ArticlePLoS genetics2020
ELF5 modulates the estrogen receptor cistrome in breast cancer.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The role of CUEDC1 in suppressing JAK1/STAT3 signaling pathway in esophageal cancer.Scientific reports · 2026Article
- DNA-PKcs, a player winding and dancing with RNA metabolism and diseases.Cellular & molecular biology letters · 2025Review
- Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Review
- E74‑like ETS transcription factor 5 facilitates cell proliferation through regulating the expression of adenomatous polyposis coli 2 in non‑small cell lung cancer.International journal of molecular medicine · 2023Article
- The ELF3 transcription factor is associated with an epithelial phenotype and represses epithelial-mesenchymal transition.Journal of biological engineering · 2023Article
- TF-Prioritizer: a Java pipeline to prioritize condition-specific transcription factors.GigaScience · 2022Article
- Mammary-Enriched Transcription Factors Synergize to Activate theInternational journal of molecular sciences · 2022Article
- Human Molecular Genetics and the long road to treating cystic fibrosis.Human molecular genetics · 2021Review
- Breast-Specific Molecular Clocks Comprised ofCancer prevention research (Philadelphia, Pa.) · 2021Article
- ELF5 inhibits the proliferation and invasion of breast cancer cells by regulating CD24.Molecular biology reports · 2021Article
- Time-varying effects of FOXA1 on breast cancer prognosis.Breast cancer research and treatment · 2021Article
- Acetylation of ELF5 suppresses breast cancer progression by promoting its degradation and targeting CCND1.NPJ precision oncology · 2021Article
- Reciprocal fine-tuning of progesterone and prolactin-regulated gene expression in breast cancer cells.Molecular and cellular endocrinology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Acquired resistance to endocrine therapy is responsible for half of the therapeutic failures in the treatment of breast cancer. Recent findings have implicated increased expression of the ETS transcription factor ELF5 as a potential modulator of estrogen action and driver of endocrine resistance, and here we provide the first insight into the mechanisms by which ELF5 modulates estrogen sensitivity. Using chromatin immunoprecipitation sequencing we found that ELF5 binding overlapped with FOXA1 and ER at super enhancers, enhancers and promoters, and when elevated, caused FOXA1 and ER to bind to new regions of the genome, in a pattern that replicated the alterations to the ER/FOXA1 cistrome caused by the acquisition of resistance to endocrine therapy. RNA sequencing demonstrated that these changes altered estrogen-driven patterns of gene expression, the expression of ER transcription-complex members, and 6 genes known to be involved in driving the acquisition of endocrine resistance. Using rapid immunoprecipitation mass spectrometry of endogenous proteins, and proximity ligation assays, we found that ELF5 interacted physically with members of the ER transcription complex, such as DNA-PKcs. We found 2 cases of endocrine-resistant brain metastases where ELF5 levels were greatly increased and ELF5 patterns of gene expression were enriched, compared to the matched primary tumour. Thus ELF5 alters ER-driven gene expression by modulating the ER/FOXA1 cistrome, by interacting with it, and by modulating the expression of members of the ER transcriptional complex, providing multiple mechanisms by which ELF5 can drive endocrine resistance.
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Registered trials
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.