Related Experiment Video
Updated: Apr 2, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
APOBEC3B-Mediated Cytidine Deamination Is Required for Estrogen Receptor Action in Breast Cancer
Manikandan Periyasamy1, Hetal Patel1, Chun-Fui Lai1
1Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.
Abstract:
Estrogen receptor α (ERα) is the key transcriptional driver in a large proportion of breast cancers. We report that APOBEC3B (A3B) is required for regulation of gene expression by ER and acts by causing C-to-U deamination at ER binding regions. We show that these C-to-U changes lead to the generation of DNA strand breaks through activation of base excision repair (BER) and to repair by non-homologous end-joining (NHEJ) pathways. We provide evidence that transient cytidine deamination by A3B aids chromatin modification and remodelling at the regulatory regions of ER target genes that promotes their expression. A3B expression is associated with poor patient survival in ER+ breast cancer, reinforcing the physiological significance of A3B for ER action.
Insights
APOBEC3B (A3B) deaminates DNA at estrogen receptor binding sites, promoting gene expression in ER+ breast cancer. This mechanism, involving DNA repair pathways, is linked to poorer patient survival.
Area of Science:
- Molecular Biology
- Genetics
- Cancer Research
Background:
- Estrogen receptor alpha (ERα) is a critical driver in many breast cancers.
- The precise mechanisms by which ERα regulates gene expression are complex and still under investigation.
Purpose of the Study:
- To investigate the role of APOBEC3B (A3B) in the regulation of gene expression by ERα.
- To elucidate the molecular mechanisms by which A3B influences ERα target gene activity.
Main Methods:
- Assessing C-to-U deamination at ER binding regions.
- Investigating DNA strand break generation via base excision repair (BER).
- Analyzing repair by non-homologous end-joining (NHEJ) pathways.
Main Results:
- APOBEC3B (A3B) causes C-to-U deamination at ER binding regions, facilitating ER-mediated gene regulation.
- A3B-induced deamination triggers DNA strand breaks, repaired by BER and NHEJ.
- Transient deamination by A3B promotes chromatin modification and remodelling at ER target gene regulatory regions, enhancing their expression.
Conclusions:
- APOBEC3B is essential for ER-mediated gene regulation in ER+ breast cancer.
- The A3B-driven mechanism involving DNA deamination and repair influences chromatin dynamics and gene expression.
- A3B expression correlates with poor patient survival in ER+ breast cancer, highlighting its clinical relevance.
More Related Videos
Related Concept Videos
RNA Editing
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Mitogens and the Cell Cycle
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Inhibition of Cdk Activity
Abnormal Proliferation

