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dc.contributor.author Molina, Luis
dc.contributor.author Bustamante, Felipe
dc.contributor.author Ortloff, Alexander
dc.contributor.author Ramos, Iraidi
dc.contributor.author Ehrenfeld, Pamela
dc.contributor.author Figueroa, Carlos D.
dc.date.accessioned 2024-09-26T00:26:45Z
dc.date.available 2024-09-26T00:26:45Z
dc.date.issued 2020-09-30
dc.identifier.issn 1664-2392
dc.identifier.uri https://repositorio.uss.cl/handle/uss/12171
dc.description Publisher Copyright: © Copyright © 2020 Molina, Bustamante, Ortloff, Ramos, Ehrenfeld and Figueroa.
dc.description.abstract GPER-1 is a novel membrane sited G protein-coupled estrogen receptor. Clinical studies have shown that patients suffering an estrogen receptor α (ERα)/GPER-1 positive, breast cancer have a lower survival rate than those who have developed ERα-positive/GPER-1 negative tumors. Moreover, absence of GPER-1 improves the prognosis of patients treated with tamoxifen, the most used selective estrogen receptor modulator to treat ERα-positive breast cancer. MCF-7 breast cancer cells were continuously treated with 1,000 nM tamoxifen for 7 days to investigate its effect on GPER-1 protein expression, cell proliferation and intracellular [Ca2+]i mobilization, a key signaling pathway. Breast cancer cells continuously treated with tamoxifen, exhibited a robust [Ca2+]i mobilization after stimulation with 1,000 nM tamoxifen, a response that was blunted by preincubation of cells with G15, a commercial GPER-1 antagonist. Continuously treated cells also displayed a high [Ca2+]i mobilization in response to a commercial GPER-1 agonist (G1) and to estrogen, in a magnitude that doubled the response observed in untreated cells and was almost completely abolished by G15. Proliferation of cells continuously treated with tamoxifen and stimulated with 2,000 nM tamoxifen, was also higher than that observed in untreated cells in a degree that was approximately 90% attributable to GPER-1. Finally, prolonged tamoxifen treatment did not increase ERα expression, but did overexpress the kinin B1 receptor, another GPCR, which we have previously shown is highly expressed in breast tumors and increases proliferation of breast cancer cells. Although we cannot fully extrapolate the results obtained in vitro to the patients, our results shed some light on the occurrence of drug resistance in breast cancer patients who are ERα/GPER-1 positive, have been treated with tamoxifen and display low survival rate. Overexpression of kinin B1 receptor may explain the increased proliferative response observed in breast tumors under continuous treatment with tamoxifen. en
dc.language.iso eng
dc.relation.ispartof vol. 11 Issue: Pages:
dc.source Frontiers in Endocrinology
dc.title Continuous Exposure of Breast Cancer Cells to Tamoxifen Upregulates GPER-1 and Increases Cell Proliferation en
dc.type Artículo
dc.identifier.doi 10.3389/fendo.2020.563165
dc.publisher.department Facultad de Medicina y Ciencia


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