ArticleNucleic acids research2019
A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- DeCTCF: Decoding CTCF binding sequences by leveraging predicted epigenomic features.PLoS computational biology · 2026Article
- Endocrine therapy reprogramming of breast cancer facilitates metastatic escape via upregulation of P-Rex1/Rac1 signalling.Nature communications · 2026Article
- Ectopic Recruitment of the CTCF N-Terminal Domain with Two Proximal Zinc-Finger Domains as a Tool for 3D Genome Engineering.International journal of molecular sciences · 2025Article
- CRISPR screening approaches in breast cancer research.Cancer metastasis reviews · 2025Review
- CTCF enhances pancreatic cancer progression via FLG-AS1-dependent epigenetic regulation and macrophage polarization.Cell death and differentiation · 2025Article
- Defining the regulatory logic of breast cancer using single-cell epigenetic and transcriptome profiling.Cell genomics · 2025Article
- Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Chromatin architectural factor CTCF is essential for progesterone-dependent uterine maturation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Chromatin Organization and Transcriptional Programming of Breast Cancer Cell Identity.Endocrinology · 2023Review
- CRISPR-Cas9 screen reveals a role of purine synthesis for estrogen receptor α activity and tamoxifen resistance of breast cancer cells.Science advances · 2023Article
- BAP18 facilitates CTCF-mediated chromatin accessible to regulate enhancer activity in breast cancer.Cell death and differentiation · 2023Article
- Network-informed discovery of multidrug combinations for ERα+/HER2-/PI3Kα-mutant breast cancer.Cellular and molecular life sciences : CMLS · 2023Article
- Gene editing and its applications in biomedicine.Science China. Life sciences · 2022Review
- Strategies to overcome the main challenges of the use of CRISPR/Cas9 as a replacement for cancer therapy.Molecular cancer · 2022Review
- Comparison and Characterization of a Cell Wall Invertase Promoter from Cu-Tolerant and Non-Tolerant Populations ofInternational journal of molecular sciences · 2021Article
- Using CRISPR to understand and manipulate gene regulation.Development (Cambridge, England) · 2021Review
- Genome-Wide Estrogen Receptor Activity in Breast Cancer.Endocrinology · 2021Review
- PtdIns(3,4,5)PProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Intrinsic and Extrinsic Factors Governing the Transcriptional Regulation of ESR1.Hormones & cancer · 2020Review
- The double dealing of cyclin D1.Cell cycle (Georgetown, Tex.) · 2020Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptor α (ERα) is an enhancer activating transcription factor, a key driver of breast cancer and a main target for cancer therapy. ERα-mediated gene regulation requires proper chromatin-conformation to facilitate interactions between ERα-bound enhancers and their target promoters. A major determinant of chromatin structure is the CCCTC-binding factor (CTCF), that dimerizes and together with cohesin stabilizes chromatin loops and forms the boundaries of topologically associated domains. However, whether CTCF-binding elements (CBEs) are essential for ERα-driven cell proliferation is unknown. To address this question in a global manner, we implemented a CRISPR-based functional genetic screen targeting CBEs located in the vicinity of ERα-bound enhancers. We identified four functional CBEs and demonstrated the role of one of them in inducing chromatin conformation changes in favor of activation of PREX1, a key ERα target gene in breast cancer. Indeed, high PREX1 expression is a bona-fide marker of ERα-dependency in cell lines, and is associated with good outcome after anti-hormonal treatment. Altogether, our data show that distinct CTCF-mediated chromatin structures are required for ERα- driven breast cancer cell proliferation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.