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The present study aimed to reveal the sensitivity of GPR30 to gefitinib in non-small cell lung cancer (NSCLC) cells.<\/jats:p>\n                  <jats:p>Methods: Cell viability and proliferation were detected using cell counting kit 8 and 5-ethynyl-2'-deoxyuridine assays, respectively. Western blotting and quantitative real-time reverse transcription PCR were used to detect GPR30 or epithelial-mesenchyme transition (EMT)-related mRNA and protein expression.<\/jats:p>\n                  <jats:p>Results: The results showed that GPR30 expression is associated with gefitinib sensitivity. G15, as a GPR30 antagonist, reduced GPR30 expression. We chose the maximum concentration of G15 with minimal cytotoxicity to detect cell viability after combined treatment with gefitinib in NSCLC cells, which indicated that G15 could increase sensitivity to gefitinib. However, the effect of G15 on gefitinib sensitivity disappeared after treatment with a small interfering RNA targeting GPR30. Further research showed that G15 or GPR30 siRNA treatment could upregulate E-cadherin and downregulate vimentin levels.<\/jats:p>\n                  <jats:p>Conclusion: Taken together, these data suggested that G15 could enhance NSCLC sensitivity to gefitinib by inhibition of GPR30 and EMT.<\/jats:p>","DOI":"10.1177\/03946320231210737","type":"journal-article","created":{"date-parts":[[2023,10,27]],"date-time":"2023-10-27T15:45:52Z","timestamp":1698421552000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Inhibition of GPR30 sensitized gefitinib to NSCLC cells via regulation of epithelial-mesenchymal transition"],"prefix":"10.1177","volume":"37","author":[{"given":"Xiaomin","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Pharmacy, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 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