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ERalpha suppresses slug expression directly by transcriptional repression
Yin Ye1, Yi Xiao, Wenting Wang
1Department of Pathology, The Ohio State University College of Medicine, 129 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210, USA.
The Biochemical Journal
|July 1, 2008
Summary
Ligand-activated oestrogen receptor (ER) directly suppresses slug expression by repressing transcription. This study reveals a direct interaction between ER signalling and the slug epithelial-mesenchymal transition pathway in breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Breast cancer involves complex signalling pathways, including oestrogen receptor (ER) activation and epithelial-mesenchymal transition (EMT) regulated by slug.
- Previous understanding suggested indirect interactions between ER signalling and EMT pathways.
Purpose of the Study:
- To investigate the direct interaction between ER ligand activation and the slug EMT pathway.
- To elucidate the mechanism by which ER regulates slug expression.
Main Methods:
- RNA interference (RNAi) for ERalpha knockdown.
- Transfection of ERalpha-negative cells with ERalpha.
- Treatment with 17beta-oestradiol (E2).
- Sequential chromatin immunoprecipitation (ChIP) assays.
- Analysis of slug gene expression in MDA-MB-468 and MCF-7 cell lines.
Main Results:
- Ligand-activated ERalpha directly suppresses slug expression via transcriptional repression.
- Knockdown of ERalpha increases slug expression.
- ERalpha forms a co-repressor complex with HDAC1 and N-CoR to repress slug transcription.
- Slug is confirmed as an E2-responsive gene.
Conclusions:
- Establishes a direct regulatory link between ERalpha signalling and slug expression.
- Demonstrates ERalpha's role in suppressing EMT by repressing slug transcription.
- Highlights the therapeutic potential of targeting ER-slug interaction in breast cancer treatment.
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