ArticleCell reports2022
Estrone, the major postmenopausal estrogen, binds ERa to induce SNAI2, epithelial-to-mesenchymal transition, and ER+ breast cancer metastasis.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Menopause and neurological disorders: a roadmap for research.Nature reviews. Neurology · 2026Review
- Exploring the Role of HSD17B2 in Colorectal Cancer Through Bioinformatic Analysis: Preliminary Insights for Prognostic Evaluation.International journal of molecular sciences · 2026Article
- Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women.Nature aging · 2026Article
- Oestrogen changes at menopause: insights into obesity-associated breast risk and outcomes.Nature reviews. Endocrinology · 2026Review
- Differentiated Thyroid Cancer Is Associated With Sex-specific Immune Response.Journal of the Endocrine Society · 2026Article
- The Pre-metastatic Niche-related Index Reveals the Immune Signature and Immunotherapy Response in Lung Adenocarcinoma.Current medicinal chemistry · 2026Article
- Predicting preoperative axillary lymph node metastasis to guide surgical decisions in invasive breast cancer.Frontiers in oncology · 2026Article
- Silver and polystyrene nanoparticles activate oestrogen signalling via cytoplasmic oestrogen receptor.Scientific reports · 2025Article
- The influence of menstrual cycle and endometriosis on endometrial expression of epithelial-to-mesenchymal transition (EMT)-related genes.Reproductive biology and endocrinology : RB&E · 2025Article
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- Class IIa HDACs Are Important Signal Transducers with Unclear Enzymatic Activities.Biomolecules · 2025Review
- Comparison of Estrone/Estradiol Ratio and Levels in Transfeminine Individuals on Different Routes of Estradiol.Transgender health · 2025Article
- Biological functions of 5-methylcytosine RNA-binding proteins and their potential mechanisms in human cancers.Frontiers in oncology · 2025Review
- Interaction of GPER-1 with the endocrine signaling axis in breast cancer.Frontiers in endocrinology · 2025Review
- Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan.Frontiers in endocrinology · 2025Review
- The Age-Male-Albumin-Bilirubin-Platelets (aMAP) Risk Score Predicts Liver Metastasis Following Surgery for Breast Cancer in Chinese Population: A Retrospective Study.ImmunoTargets and therapy · 2024Article
- Assessment of the albumin-bilirubin score in breast cancer patients with liver metastasis after surgery.Heliyon · 2023Article
- Breast cancers as ecosystems: a metabolic perspective.Cellular and molecular life sciences : CMLS · 2023Review
- Exome sequencing identified rare recurrent copy number variants and hereditary breast cancer susceptibility.PLoS genetics · 2023Article
- Mechanisms of drug resistance in breast cancer liver metastases: Dilemmas and opportunities.Molecular therapy oncolytics · 2023Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Recent work showed that the dominant post-menopausal estrogen, estrone, cooperates with nuclear factor κB (NF-κB) to stimulate inflammation, while pre-menopausal 17β-estradiol opposes NF-κB. Here, we show that post-menopausal estrone, but not 17β-estradiol, activates epithelial-to-mesenchymal transition (EMT) genes to stimulate breast cancer metastasis. HSD17B14, which converts 17β-estradiol to estrone, is higher in cancer than normal breast tissue and in metastatic than primary cancers and associates with earlier metastasis. Treatment with estrone, but not 17β-estradiol, and HSD17B14 overexpression both stimulate an EMT, matrigel invasion, and lung, bone, and liver metastasis in estrogen-receptor-positive (ER+) breast cancer models, while HSD17B14 knockdown reverses the EMT. Estrone:ERα recruits CBP/p300 to the SNAI2 promoter to induce SNAI2 and stimulate an EMT, while 17β-estradiol:ERα recruits co-repressors HDAC1 and NCOR1 to this site. Present work reveals novel differences in gene regulation by these estrogens and the importance of estrone to ER+ breast cancer progression. Upon loss of 17β-estradiol at menopause, estrone-liganded ERα would promote ER+ breast cancer invasion and metastasis.
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