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Updated: Nov 27, 2025
Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
Genome-Wide Estrogen Receptor Activity in Breast Cancer
Anca M Farcas1,2, Sankari Nagarajan2,3, Sabina Cosulich4
1Bioscience, Oncology R&D, AstraZeneca, Cambridge, UK.
Abstract:
The largest subtype of breast cancer is characterized by the expression and activity of the estrogen receptor alpha (ERalpha/ER). Although several effective therapies have significantly improved survival, the adaptability of cancer cells means that patients frequently stop responding or develop resistance to endocrine treatment. ER does not function in isolation and multiple associating factors have been reported to play a role in regulating the estrogen-driven transcriptional program. This review focuses on the dynamic interplay between some of these factors which co-occupy ER-bound regulatory elements, their contribution to estrogen signaling, and their possible therapeutic applications. Furthermore, the review illustrates how some ER association partners can influence and reprogram the genomic distribution of the estrogen receptor. As this dynamic ER activity enables cancer cell adaptability and impacts the clinical outcome, defining how this plasticity is determined is fundamental to our understanding of the mechanisms of disease progression.
Insights
Estrogen receptor alpha (ER) drives breast cancer. Understanding how ER interacts with other factors is key to overcoming endocrine resistance and improving patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Estrogen receptor alpha (ER) drives the most common breast cancer subtype.
- Endocrine therapies are effective but cancer cells develop resistance.
- ER function is regulated by multiple interacting factors.
Purpose of the Study:
- Review the dynamic interplay of ER-associated factors.
- Explore their role in estrogen signaling and therapeutic potential.
- Understand how these factors influence ER genomic distribution.
Main Methods:
- Literature review of studies on ERalpha co-regulators.
- Analysis of mechanisms driving estrogen signaling pathways.
- Examination of therapeutic strategies targeting ER interactions.
Main Results:
- ER function is modulated by co-occupying factors at regulatory elements.
- These interactions influence estrogen-driven transcription and cancer adaptability.
- ER association partners can reprogram ER's genomic binding sites.
Conclusions:
- Understanding ER plasticity is crucial for overcoming treatment resistance.
- Targeting ER-associated factors offers potential therapeutic applications.
- Defining ER dynamics is fundamental to understanding breast cancer progression.
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