Journal
MOLECULAR CELL
Volume 21, Issue 3, Pages 393-404Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2005.12.016
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Funding
- NCI NIH HHS [R01 CA69065, P50 CA113001] Funding Source: Medline
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In breast cancer and normal estrogen target tissues, estrogen receptor-alpha (ER alpha) signaling results in the establishment of spatiotemporal patterns of gene expression. Whereas primary target gene regulation by ER alpha involves recruitment of coregulatory proteins, co-activators, or corepressors, activation of these downstream promoters by receptor signaling may also involve partnership of ER alpha with other transcription factors. By using an integrated, genome-wide approach that involves ChIP-chip and computational modeling, we uncovered 13 ER alpha-responsive promoters containing both ER alpha and c-MYC binding elements located within close proximity (13-214 bp) to each other. Estrogen stimulation enhanced the c-MYC-ER alpha interaction and facilitated the association of ER alpha, c-MYC, and the coactivator TRRAP with these estrogen-responsive promoters, resulting in chromatin remodeling and increased transcription. These results suggest that ER alpha and c-MYC physically interact to stabilize the ER alpha-coactivator complex, thereby permitting other signal transduction pathways to fine-tune estrogen-mediated signaling networks.
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