ArticlePLoS biology2012
ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.
Article in PLoS biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 82 citations in OpenAlex.
- Clinical and genomic analysis of a randomised phase II study evaluating anastrozole and fulvestrant in postmenopausal patients treated for large operable or locally advanced hormone-receptor-positive breast cancer.British journal of cancer · 2015Trial
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- Integrated Multiomic Profiling Identifies BRD8/EP400 as a Pivotal Chromatin Module Mediating Anti-HER2 Response in HR+/HER2+ Breast Cancer.Cancer research · 2026Article
- The Human Male Mammary Gland has Similar Epithelial Populations to Female but Distinct Composition and Transcriptional Properties.bioRxiv : the preprint server for biology · 2026Article
- A weight-sharing Bayesian neural network for consistent feature selection with applications in cancer gene expression data.BMC bioinformatics · 2026Article
- Molecular profiling of the Basal-like intrinsic molecular subtype in primary ER-positive HER2-negative breast cancer.Genome medicine · 2025Article
- Classification of Breast Cancer Through the Perspective of Cell Identity Models.Advances in experimental medicine and biology · 2025Review
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- GWAS-significant loci and severe COVID-19: analysis of associations, link with thromboinflammation syndrome, gene-gene, and gene-environmental interactions.Frontiers in genetics · 2024Article
- 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
- ELF5 is a potential respiratory epithelial cell-specific risk gene for severe COVID-19.Nature communications · 2022Article
- Review
- Review
- 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
- Acetylation of ELF5 suppresses breast cancer progression by promoting its degradation and targeting CCND1.NPJ precision oncology · 2021Article
- Immune microenvironment in different molecular subtypes of ductal breast carcinoma.Breast cancer research and treatment · 2021Review
- Nuclear Mechanisms Involved in Endocrine Resistance.Frontiers in oncology · 2021Review
- Systems biology comprehensive analysis on breast cancer for identification of key gene modules and genes associated with TNM-based clinical stages.Scientific reports · 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
30 authors at 7 institutions in 2 countries.
Funding
Abstract
We have previously shown that during pregnancy the E-twenty-six (ETS) transcription factor ELF5 directs the differentiation of mammary progenitor cells toward the estrogen receptor (ER)-negative and milk producing cell lineage, raising the possibility that ELF5 may suppress the estrogen sensitivity of breast cancers. To test this we constructed inducible models of ELF5 expression in ER positive luminal breast cancer cells and interrogated them using transcript profiling and chromatin immunoprecipitation of DNA followed by DNA sequencing (ChIP-Seq). ELF5 suppressed ER and FOXA1 expression and broadly suppressed ER-driven patterns of gene expression including sets of genes distinguishing the luminal molecular subtype. Direct transcriptional targets of ELF5, which included FOXA1, EGFR, and MYC, accurately classified a large cohort of breast cancers into their intrinsic molecular subtypes, predicted ER status with high precision, and defined groups with differential prognosis. Knockdown of ELF5 in basal breast cancer cell lines suppressed basal patterns of gene expression and produced a shift in molecular subtype toward the claudin-low and normal-like groups. Luminal breast cancer cells that acquired resistance to the antiestrogen Tamoxifen showed greatly elevated levels of ELF5 and its transcriptional signature, and became dependent on ELF5 for proliferation, compared to the parental cells. Thus ELF5 provides a key transcriptional determinant of breast cancer molecular subtype by suppression of estrogen sensitivity in luminal breast cancer cells and promotion of basal characteristics in basal breast cancer cells, an action that may be utilised to acquire antiestrogen 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.