ArticleNature cell biology2020
Enhancer reprogramming driven by high-order assemblies of transcription factors promotes phenotypic plasticity and breast cancer endocrine resistance.
Article in Nature cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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.
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Who cites it
100 citing papers in PubMed, 132 citations in OpenAlex.
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
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- Nanoclustering of a plant transcription factor enables strong yet specific DNA binding.Science advances · 2026Article
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- A transient epithelial plasticity state defines the developmental window for uterine gland specification.bioRxiv : the preprint server for biology · 2026Article
- Transcriptionally Informed Nucleosome Profiling of Circulating Cell-Free DNA Predicts Breast Cancer Recurrence.Cancer research communications · 2026Article
- Endocrine therapy-specific lineage and partial epithelial-mesenchymal reprogramming defines divergent resistant cell-states in ER+ breast cancer.bioRxiv : the preprint server for biology · 2026Article
- BCR::ABL1-Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B-ALL Cells to Enhancer-Targeting Drugs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026Review
- The GATA3-RFPL3-ASK1 axis suppresses breast cancer growth and lung metastasis.Apoptosis : an international journal on programmed cell death · 2026Article
- Targeting pre-existing club-like cells in prostate cancer potentiates androgen deprivation therapy.EMBO molecular medicine · 2026Article
- KIF18B Is Essential for Lung Adenocarcinoma Progression Through the E2F Transcriptional Network.International journal of molecular sciences · 2026Article
- Mechanisms and implications of epithelial cell plasticity in the bladder.Nature reviews. Urology · 2026Review
- Navigating the complexities of epigenetic dysregulation in breast cancer and its implication in therapeutic interventions: a comprehensive overview.Molecular and cellular biochemistry · 2026Review
- Targeting MED23 inhibits hepatocellular carcinoma development by suppressing compensatory proliferation and facilitating ROS-mediated cell death.Cell death & disease · 2025Article
- Review
- Genomic Crosstalk Between Nuclear Receptors in Hormone-dependent Cancers.Endocrinology · 2025Review
- SOX9 drives a stem-like transcriptional state and platinum resistance in high-grade serous ovarian cancer.The Journal of clinical investigation · 2025Article
- Integrated analysis of differential intra-chromosomal community interactions: A study of breast cancer.Artificial intelligence in medicine · 2025Article
- Endogenous Real Time Imaging Reveals Dynamic Chromosomal Mobility During Ligand-Mediated Transcriptional Burst Events.bioRxiv : the preprint server for biology · 2025Article
40 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
Acquired therapy resistance is a major problem for anticancer treatment, yet the underlying molecular mechanisms remain unclear. Using an established breast cancer cellular model, we show that endocrine resistance is associated with enhanced phenotypic plasticity, indicated by a general downregulation of luminal/epithelial differentiation markers and upregulation of basal/mesenchymal invasive markers. Consistently, similar gene expression changes are found in clinical breast tumours and patient-derived xenograft samples that are resistant to endocrine therapies. Mechanistically, the differential interactions between oestrogen receptor α and other oncogenic transcription factors, exemplified by GATA3 and AP1, drive global enhancer gain/loss reprogramming, profoundly altering breast cancer transcriptional programs. Our functional studies in multiple culture and xenograft models reveal a coordinated role of GATA3 and AP1 in re-organizing enhancer landscapes and regulating cancer phenotypes. Collectively, our study suggests that differential high-order assemblies of transcription factors on enhancers trigger genome-wide enhancer reprogramming, resulting in transcriptional transitions that promote tumour phenotypic plasticity and therapy 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.