ArticleNature communications2015
Differential epigenetic reprogramming in response to specific endocrine therapies promotes cholesterol biosynthesis and cellular invasion.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.
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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
79 citing papers in PubMed, 134 citations in OpenAlex.
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- GLYATL1 is associated with metabolic and epigenetic changes and with endocrine resistance in luminal breast cancer.Clinical epigenetics · 2026Article
- The Contribution of Cholesterol and Squalene Synthase in Cancer: Molecular Mechanisms, Lipid Rafts and Therapeutic Approaches.Medicinal research reviews · 2026Review
- Squalene synthase induces ERα expression via cholesterol supplementation to confer statin resistance in lung cancer cells.Cancer cell international · 2026Article
- Cholesterol Reprograms Oxysterol Metabolism via the LOX1/CH25H/CYP7B1 Signaling Axis to Drive Multidrug Resistance in Colorectal Cancer.Human mutation · 2026Article
- 27-Hydroxycholesterol in cancer development and drug resistance.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Super-enhancer profiling reveals ThPOK/ZBTB7B, a CD4Cellular and molecular life sciences : CMLS · 2025Article
- A histone-centric multi-omics study shows that increased H3K4 methylation sustains triple-negative breast cancer phenotypes.Nature communications · 2025Article
- Molecular Mechanisms and Therapeutic Strategies to Overcome Resistance to Endocrine Therapy and CDK4/6 Inhibitors in Advanced ER+/HER2- Breast Cancer.International journal of molecular sciences · 2025Review
- Therapeutic Potential of Simvastatin: Cellular Mechanism, Binding Energetics, and Resistance Developments.Current topics in medicinal chemistry · 2025Review
- A Functional Survey of the Regulatory Landscape of Estrogen Receptor-Positive Breast Cancer Evolution.Cancer discovery · 2024Article
- CRISPR screens in 3D tumourspheres identified miR-4787-3p as a transcriptional start site miRNA essential for breast tumour-initiating cell growth.Communications biology · 2024Article
- Novel Treatment Strategies for Hormone Receptor (HR)-Positive, HER2-Negative Metastatic Breast Cancer.Journal of clinical medicine · 2024Review
- Oestrogen receptor positive breast cancer and its embedded mechanism: breast cancer resistance to conventional drugs and related therapies, a review.Open biology · 2024Review
- Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells.Cancer discovery · 2024Article
- The breast cancer tumor microenvironment and precision medicine: immunogenicity and conditions favoring response to immunotherapy.Journal of the National Cancer Center · 2024Review
- Characters of KRT80 and its roles in neoplasms diseases.Cancer medicine · 2023Review
- DAXX drives de novo lipogenesis and contributes to tumorigenesis.Nature communications · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
Endocrine therapies target the activation of the oestrogen receptor alpha (ERα) via distinct mechanisms, but it is not clear whether breast cancer cells can adapt to treatment using drug-specific mechanisms. Here we demonstrate that resistance emerges via drug-specific epigenetic reprogramming. Resistant cells display a spectrum of phenotypical changes with invasive phenotypes evolving in lines resistant to the aromatase inhibitor (AI). Orthogonal genomics analysis of reprogrammed regulatory regions identifies individual drug-induced epigenetic states involving large topologically associating domains (TADs) and the activation of super-enhancers. AI-resistant cells activate endogenous cholesterol biosynthesis (CB) through stable epigenetic activation in vitro and in vivo. Mechanistically, CB sparks the constitutive activation of oestrogen receptors alpha (ERα) in AI-resistant cells, partly via the biosynthesis of 27-hydroxycholesterol. By targeting CB using statins, ERα binding is reduced and cell invasion is prevented. Epigenomic-led stratification can predict resistance to AI in a subset of ERα-positive patients.
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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.