ArticleCarcinogenesis2017
Bisphenol A activates EGFR and ERK promoting proliferation, tumor spheroid formation and resistance to EGFR pathway inhibition in estrogen receptor-negative inflammatory breast cancer cells.
Article in Carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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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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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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Unlocking the Potential of Spheroids in Personalized Medicine: A Systematic Review of Seeding Methodologies.International journal of molecular sciences · 2025Pooled it
- Elucidating the molecular mechanisms linking bisphenol A to breast cancer: an integrated study of bioinformatics, machine learning, and molecular docking.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Article
- More than alternative estrogen receptors: the emerging role of GPER-1 and ERα36 in breast cancer.Exploration of targeted anti-tumor therapy · 2026Review
- Bisphenol A (BPA) Modifies Cancer Signaling Pathways: A Neglected Global Health Threat.Journal of xenobiotics · 2025Review
- Epidermal growth factor receptor in placental health and disease: pathways, dysfunction, and chemical disruption.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Reduced bioenergetics and mitochondrial fragmentation in human primary cytotrophoblasts induced by an EGFR-targeting chemical mixture.Chemosphere · 2024Article
- Chemical mixture that targets the epidermal growth factor pathway impairs human trophoblast cell functions.Toxicology and applied pharmacology · 2024Article
- Cumulative environmental quality is associated with breast cancer incidence differentially by summary stage and urbanicity.Scientific reports · 2023Article
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Combined Toxic Effects of BPA and Its Two Analogues BPAP and BPC in a 3D HepG2 Cell Model.Molecules (Basel, Switzerland) · 2023Article
- Adverse (geno)toxic effects of bisphenol A and its analogues in hepatic 3D cell model.Environment international · 2023Article
- Bisphenol S Increases Cell Number and Stimulates Migration of Endometrial Epithelial Cells.Journal of the ASEAN Federation of Endocrine Societies · 2023Article
- Multimodal interactions of drugs, natural compounds and pollutants with the gut microbiota.Nature reviews. Microbiology · 2022Review
- Bisphenol S Impairs Invasion and Proliferation of Extravillous Trophoblasts Cells by Interfering with Epidermal Growth Factor Receptor Signaling.International journal of molecular sciences · 2022Article
- Bisphenol A Promotes the Progression of Colon Cancer Through Dual-Targeting of NADPH Oxidase and Mitochondrial Electron-Transport Chain to Produce ROS and Activating HIF-1α/VEGF/PI3K/AKT Axis.Frontiers in endocrinology · 2022Article
- Anti-neoplastic characteristics and potential targets of calycosin against bisphenol A-related osteosarcoma: bioinformatics analysis.Bioengineered · 2021Article
- Identification of harmine and β-carboline analogs from a high-throughput screen of an approved drug collection; profiling as differential inhibitors of DYRK1A and monoamine oxidase A and for in vitro and in vivo anti-cancer studies.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2021Article
- Using the Key Characteristics of Carcinogens to Develop Research on Chemical Mixtures and Cancer.Environmental health perspectives · 2021Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Emerging evidence from epidemiological studies suggests a link between environmental chemical exposure and progression of aggressive breast cancer subtypes. Of all clinically distinct types of breast cancers, the most lethal phenotypic variant is inflammatory breast cancer (IBC). Overexpression of epidermal growth factor receptors (EGFR/HER2) along with estrogen receptor (ER) negativity is common in IBC tumor cells, which instead of a solid mass present as rapidly proliferating diffuse tumor cell clusters. Our previous studies have demonstrated a role of an adaptive response of increased antioxidants in acquired resistance to EGFR-targeting drugs in IBC. Environmental chemicals are known to induce oxidative stress resulting in perturbations in signal transduction pathways. It is therefore of interest to identify chemicals that can potentiate EGFR mitogenic effects in IBC. Herein, we assessed in ER-negative IBC cells a subset of chemicals from the EPA ToxCast set for their effect on EGFR activation and in multiple cancer phenotypic assays. We demonstrated that endocrine-disrupting chemicals such as bisphenol A (BPA) and 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane can increase EGFR/ERK signaling. BPA also caused a corresponding increase in expression of SOD1 and anti-apoptotic Bcl-2, key markers of antioxidant and anti-apoptotic processes. BPA potentiated clonogenic growth and tumor spheroid formation in vitro, reflecting IBC-specific pathological characteristics. Furthermore, we identified that BPA was able to attenuate the inhibitory effect of an EGFR targeted drug in a longer-term anchorage-independent growth assay. These findings provide a potential mechanistic basis for environmental chemicals such as BPA in potentiating a hyperproliferative and death-resistant phenotype in cancer cells by activating mitogenic pathways to which the tumor cells are addicted for survival.
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Registered trials
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.