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Estrogen Receptor Inhibition of NF-kB Activity in Breast Cancer
Annual summary rept. 28 May 2001-27 May 2004
CHICAGO UNIV IL
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Estrogen Receptor-alpha ER mediated inhibition of NF-kappaB contributes to the anti-inflammatory and protective effects of estrogen in bone, cardiovasculature, and breast cancer. Cross talk could be caused by direct or 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 MCF-7 SS display ER mediated inhibition of NF-kappaB transcriptional activity. Transient transfection of various coactivators into the MCF-7SS cells revealed that only CBP and p300 were able to promote an inhibitory effect of estradiolon NF-kappaB activity. Western Bolt analysis showed that CBP protein levels were reduced in this cell line relative to the MCF-7SI cells. Both immunofluorescent microscopy and co-immunoprecipitation shoed an associated between ER and NF-kappaB in the MCF-7SI cells. CBP also immunoprecipitated with both ER and NF-kappaB.
APPROVED FOR PUBLIC RELEASE