Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2026
MEHP promotes breast cancer progression via GPR30-mediated epithelial-mesenchymal transition.
СтатьяНазвание и аннотация: Перевод в очереди
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Qi Wen, Wang Jia, Wang Yunlong, Cui Jianwei, Wu Xiaotong, Ding Ziji, Jiang Tao, Liu Wanyu, Zhai Xueyu, Jin Shunzi, Ye Lin
Аннотация
PURPOSE: Mono-(2-ethylhexyl) phthalate (MEHP), the primary metabolite of di-(2-ethylhexyl) phthalate (DEHP), is a well-documented environmental endocrine disruptor with estrogen-like effects that promote the development of hormone receptor-positive tumors. G protein-coupled receptor 30 (GPR30), also known as G protein-coupled estrogen receptor 1, has emerged as a key factor in the pathogenesis and progression of hormone-dependent tumors. This study elucidates the mechanism by which MEHP promotes breast cancer development via GPR30.
METHODS: MCF-7 cells were exposed to different concentrations of MEHP, and GPR30 expression was inhibited using G15. Cell proliferation and cell cycle were assessed using the CCK-8 and flow cytometry, respectively. Cell migration and cell invasion were evaluated via scratch-wound assays and transwell migration assay. Western blotting and quantitative real-time reverse transcription PCR were performed to analyze the expression of GPR30 and epithelial-mesenchymal transition (EMT)-related mRNAs and proteins.
RESULTS: Our findings demonstrate that MEHP exposure promotes the proliferation, migration, and invasion of MCF-7 cells, while concomitantly modulating the expression of GPR30, cell cycle-related and EMT-associated mRNAs and proteins. After inhibiting GPR30, the promoting effect of MEHP on MCF-7 cell proliferation and migration decreased.
CONCLUSION: Notably, GPR30 inhibition attenuated MEHP-induced promotion of MCF-7 cell proliferation and migration through modulating the EMT process.
METHODS: MCF-7 cells were exposed to different concentrations of MEHP, and GPR30 expression was inhibited using G15. Cell proliferation and cell cycle were assessed using the CCK-8 and flow cytometry, respectively. Cell migration and cell invasion were evaluated via scratch-wound assays and transwell migration assay. Western blotting and quantitative real-time reverse transcription PCR were performed to analyze the expression of GPR30 and epithelial-mesenchymal transition (EMT)-related mRNAs and proteins.
RESULTS: Our findings demonstrate that MEHP exposure promotes the proliferation, migration, and invasion of MCF-7 cells, while concomitantly modulating the expression of GPR30, cell cycle-related and EMT-associated mRNAs and proteins. After inhibiting GPR30, the promoting effect of MEHP on MCF-7 cell proliferation and migration decreased.
CONCLUSION: Notably, GPR30 inhibition attenuated MEHP-induced promotion of MCF-7 cell proliferation and migration through modulating the EMT process.