Endogenous Purification Reveals GREB1 as a Key Estrogen Receptor Regulatory Factor

Hisham Mohammed(Cancer Research UK), Clive S. D’Santos(Cancer Research UK), Aurélien A. Sérandour(Cancer Research UK), H. Raza Ali(Cambridge University Hospitals NHS Foundation Trust), Gordon D. Brown(Cancer Research UK), A.R. Atkins(Thermo Fisher Scientific (Israel)), Oscar M. Rueda(Cancer Research UK), Kelly A. Holmes(Cancer Research UK), Vassiliki Theodorou(Cancer Research UK), Jessica Robinson(Cancer Research UK), Wilbert Zwart(The Netherlands Cancer Institute), Amel Saadi(Cancer Research UK), Caryn S. Ross-Innes(Cancer Research UK), Suet‐Feung Chin(Cancer Research UK), Suraj Menon(Cancer Research UK), Julia Stingl(University of Cambridge), Carlo Palmieri(Imperial College Healthcare NHS Trust), Carlos Caldas(Cancer Research UK), Jason S. Carroll(University of Cambridge)
Cell Reports
February 1, 2013
Cited by 404Open Access
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Abstract

Estrogen receptor-α (ER) is the driving transcription factor in most breast cancers, and its associated proteins can influence drug response, but direct methods for identifying interacting proteins have been limited. We purified endogenous ER using an approach termed RIME (rapid immunoprecipitation mass spectrometry of endogenous proteins) and discovered the interactome under agonist- and antagonist-liganded conditions in breast cancer cells, revealing transcriptional networks in breast cancer. The most estrogen-enriched ER interactor is GREB1, a potential clinical biomarker with no known function. GREB1 is shown to be a chromatin-bound ER coactivator and is essential for ER-mediated transcription, because it stabilizes interactions between ER and additional cofactors. We show a GREB1-ER interaction in three xenograft tumors, and using a directed protein-protein approach, we find GREB1-ER interactions in half of ER(+) primary breast cancers. This finding is supported by histological expression of GREB1, which shows that GREB1 is expressed in half of ER(+) cancers, and predicts good clinical outcome. These findings reveal an unexpected role for GREB1 as an estrogen-specific ER cofactor that is expressed in drug-sensitive contexts.


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