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Estrogen receptor  β  (ER β ) can regulate cellular signaling through non-genomic mechanisms, potentially promoting resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). However, the mechanisms underlying the ER β -mediated resistance to EGFR TKIs remain poorly understood. In this study, we investigated the role of the interaction between ER β 1 and ER β 5 in non-genomic signaling in lung adenocarcinoma. We established PC9 cell lines stably overexpressing ER β 1 or ER β 1/ER β 5. Immunofluorescence revealed that ER β 5 overexpression partly retained ER β 1 in the cytoplasm. Immunoblotting analyses revealed that EGFR pathway activation levels were higher in PC9/ER β 1/5 cells than those in PC9/ER β 1 or control PC9 cells. In the presence of estradiol, PI3K/AKT/mTOR pathway activation levels were higher in ER β 1/5-expressing cells than those in ER β 1-expressing cells. Additionally, PC9/ER β 1/5 cells were less prone to the cytotoxic and pro-apoptotic effects of gefitinib compared with PC9/ER β 1 or control PC9 cells. Cytoplasmic ER β 1 was associated with poor progression-free survival in lung cancer patients treated with EGFR TKIs. These results suggest that cytoplasmic ER β 1 was responsible for EGFR TKI resistance slightly through non-genomic mechanism in EGFR mutant lung adenocarcinoma.

frontiers in oncology

Estrogen Receptor β1 Expression Patterns Have Different Effects on Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors’ Treatment Response in Epidermal Growth Factor Receptor Mutant Lung Adenocarcinoma