ArticleOncotarget2018
ERβ alters the chemosensitivity of luminal breast cancer cells by regulating p53 function.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Estrogen receptor β stimulation as a possible novel therapeutic target for cutaneous T-cell lymphoma.Blood advances · 2025Article
- Interaction between Estrogen Receptors and p53: A Broader Role for Tamoxifen?Endocrinology · 2025Review
- The expression and clinical significance of ERβ/ERα in ovarian cancer: can we predict the effectiveness of platinum plus taxane therapy?Irish journal of medical science · 2022Article
- In Vitro Evaluation of the Antioxidant Activity and Chemopreventive Potential in Human Breast Cancer Cell Lines of the Standardized Extract Obtained from the Aerial Parts of Zigzag Clover (Pharmaceuticals (Basel, Switzerland) · 2022Article
- Estrogen Receptor β-Mediated Inhibition of Actin-Based Cell Migration Suppresses Metastasis of Inflammatory Breast Cancer.Cancer research · 2021Article
- Moonlight human ribosomal protein L13a downregulation is associated with p53 and HER2/neu expression in breast cancer.Journal of applied biomedicine · 2020Article
- Optimized immunohistochemical detection of estrogen receptor beta using two validated monoclonal antibodies confirms its expression in normal and malignant breast tissues.Breast cancer research and treatment · 2020Article
- The role of estrogen receptor beta in breast cancer.Biomarker research · 2020Review
- ERβ modulates genistein's cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway.Molecular and cellular biochemistry · 2019Article
- Estrogen receptor beta enhances chemotherapy response of GBM cells by down regulating DNA damage response pathways.Scientific reports · 2019Article
- Overexpression Of ERβ Participates In The Progression Of Liver Cancer Via Inhibiting The Notch Signaling Pathway.OncoTargets and therapy · 2019Article
- Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence.Cancers · 2018Review
- Histone deacetylase inhibitors enhance estrogen receptor beta expression and augment agonist-mediated tumor suppression in glioblastoma.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptor α (ERα)-positive breast cancers tend to develop resistance to both endocrine therapy and chemotherapy. Despite recent progress in defining molecular pathways that confer endocrine resistance, the mechanisms that regulate chemotherapy response in luminal tumors remain largely elusive. Luminal tumors often express wild-type p53 that is a major determinant of the cellular DNA damage response. Similar to p53, the second ER subtype, ERβ, has been reported to inhibit breast tumorigenesis by acting alone or in collaboration with p53. However, a synergistic mechanism of action has not been described. Here, we suggest that ERβ relies on p53 to elicit its tumor repressive actions in ERα-positive breast cancer cells. Upregulation of ERβ and treatment with ERβ agonists potentiates the tumor suppressor function of p53 resulting in decreased survival. This effect requires molecular interaction between the two proteins that disrupts the inhibitory action of ERα on p53 leading to increased transcriptional activity of p53. In addition, we show that the same interaction alters the chemosensitivity of endocrine-resistant cells including their response to tamoxifen therapy. Our results suggest a collaboration of ERβ and p53 tumor suppressor activity in breast cancer cells that indicates the importance of ligand-regulated ERβ as a tool to target p53 activity and improve the clinical management of resistant disease.
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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.