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Vol. 12, No. 22, pp. 3488-3498, November 15, 1998
1 Division of Molecular Carcinogenesis, The Netherlands
Cancer Institute, 1066 CX Amsterdam, The Netherlands;
2 Prolifix Ltd., Abindgon, Oxfordshire OX14 4RY, UK
The estrogen receptor (ER) is an important regulator of growth and
differentiation of breast epithelium. Transactivation by ER depends on
a leucine-rich motif, which constitutes a ligand-regulated binding site
for steroid receptor coactivators (SRCs). Cyclin D1 is frequently
amplified in breast cancer and can activate ER through direct binding.
We show here that cyclin D1 also interacts in a ligand-independent
fashion with coactivators of the SRC-1 family through a motif that
resembles the leucine-rich coactivator binding motif of nuclear
receptors. By acting as a bridging factor between ER and SRCs, cyclin
D1 can recruit SRC-family coactivators to ER in the absence of ligand.
A cyclin D1 mutant that binds to ER but fails to recruit coactivators
preferentially interferes with ER activation in breast cancer cells
that have high levels of cyclin D1. These data support that cyclin D1
contributes significantly to ER activation in breast cancers in which
the protein is overexpressed. Our present results reveal a novel route
of coactivator recruitment to ER and establish a direct role for cyclin
D1 in regulation of transcription.
[Key Words: Estrogen receptor; cyclin D1; breast cancer; SRC-1; coactivator]
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