Estrogen Receptor Inhibition of NF- (kappa) B Activity in Breast Cancer
Abstract
Estrogen Receptor-alpha (ER) mediated inhibition of NF-kappaB contributes to the anti- inflammatory and protective effects of estrogen in bone, cardovasculature, and breast cancer. Cross talk could be caused by direct of indirect association of these transcription factors, or by competition for other components of the transcriptional apparatus. In order to distinguish among these possibilities, we identified clonal variants of ER(+) MCF-7 breast cancer cells that either do (MCF-7 SI) or do not (MCF7 55) display ER mediated inhibition of NF-kappaB transcriptional activity. Transient transfection of various coactivators intot he MCF-7SS cells revealed that only CBP and p3OO were able to promote an inhibitory effect ofestradiolon NF-kappa B activity. Western Bolt analysis showed that CEP protein levels were reduced in this cell line relate to the MCF-7S1 cells. Both iminunofluorescent microscopy and co-immunoprecipitation shoed an associated between ER and NF-kappaB in the MCF-7ST cells. CBP also immunoprecipitated with both ER and NF-kappaB. The use of deletion constructs demonstrated that the ER ligand binding domain was necessary and sufficient for...
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2003
- Accession Number
- ADA425643
Entities
People
- Geoffrey L Greene
- Kendall W Nettles
Organizations
- University of Chicago