Estrogen receptor pathways to AP-1

Kushner, Peter J.; Agard, David A.; Greene, Geoffrey L.; Scanlan, Thomas S.; Shiau, Andrew K.; Uht, Rosalie Maire; Webb, Paul

doi:10.1016/s0960-0760(00)00108-4

Cited by 776 publications

(574 citation statements)

References 34 publications

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“…Indirect loading of ER␣ to transcriptional regulatory sites has already been documented and could represent an important pathway through which this factor acts (Hall et al 2001). Interestingly, several transcription factors recruited to the CCND1 regulatory regions have been shown to physically interact with hormone-activated ER␣ and could therefore tether it to these regions: C/EBP␤ (Chang et al 2005), c-jun (Kushner et al 2000), and Sp1 (Safe 2001;Kim et al 2005). ER␣ ChIP experiments following Sp1 silencing revealed a decrease in ER␣ recruitment at enh2 (Supplementary Fig.…”

Section: Genes and Development 2521mentioning

confidence: 75%

“…1). However, ER␣ has the ability to regulate target genes through interaction with other transcription factors that tether ER␣ to the DNA (Kushner et al 2000;Safe 2001). In keeping with the relatively low E2 sensitivity of indirect regulatory sites reported in reporter assays (Xie et al 1999;Stoner et al 2004), transient transfections performed in MCF7 cells showed that enh2 activity could be modestly enhanced by E2 ( Supplementary Fig.…”

Section: Enh2 Is An Estradiol (E2)-responsive Enhancer Corresponding mentioning

confidence: 99%

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A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer

Eeckhoute¹,

Carroll²,

Geistlinger³

et al. 2006

Genes Dev.

268

239

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Estrogen stimulates the proliferation of the most common type of human breast cancer that expresses estrogen receptor ␣ (ER␣) through the activation of the cyclin D1 (CCND1) oncogene. However, our knowledge of ER␣ transcriptional mechanisms remains limited. Hence, it is still elusive why ER␣ ectopically expressed in ER-negative breast cancer cells (BCC) is functional on ectopic reporter constructs but lacks activity on many endogenous target genes, including CCND1. Here, we show that estradiol (E2) stimulation of CCND1 expression in BCC depends on a novel cell-type-specific enhancer downstream from the CCND1 coding region, which is the primary ER␣ recruitment site in estrogen-responsive cells. The pioneer factor FoxA1 is specifically required for the active chromatin state of this enhancer and as such is crucial for both CCND1 expression and subsequent cell cycle progression. Interestingly, even in BCC, CCND1 levels and proliferation are tightly controlled by E2 through the establishment of a negative feedforward loop involving the induction of NFIC, a putative tumor suppressor capable of directly repressing CCND1 transcription. Taken together, our results reveal an estrogen-regulated combinatorial network including cell-specific cis-and trans-regulators of CCND1 expression where ER␣ collaborates with other transcription factors associated with the ER-positive breast cancer phenotype, including FoxA1 and NFIC.[Keywords: Breast cancer; estrogen receptor; cyclin D1; transcription; enhancer; chromatin] Supplemental material is available at http://www.genesdev.org.

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Section: Genes and Development 2521mentioning

confidence: 75%

Section: Enh2 Is An Estradiol (E2)-responsive Enhancer Corresponding mentioning

confidence: 99%

A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer

Eeckhoute¹,

Carroll²,

Geistlinger³

et al. 2006

Genes Dev.

268

239

View full text Add to dashboard Cite

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“…But additional pathways for estrogen action have been are suggested (Coleman and Smith, 2001) including ER modulating gene expression via protein-protein binding with c-Fos/c-Jun B (AP-1), Sp1 or through NF-κB (Ray et al, 1994;Kushner et al, 2000;Safe, 2001). …”

Section: Discussionmentioning

confidence: 99%

Time dependency of uterine effects of naringenin type phytoestrogens in vivo

Zierau

Kretzschmar

Möller

et al. 2008

Molecular and Cellular Endocrinology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 29A c c e p t e d M a n u s c r i p t

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“…The ER␣ could potentially be tethered to the MHRE and co-occupy the region with DNAbound ERRs (29) or, alternatively, may be tethered to AP1 (67)(68)(69) or SP1 (7,70) complexes bound to their consensus binding sites located upstream as well as within the MHRE nucleosome. To discern among these possibilities, we first used ChIP assays to demonstrate that ERR␣ and AP1 interact with their corresponding binding elements in the nucleosome (Fig.…”

Section: Estrogen Induces Err␣ Expression In Mcf-7 Cells Via An Er␣-mmentioning

confidence: 99%

Estrogen Induces Estrogen-related Receptor α Gene Expression and Chromatin Structural Changes in Estrogen Receptor (ER)-positive and ER-negative Breast Cancer Cells

Kinyamu

Wang

et al. 2008

Journal of Biological Chemistry

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Estrogen-related receptor ␣ (ERR␣), a member of the nuclear receptor superfamily, is closely related to the estrogen receptors (ER␣ and ER␤). The ERR␣ gene is estrogen-responsive in several mouse tissues and cell lines, and a multiple hormone-response element (MHRE) in the promoter is an important regulatory region for estrogen-induced ERR␣ gene expression. ERR␣ was recently shown to be a negative prognostic factor for breast cancer survival, with its expression being highest in cancer cells lacking functional ER␣. The contribution of ERR␣ in breast cancer progression remains unknown but may have important clinical implications. In this study, we investigated ERR␣ gene expression and chromatin structural changes under the influence of 17␤-estradiol in both ER-positive MCF-7 and ER-negative SKBR3 breast cancer cells. We mapped the nucleosome positions of the ERR␣ promoter around the MHRE region and found that the MHRE resides within a single nucleosome. Local chromatin structure of the MHRE exhibited increased restriction enzyme hypersensitivity and enhanced histone H3 and H4 acetylation upon estrogen treatment. Interestingly, estrogen-induced chromatin structural changes could be repressed by estrogen antagonist ICI 182 780 in MCF-7 cells yet were enhanced in SKBR3 cells. We demonstrated, using chromatin immunoprecipitation assays, that 17␤-estradiol induces ERR␣ gene expression in MCF-7 cells through active recruitment of co-activators and release of co-repressors when ERR␣ and AP1 bind and ER␣ is tethered to the MHRE. We also found that this estrogen effect requires the MAPK signaling pathway in both cell lines.Estradiol (E 2 ) 2 is required for the development and function of multiple tissue types and physiological systems in mammals, and it has been implicated in a range of pathological conditions, including the initiation and progression of breast cancer (Refs.

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Estrogen receptor pathways to AP-1

Cited by 776 publications

References 34 publications

A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer

A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer

Time dependency of uterine effects of naringenin type phytoestrogens in vivo

Estrogen Induces Estrogen-related Receptor α Gene Expression and Chromatin Structural Changes in Estrogen Receptor (ER)-positive and ER-negative Breast Cancer Cells

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