Related Experiment Video
Updated: Feb 2, 2026
07:42
Imaging of Estrogen Receptor-α in Rat Pial Arterioles using a Digital Immunofluorescent Microscope
Published on: November 29, 2011
12.8K
Genome-wide Estrogen Receptor-α activation is sustained, not cyclical
Andrew N Holding1, Amy E Cullen1, Florian Markowetz1
1Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, United Kingdom.
Elife
|November 21, 2018
Summary
Estrogen Receptor-alpha (ER) binding in breast cancer is complex. Our study reveals sustained ER binding and estra-2-diol independent sites, challenging previous cyclical models.
Area of Science:
- Endocrinology
- Cancer Biology
- Genomics
Background:
- Estrogen Receptor-alpha (ER) drives a majority of breast cancers.
- ER activation by estra-2-diol forms transcriptionally active complexes.
- Previous research suggested cyclical ER binding patterns, but lacked comprehensive data.
Purpose of the Study:
- To conduct a genome-wide analysis of ER binding dynamics after activation.
- To investigate the robustness and generality of ER binding patterns.
- To develop a new model reconciling conflicting findings on ER binding.
Main Methods:
- Utilized Parallel-Factor ChIP-seq for precise quantification of ER binding.
- Performed analysis across 6 replicates and 10 time-points post-activation.
- Integrated quantitative re-analysis of independent studies.
Main Results:
- Identified a sustained increase in ER binding affinity.
- Discovered a subset of estra-2-diol independent ER binding sites.
- Reconciled conflicting previous findings regarding ER binding at the TFF1 promoter.
Conclusions:
- ER binding dynamics are more complex than previously understood, involving sustained affinity and independent sites.
- The findings provide a detailed understanding of ER's role in breast cancer.
- This research offers insights into ER as both a driver and therapeutic target in breast cancer.
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