ArticleMolecular carcinogenesis2013
Endocrine disrupting chemicals promote the growth of ovarian cancer cells via the ER-CXCL12-CXCR4 signaling axis.
Article in Molecular carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 60 citations in OpenAlex.
- Exposures to Drinking Water Contaminants in Community Water Systems and Risk of Ovarian Cancer in the California Teachers Study Cohort.Environmental health perspectives · 2026Article
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- A mechanistic study of bisphenol a exposure on asthma through integrating clinical research, network toxicology, machine learning, and multi-omics.Frontiers in pharmacology · 2026Article
- Bisphenol A and ovarian cancer: emerging evidence and potential biological mechanisms.Frontiers in cell and developmental biology · 2026Review
- AOH induces oxidative stress and DNA damage in ovarian cancer cells via modulation of GPER1 and HIF1α/PI3K/CLDNs signaling pathway.Scientific reports · 2025Article
- Bisphenol A in the Urine: Association with Urinary Creatinine, Impaired Kidney Function, Use of Plastic Food and Beverage Storage Products but Not with Serum Anti-Müllerian Hormone in Ovarian Malignancies.International journal of molecular sciences · 2025Article
- Impact of Endocrine Disruptors on the Genitourinary Tract.Journal of xenobiotics · 2024Review
- In Vitro and Vivo Identification, Metabolism and Action of Xenoestrogens: An Overview.International journal of molecular sciences · 2021Review
- Serum concentration of bisphenol A in elderly cats and its association with clinicopathological findings.Journal of feline medicine and surgery · 2021Article
- Carcinogenic effects of bisphenol A in breast and ovarian cancers.Oncology letters · 2020Review
- Review
- Article
- Bisphenol A (BPA) the mighty and the mutagenic.Toxicology reports · 2018Review
- miR-9 functions as a tumor inhibitor of cell proliferation in epithelial ovarian cancer through targeting the SDF-1/CXCR4 pathway.Experimental and therapeutic medicine · 2017Article
- Environmental Factors Impacting Bone-Relevant Chemokines.Frontiers in endocrinology · 2017Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals.Endocrine reviews · 2015Review
- Endocrine disrupting chemicals (EDCs) and female cancer: Informing the patients.Reviews in endocrine & metabolic disorders · 2015Review
- Akt2/ZEB2 may be a biomarker for exfoliant cells in ascitic fluid in advanced grades of serous ovarian carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis.Carcinogenesis · 2015Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The majority of ovarian cancers over-express the estrogen receptor (ERα) and grow in response to estrogens. We previously demonstrated that ER induction of the chemokine CXCL12 (stromal cell-derived factor-1) is required for estradiol (E2)-stimulated proliferation of human ovarian carcinoma cells. In the current study, we report that known "endocrine disrupting chemicals" (EDCs) display mitogenic activities in ovarian cancer cells via their ability to activate the ER and upregulate CXCL12 expression. Notably, the EDCs genistein, bisphenol A and HPTE stimulated both cell proliferation and induction of CXCL12 mRNA and protein in a manner comparable to estradiol. The effects were completely attenuated by the ER antagonist ICI 182,780, revealing that observed activities of these agents were receptor-mediated. In cell proliferation assays, the mitogenic effects of estradiol and EDCs were obviated by siRNAs targeting CXCL12 and restored upon addition of exogenous CXCL12. Furthermore, an inhibitor to the CXCL12 receptor CXCR4 completely attenuated growth-stimulatory effects of E2 and EDCs. These studies highlight a potential role of EDCs possessing estrogenic activities in the etiology of ovarian cancer. Moreover, they suggest that the ER-CXCL12-CXCR4 signaling axis may represent a promising target for development of therapeutics for ER+ ovarian cancers.
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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.