Estrogen Receptor-mediated Activation of the Serum Response Element in MCF-7 Cells through MAPK-dependent Phosphorylation of Elk-1

Duan, Renqin; Xie, Wen; Burghardt, Robert C.; Safe, Stephen

doi:10.1074/jbc.m005492200

Cited by 140 publications

(125 citation statements)

References 59 publications

Supporting

Mentioning

111

Contrasting

Unclassified

Order By: Relevance

“…In the particular context of tumor growth, hormone-induced non-genomic activation of the MAPK pathway is generally believed to be of greater consequence to estrogen receptor action in breast cancer (47,48) than to AR action in prostate cancer. Indeed, the principal effect of the cross-talk between the androgen signaling axis and MAPK signaling on prostate cancer growth appears to be via enhancement of the transcriptional activity of AR through phosphorylation of AR as noted in the Introduction.…”

Section: Discussionmentioning

confidence: 99%

The ETS Domain Transcription Factor ELK1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer Cells

Patki

Chari

Sivakumaran

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Mechanisms that redirect androgen receptor signaling to primarily support prostate tumor growth are poorly understood. Results: Prostate cancer cells were addicted to ELK1, which tethered AR to activate growth genes in hormone-dependent and castration-recurrent PC without ELK1 phosphorylation. Conclusion: ELK1 directs a critical arm of transcriptional growth signaling by AR that is preserved in CRPC. Significance: The ELK1-AR interaction offers a functionally tumor-selective drug target.

show abstract

Section: Discussionmentioning

confidence: 99%

The ETS Domain Transcription Factor ELK1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer Cells

Patki

Chari

Sivakumaran

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…The non-classical oestrogen pathways were investigated by examining transcription of Igf1, reflecting Ap1 signalling (Umayahara et al 1994) and c-fos reflecting transcription activated via phosphorylation cascades (Duan et al 2001). In uterus, both OE 2 and raloxifene treatment increased IGFI expression compared with vehicle treatment (99-fold, P!0 .…”

Section: Oe 2 and Raloxifene Effects Via Non-classical Pathwaysmentioning

confidence: 99%

In vivo activation of gene transcription via oestrogen response elements by a raloxifene analogue

Engdahl

Jochéms

Gustafsson

et al. 2009

Journal of Endocrinology

View full text Add to dashboard Cite

Raloxifene is a selective oestrogen receptor modulator with tissue-specific effects. The mechanisms behind the effects of raloxifene are partly unclear, and the aim of the present study was to investigate whether raloxifene can activate the classical oestrogen-signalling pathway in vivo in three known oestrogen-responsive organs, uterus (reproductive organ), bone (non-reproductive organ) and thymus (immune organ). For this purpose, we have used reporter mice with a luciferase gene under control of oestrogen-responsive elements (EREs), enabling detection of in vivo activation of gene transcription via the classical oestrogen pathway. Three-month-old ovariectomized ERE-luciferase mice were treated with the raloxifene analogue (LY117018), oestradiol (OE 2 ) or vehicle for 3 weeks. Luciferase activation was measured in bone, uterus and thymus, and compared to bone parameters, and uterus and thymus weights. The raloxifene analogue affected bone mineral density (BMD) to the same extent as OE 2 , and both treatments resulted in increased luciferase activity in bone. As expected, OE 2 treatment resulted in increased uterus weight and increased uterine luciferase activity, while the effect of LY117018 on uterus weight and luciferase activity was modest and significantly lower than the effect of OE 2 . LY117018 and OE 2 treatment resulted in similar luciferase activation in thymus. However, only OE 2 treatment resulted in thymic atrophy, while no effect on thymus weight was seen after LY117018 treatment. In summary, the raloxifene analogue LY117018 can activate the classical oestrogen pathway in bone, uterus and thymus in vivo, and this activation is associated with BMD and uterus weight, but not thymus weight.

show abstract

“…The present study was instigated by the notion that essentially all cellular responses to estrogenic stimuli culminate in transcriptional regulation, even though some of the known effects are considered indirect or non-genomic (Duan et al 2001, McDonnell & Norris 2002, Levin 2003. Thus, oligonucleotide-based microarrays, which are able to detect global expression profiles at the transcriptional level, provide a convenient molecular approach to analyze biological endpoints of phytoestrogen exposure.…”

Section: Introductionmentioning

confidence: 99%

Global gene expression profiles induced by phytoestrogens in human breast cancer cells

Dip

Lenz

Antignac

et al. 2008

Endocrine Related Cancer

View full text Add to dashboard Cite

Estrogen Receptor-mediated Activation of the Serum Response Element in MCF-7 Cells through MAPK-dependent Phosphorylation of Elk-1

Abstract: 17␤-Estradiol (E2) induces c-fos protooncogene expression in MCF-

Cited by 140 publications

References 59 publications

The ETS Domain Transcription Factor ELK1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer Cells

The ETS Domain Transcription Factor ELK1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer Cells

In vivo activation of gene transcription via oestrogen response elements by a raloxifene analogue

Global gene expression profiles induced by phytoestrogens in human breast cancer cells

Contact Info

Product

Resources

About