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• W2332655319 abstract "Vol. 124, No. 4 CorrespondenceOpen AccessResponse to “Comment on ‘Effects of Atrazine on Estrogen Receptor α– and G Protein–Coupled Receptor 30–Mediated Signaling and Proliferation in Cancer Cells and Cancer-Associated Fibroblasts’” Rosamaria Lappano, Marco Pupo, and Marcello Maggiolini Rosamaria Lappano Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy Search for more papers by this author , Marco Pupo Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy Department of Cellular Biology, University of Geneva, Geneva, Switzerland Search for more papers by this author , and Marcello Maggiolini †Address correspondence to M. Maggiolini, Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy. E-mail: E-mail Address: [email protected]; E-mail Address: [email protected] Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy Search for more papers by this author Published:1 April 2016https://doi.org/10.1289/ehp.1611288AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit In their letter to the editor, Chevalier et al. wrote that a single chemical can elicit both agonist and antagonist activity through a specific receptor in different types of cancer cells, while two different chemicals can elicit opposite biological effects through the same receptor in the same cancer cell type, with the disparity lying in the receptor’s activation and in whether the action is primarily genomic versus nongenomic. Chevalier et al. also raised interesting issues regarding the level of exposure to chemicals and the cell context–dependent involvement of different transduction pathways by one chemical through the same receptor. These issues are complicated by the fact that the cumulative and final action may be triggered by a mixture of pollutants, in which the signal(s) that is/are activated by one or more compounds depend on the nature of the stimulus, its length, and the cell-related gene profile that characterizes a distinct cell context (Diamanti-Kandarakis et al. 2009).For instance, as Chevalier et al. mention, 17α-estradiol (E2) inhibited cell proliferation through estrogen receptor (ER) β in human testicular seminoma–derived JKT-1 cells and seminoma tumors, whereas bisphenol A (BPA) promoted growth responses through G protein–coupled estrogen receptor (GPER) and the activation of protein kinase A and protein kinase G transduction pathways, but not through extracellular-signal-regulated kinase (ERK) signaling (Bouskine et al. 2009). Nevertheless, the epidermal growth factor receptor/ERK transduction pathway mediated the proliferation of spermatogonial GC-1 cells induced by BPA (Sheng and Zhu 2011) in accordance with our results obtained in breast cancer cells and cancer-associated fibroblasts (Pupo et al. 2012). Chevalier et al. also cited findings on atrazine action through GPER toward the suppression of JKT-1 cell proliferation (Fénichel et al. 2013). However, as we demonstrated in our study, GPER was able, on its own, to trigger the stimulatory effects induced by atrazine in ERα-negative breast cancer cells and cancer-associated fibroblasts, whereas atrazine stimulation involved a functional cooperation between ERα and GPER in ovarian cancer cells.Although these data may appear contradictory, it is not surprising that the intricate network of ligand-activated cell responses could lead to divergent biological outcomes, as discussed above. In this regard, well-designed assays have recently shown how the differential engagement of feedback and feed-forward regulation by different ligands leads to different dynamics of pathway activity, which in turn alters cell fate (Ryu et al. 2015). One plausible network motif that drives these responses at least in part may be a transient, pulsing, or prolonged activation of certain transduction pathway(s) beyond a threshold level. Hence, different signaling frequencies and amplitudes could uncover the timescales of major network components determining ultimate cell choices (Purvis and Lahav 2013). As Chevalier et al. suggest, we need to boost research and innovative tools to better appreciate the multifaceted mechanisms of action and the biological effects of environmental contaminants on human health.The authors’ research was supported by Associazione Italiana per la Ricerca sul Cancro grant 16719/2015 and Ministero della Salute grant 67/GR-2010-2319511. The authors declare they have no actual or potential competing financial interests.ReferencesBouskine A, Nebout M, Brücker-Davis F, Benahmed M, Fènichel P. 2009. Low doses of bisphenol A promote human seminoma cell proliferation by activating PKA and PKG via a membrane G-protein-coupled estrogen receptor.Environ Health Perspect 117(7):1053-1058, doi:10.1289/ehp.080036719654912. Link, Google ScholarDiamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AMet al.. 2009. Endocrine-disrupting chemicals: an Endocrine Society scientific statement.Endocr Rev 30(4):293-342, doi:10.1210/er.2009-000219502515. Crossref, Medline, Google ScholarFénichel P, Chevalier N, Brucker-Davis F. 2013. Bisphenol A: an endocrine and metabolic disruptor.Ann Endocrinol (Paris) 74(3):211-220, doi:10.1016/j.ando.2013.04.00223796010. Crossref, Medline, Google ScholarPupo M, Pisano A, Lappano R, Santolla MF, De Francesco EM, Abonante Set al.. 2012. Bisphenol A induces gene expression changes and proliferative effects through GPER in breast cancer cells and cancer-associated fibroblasts.Environ Health Perspect 120(8):1177-1182, doi:10.1289/ehp.110452622552965. Link, Google ScholarPurvis JE, Lahav G. 2013. Encoding and decoding cellular information through signaling dynamics.Cell 152(5):945-956, doi:10.1016/j.cell.2013.02.00523452846. Crossref, Medline, Google ScholarRyu H, Chung M, Dobrzynski M, Fey D, Blum Y, Lee SSet al.. 2015. Frequency modulation of ERK activation dynamics rewires cell fate.Mol Syst Biol 11(11):838, doi:10.15252/msb.2015645826613961. Crossref, Medline, Google ScholarSheng ZG, Zhu BZ. 2011. Low concentrations of bisphenol A induce mouse spermatogonial cell proliferation by G protein–coupled receptor 30 and estrogen receptor-α.Environ Health Perspect 119(12):1775-1780, doi:10.1289/ehp.110378121813366. Link, Google ScholarFiguresReferencesRelatedDetails Vol. 124, No. 4 April 2016Metrics About Article Metrics Publication History Originally published1 April 2016Published in print1 April 2016 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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