ArticleInternational journal of oncology2019
Arsenic‑induced BRCA1 CpG promoter methylation is associated with the downregulation of ERα and resistance to tamoxifen in MCF7 breast cancer cells and mouse mammary tumor xenografts.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Pooled it
- Article
- Arsenic induced Hippo pathway dysregulation linked to hTERT hypo-methylation in breast cancer patients.Frontiers in epigenetics and epigenomics · 2026Article
- DNA methylation signatures of arsenic exposure and obesity.Environmental epigenetics · 2025Article
- Crosstalk of methylation and tamoxifen in breast cancer (Review).Molecular medicine reports · 2024Review
- Arsenic and Human Health: New Molecular Mechanisms For Arsenic-Induced Cancers.Current pollution reports · 2023Article
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Effect of PINK1 and Parkin gene silencing on sodium arsenite-induced mitophagy in normal rat liver cells (BRL-3A).Toxicology research · 2022Article
- Sodium arsenite-mediated upregulation of circDHX34 promotes apoptosis in hormone-independent breast cancer cells by regulating apoptotic genes.Environmental science and pollution research international · 2022Article
- Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins.Seminars in cancer biology · 2021Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- ELOVL2: a novel tumor suppressor attenuating tamoxifen resistance in breast cancer.American journal of cancer research · 2021Article
- Health Effects Associated With Pre- and Perinatal Exposure to Arsenic.Frontiers in genetics · 2021Review
- Effects of arsenic and heavy metals on metabolic pathways in cells of human origin: Similarities and differences.Toxicology reports · 2021Article
- Inorganic arsenic promotes luminal to basal transition and metastasis of breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- ERα, A Key Target for Cancer Therapy: A Review.OncoTargets and therapy · 2020Review
- Effect, sensitivity, specificity and accuracy of ultrasonic assessment of axillary lymph node-negative breast cancer.Pakistan journal of medical sciencesArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
A significant percentage (~30%) of estrogen receptor‑α (ERα)‑positive tumors become refractory to endocrine therapies; however, the mechanisms responsible for this resistance remain largely unknown. Chronic exposure to arsenic through foods and contaminated water has been linked to an increased incidence of several tumors and long‑term health complications. Preclinical and population studies have indicated that arsenic exposure may interfere with endocrine regulation and increase the risk of breast tumorigenesis. In this study, we examined the effects of sodium arsenite (NaAsIII) exposure in ERα‑positive breast cancer cells in vitro and in mammary tumor xenografts. The results revealed that acute (within 4 days) and long‑term (10 days to 7 weeks) in vitro exposure to environmentally relevant doses reduced breast cancer 1 (BRCA1) and ERα expression associated with the gain of cyclin D1 (CCND1) and folate receptor 1 (FOLR1), and the loss of methylenetetrahydrofolate reductase (MTHFR) expression. Furthermore, long‑term exposure to NaAsIII induced the proliferation and compromised the response of MCF7 cells to tamoxifen (TAM). The in vitro exposure to NaAsIII induced BRCA1 CpG methylation associated with the increased recruitment of DNA methyltransferase 1 (DNMT1) and the loss of RNA polymerase II (PolII) at the BRCA1 gene. Xenografts of NaAsIII‑preconditioned MCF7 cells (MCF7NaAsIII) into the mammary fat pads of nude mice produced a larger tumor volume compared to tumors from control MCF7 cells and were more refractory to TAM in association with the reduced expression of BRCA1 and ERα, CpG hypermethylation of estrogen receptor 1 (ESR1) and BRCA1, and the increased expression of FOLR1. These cumulative data support the hypothesis that exposure to AsIII may contribute to reducing the efficacy of endocrine therapy against ERα‑positive breast tumors by hampering the expression of ERα and BRCA1 via CpG methylation, respectively of ESR1 and BRCA1.
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Registered trials
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