ArticleMolecular nutrition & food research2013
In vitro mechanism for downregulation of ER-α expression by epigallocatechin gallate in ER+/PR+ human breast cancer cells.
Article in Molecular nutrition & food research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- An Update on Antitumor Efficacy of Catechins: From Molecular Mechanisms to Clinical Applications.Food science & nutrition · 2025Review
- Review
- A systematic review and meta-analysis of the effects of green tea extracts and polyphenols in female hormone-dependent cancers for benefit-risk evaluation.Frontiers in oncology · 2025Article
- Anticancer Therapeutic Effects of Green Tea Catechins (GTCs) When Integrated with Antioxidant Natural Components.Molecules (Basel, Switzerland) · 2023Review
- Resveratrol, Epigallocatechin Gallate and Curcumin for Cancer Therapy: Challenges from Their Pro-Apoptotic Properties.Life (Basel, Switzerland) · 2023Review
- Combination Therapy Using Polyphenols: An Efficient Way to Improve Antitumoral Activity and Reduce Resistance.International journal of molecular sciences · 2022Review
- The Mediterranean Diet as a Source of Natural Compounds: Does It Represent a Protective Choice against Cancer?Pharmaceuticals (Basel, Switzerland) · 2021Article
- Nutraceuticals in the Mediterranean Diet: Potential Avenues for Breast Cancer Treatment.Nutrients · 2021Review
- Co-Adjuvant Therapy Efficacy of Catechin and Procyanidin B2 with Docetaxel on Hormone-Related Cancers In Vitro.International journal of molecular sciences · 2021Article
- Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome.International journal of molecular sciences · 2021Article
- Alternaria toxins as casein kinase 2 inhibitors and possible consequences for estrogenicity: a hybrid in silico/in vitro study.Archives of toxicology · 2020Article
- ERα36 is an effective target of epigallocatechin-3-gallate in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2019Article
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
- Pathogenesis of Keratoconus: The intriguing therapeutic potential of Prolactin-inducible protein.Progress in retinal and eye research · 2018Review
- Mechanistic evaluation of phytochemicals in breast cancer remedy: current understanding and future perspectives.RSC advances · 2018Review
- Effects of green tea on miRNA and microbiome of oral epithelium.Scientific reports · 2018Article
- Polyphenols as Promising Drugs against Main Breast Cancer Signatures.Antioxidants (Basel, Switzerland) · 2017Review
- Human in vitro Model Reveals the Effects of Collagen Cross-linking on Keratoconus Pathogenesis.Scientific reports · 2017Article
- The regulation of steroid receptors by epigallocatechin-3-gallate in breast cancer cells.Breast cancer (Dove Medical Press) · 2017Article
- Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
scopeExposure of the breast to estrogens and other sex hormones is an important cancer risk factor and estrogen receptor downregulators are attracting significant clinical interest. Epigallocatechin gallate (EGCG), a polyphenolic compound found in green tea, has gained considerable attention for its antitumor properties. Here we aimed to investigate the molecular mechanisms through which EGCG regulates ER-α expression in ER+ PR+ breast cancer cells. MATERIAL AND
methodsWestern blotting analysis, real-time PCR, and transient transfections of deletion fragments of the ER-α gene promoter show that EGCG downregulates ER-α protein, mRNA, and gene promoter activity with a concomitant reduction of ER-α genomic and nongenomic signal. These events occur through p38(MAPK) /CK2 activation, causing the release from Hsp90 of progesterone receptor B (PR-B) and its consequent nuclear translocation as evidenced by immunofluorescence studies. EMSA, and ChIP assay reveal that, upon EGCG treatment, PR-B is recruited at the half-PRE site on ER-α promoter. This is concomitant with the formation of a corepressor complex containing NCoR and HDAC1 while RNA polymerase II is displaced. The events are crucially mediated by PR-B isoform, since they are abrogated with PR-B siRNA.
conclusionOur data provide evidence for a mechanism by which EGCG downregulates ER-α and explains the inhibitory action of EGCG on the proliferation of ER+ PR+ cancer cells tested. We suggest that the EGCG/PR-B signaling should be further exploited for clinical approach.
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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.