ArticleNature communications2015
Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 123 citations in OpenAlex.
- A randomized phase II trial of nab-paclitaxel with or without mifepristone for advanced triple-negative breast cancer.Breast cancer research and treatment · 2025Trial
- Signaling Under Stress: Targeting the Glucocorticoid Receptor in Cancer.Cancer research · 2026Review
- How post-translational modifications impact glucocorticoid receptor function in human pathologies.Cell communication and signaling : CCS · 2026Review
- Identification and validation of five hypoxia- and immune-related hub targets in atrial fibrillation.Journal of cardiothoracic surgery · 2026Article
- Decoding drug-responsive cell subpopulations in triple-negative breast cancer using single-cell multiomics.iScience · 2026Article
- Article
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 2026Review
- How fasting boosts breast cancer therapy.Nature · 2026Article
- WTAP-mediated mScience China. Life sciences · 2025Article
- Levonorgestrel-induced modulation of triple negative breast cancer proliferation via glucocorticoid receptor.3 Biotech · 2025Article
- Midkine: A Cancer Biomarker Candidate and Innovative Therapeutic Approaches.European journal of breast health · 2024Article
- Association between pretreatment emotional distress and immune checkpoint inhibitor response in non-small-cell lung cancer.Nature medicine · 2024Observational
- Oxidative Stress in Breast Cancer: A Biochemical Map of Reactive Oxygen Species Production.Current issues in molecular biology · 2024Review
- PRMT5 triggers glucocorticoid-induced cell migration in triple-negative breast cancer.Life science alliance · 2023Article
- Glucocorticoid Receptor and Ovarian Cancer: From Biology to Therapeutic Intervention.Biomolecules · 2023Review
- Context-Dependent Role of Glucocorticoid Receptor Alpha and Beta in Breast Cancer Cell Behaviour.Cells · 2023Article
- The Tumor Coagulome as a Transcriptional Target and a Potential Effector of Glucocorticoids in Human Cancers.Cancers · 2023Article
- Krüppel-like factor 9 (KLF9) links hormone dysregulation and circadian disruption to breast cancer pathogenesis.Cancer cell international · 2023Article
- Nuclear Receptor Imaging In Vivo-Clinical and Research Advances.Journal of the Endocrine Society · 2023Review
- Glucocorticoid regulation of cancer development and progression.Frontiers in endocrinology · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Glucocorticoids (GCs) have been widely used as coadjuvants in the treatment of solid tumours, but GC treatment may be associated with poor pharmacotherapeutic response or prognosis. The genomic action of GC in these tumours is largely unknown. Here we find that dexamethasone (Dex, a synthetic GC)-regulated genes in triple-negative breast cancer (TNBC) cells are associated with drug resistance. Importantly, these GC-regulated genes are aberrantly expressed in TNBC patients and are associated with unfavourable clinical outcomes. Interestingly, in TNBC cells, Compound A (CpdA, a selective GR modulator) only regulates a small number of genes not involved in carcinogenesis and therapy resistance. Mechanistic studies using a ChIP-exo approach reveal that Dex- but not CpdA-liganded glucocorticoid receptor (GR) binds to a single glucocorticoid response element (GRE), which drives the expression of pro-tumorigenic genes. Our data suggest that development of safe coadjuvant therapy should consider the distinct genomic function between Dex- and CpdA-liganded GR.
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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.