Abstract

Estrogen receptor (ER) is a hormone-regulated transcription factor that controls cell division and differentiation in the ovary, breast, and uterus. The expression of ER is a common feature of the majority of breast cancers, which is used as a therapeutic target. Recent genetic studies have shown that ER binding occurs in regions distant to the promoters of estrogen target genes. These studies have also demonstrated that ER binding is accompanied with the binding of other transcription factors, which regulate the function of ER and response to anti-estrogen therapies. In this review, we explain how these factors influence the interaction of ER to chromatin and their cooperation for ER transcriptional activity. Moreover, we describe how the expression of these factors dictates the response to anti-estrogen therapies. Finally, we discuss how cytoplasmatic signaling pathways may modulate the function of ER and its cooperating transcription factors.

Highlights

  • The steroid hormone estrogen and the estrogen receptor alpha (ER) are necessary for the physiology of the femaleCommunicated by Erich NiggElisa Fiorito and Madhumohan R

  • We describe how cooperating factors influence the transcriptional activity of ER, and we speculate how these signaling pathways may modulate the function of ER and ERcooperating factors

  • Ross-Innes et al have established that hormone-resistant breast cancers still recruit ER to the chromatin, and this binding is associated with FOXA1 (Ross-Innes et al 2012)

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Summary

Introduction

The steroid hormone estrogen and the estrogen receptor alpha (ER) are necessary for the physiology of the femaleCommunicated by Erich NiggElisa Fiorito and Madhumohan R. FOXA proteins are the most studied pioneer transcription factors that bind to chromatin and enable gene activity. Ross-Innes et al have established that hormone-resistant breast cancers still recruit ER to the chromatin, and this binding is associated with FOXA1 (Ross-Innes et al 2012).

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