Abstract | BACKGROUND: METHODS: Expression levels of the coactivators p300 and CBP were manipulated by plasmid or siRNA transfections and activity of ER-β was measured by luciferase assays. Viability was measured by MTT assays and cellular migration was determined by wound-healing and Boyden chamber assays. RESULTS: High expression of ER-β was found in PC3 cells which were used for the experiments. p300 or CBP enhanced activation of ER-β by genistein. Antiestrogens did not acquire agonistic properties in the presence of increased concentrations of either coactivator. Inhibition of p300 or CBP decreased genistein stimulation of ER-β. Genistein reduced migration of PC3 prostate cancer cells and down-regulation of p300 potentiated this effect. CONCLUSIONS: p300 and CBP are implicated in regulation of ER-β activity and cellular migration in prostate cancer. These findings are important for understanding of action of ER-β in carcinoma of the prostate.
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Authors | Jan Bouchal, Frédéric R Santer, Philipp P S Höschele, Eva Tomastikova, Hannes Neuwirt, Zoran Culig |
Journal | The Prostate
(Prostate)
Vol. 71
Issue 4
Pg. 431-7
(Mar 01 2011)
ISSN: 1097-0045 [Electronic] United States |
PMID | 20859991
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2010 Wiley-Liss, Inc. |
Chemical References |
- Estrogen Receptor beta
- Genistein
- CREB-Binding Protein
- CREBBP protein, human
- E1A-Associated p300 Protein
- EP300 protein, human
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Topics |
- CREB-Binding Protein
(physiology)
- Cell Line, Tumor
- Cell Movement
(drug effects)
- E1A-Associated p300 Protein
(physiology)
- Estrogen Receptor beta
(genetics, physiology)
- Genistein
(pharmacology)
- Humans
- Male
- Prostatic Neoplasms
(pathology)
- Signal Transduction
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