2. Academic Validation
  3. MEHP promotes breast cancer progression via GPR30-mediated epithelial-mesenchymal transition

MEHP promotes breast cancer progression via GPR30-mediated epithelial-mesenchymal transition

  • Food Chem Toxicol. 2026 Jun:212:116049. doi: 10.1016/j.fct.2026.116049.
Wen Qi 1,  Jia Wang 1,  Yunlong Wang 2,  Jianwei Cui 1,  Xiaotong Wu 1,  Ziji Ding 1,  Tao Jiang 1,  Wanyu Liu 1,  Xueyu Zhai 1,  Shunzi Jin 3,  Lin Ye 4
Affiliations

Affiliations

  • 1 Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun, China.
  • 2 Department of Radiotherapy, Tumor Hospital of Jilin Province, Changchun, China.
  • 3 NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China. Electronic address: [email protected].
  • 4 Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun, China. Electronic address: [email protected].
PMID: 41780712 DOI: 10.1016/j.fct.2026.116049
Abstract

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.

Keywords

Breast cancer; EMT; GPR30; MEHP; Migration; Proliferation.

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