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• W4280625883 abstract "Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) have a good clinical efficacy in lung adenocarcinoma harboring activating-mutation EGFR. Such EGFR mutations are more frequently observed in women and non-smokers. EGFR mutations are frequently reported to correlate with estrogen receptor (ER) α and/or β-expressions in lung adenocarcinoma. However, the role of GPER1, a novel G-protein-coupled estrogen receptor, in the estrogen signaling pathway and the association between its expression and EGFR mutation in lung adenocarcinoma are less well understood. Here, we aimed to examine ERα, Erβ, and GPER1 expressions, and to analyze their roles in the mechanism of EGFR-TKIs resistance in lung adenocarcinoma. We report an enhanced cytoplasmic expression of GPER1 in tissue samples. The nuclear GPER1 positively correlated with ER expression while the nuclear and also cytoplasmic expressing GPER1 negatively correlated with ER expression. Further, TKI resistance results in higher cytoplasmic GPER1 expression and decreased ER and nuclear GPER1 expression with evidence for GPER1 translocation to cell surface during the resistance. GPER1 itself is capable of regulating ER expression with concomitant regulation of MAPK signaling, and co-inhibition of GPER1 and ERs attenuates ERK1/2 and Akt phosphorylation. The results were also verified in vivo in mice where GPER1 silencing slowed tumor progression which was further potentiated by gefitinib." @default.
• W4280625883 created "2022-05-22" @default.
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• W4280625883 date "2022-05-18" @default.
• W4280625883 modified "2023-10-01" @default.
• W4280625883 title "Role of GPER1 in the Mechanism of EGFR-TKIs Resistance in Lung Adenocarcinoma" @default.
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• W4280625883 doi "https://doi.org/10.3389/fonc.2022.869113" @default.
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