Journal
CANCER CELL
Volume 10, Issue 6, Pages 487-499Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2006.09.015
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Funding
- Intramural NIH HHS Funding Source: Medline
- NCI NIH HHS [N01-CO-12400] Funding Source: Medline
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A serious obstacle to successful treatment of estrogen receptor (ER)-positive human breast cancer is cell resistance to tamoxifen (TAM) therapy. Here we show that the electrophile disulfide benzamide (DIBA), an ER zinc finger inhibitor, blocks ligand-dependent and -independent cell growth of TAM-resistant breast cancer in vitro and in vivo. Such inhibition depends on targeting disruption of the ER DNA-binding domain and its communication with neighboring functional domains, facilitating ER alpha dissociation from its coactivator AIB1 and concomitant association with its corepressor NCoR bound to chromatin. DIBA does not affect phosphorylation of HER2, MAPK, AKT, and AIB1, suggesting that DIBA-modified ER alpha may induce a switch from agonistic to antagonistic effects of TAM on resistant breast cancer cells.
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