
2010-3-16
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pubmed:abstractText |
To investigate a presumed crosstalk between estrogen receptor alpha (ERalpha) and the TGF-beta signaling pathway in breast cancer, we analyzed the TGF-beta-induced expression of the plasminogen activator inhibitor 1 (PAI-1) gene in ER-positive MCF-7 cells. After siRNA-mediated knock-down of endogenous ERalpha, the transcription level of PAI-1 was upregulated, pointing to an attenuation of TGF-beta signaling by the presence of ERalpha. We verified these findings by a vice versa approach using a primary ER-negative cell model transiently overexpressing either ERalpha or ERbeta. We found that ERalpha, but not ERbeta, led to a strong inhibition of the TGF-beta1 signal, monitored by TGF-beta reporter assays. This attenuation was completely independent of receptor stimulation by beta-estradiol (E2) or inhibition by the pure antagonist ICI 182.780 (ICI). Our results indicate a permanent repression of PAI-1 by ERalpha and suggest a ligand-independent crosstalk between ERalpha and TGF-beta signaling in breast cancer cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1573-7217
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
357-67
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pubmed:meshHeading |
pubmed-meshheading:19370415-Blotting, Western,
pubmed-meshheading:19370415-Breast Neoplasms,
pubmed-meshheading:19370415-Cell Line, Tumor,
pubmed-meshheading:19370415-Estrogen Receptor alpha,
pubmed-meshheading:19370415-Estrogen Receptor beta,
pubmed-meshheading:19370415-Female,
pubmed-meshheading:19370415-Gene Expression,
pubmed-meshheading:19370415-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19370415-Humans,
pubmed-meshheading:19370415-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:19370415-RNA, Small Interfering,
pubmed-meshheading:19370415-Receptor Cross-Talk,
pubmed-meshheading:19370415-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19370415-Signal Transduction,
pubmed-meshheading:19370415-Transfection,
pubmed-meshheading:19370415-Transforming Growth Factor beta
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pubmed:year |
2010
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pubmed:articleTitle |
Estrogen receptor alpha attenuates transforming growth factor-beta signaling in breast cancer cells independent from agonistic and antagonistic ligands.
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pubmed:affiliation |
Dr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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