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Archive > Volume 30 Issue 10 > 2023,30(10):868-873. DOI:10.3872/j.issn.1007-385X.2023.10.003 Prev Next
Basic Research
Specific activation of G protein-coupled estrogen receptor regulates colorectal cancer cell migration through reactive oxygen species pathways
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Abstract:
Objective: To investigate the impact of specific activation of G protein-coupled estrogen receptors (GPER) on the migration of colorectal cancer (CRC) cells, and explore the potential underlying mechanism. Methods: CRC RKO and SW480 cells were cultured in vitro and treated with 0.5 or 1.0 μmol/L GPER-specific activator (G-1). CCK-8 method, scratch test, and Transwell test were used to detect the effects of G-1 on CRC cell proliferation and migration. The impact of G-1/G-1+ reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) treatment on the mRNA and protein expressions of E-cadherin (E-Cad) and fibronectin (FN) in RKO cells was measured using qPCR and WB. The level of ROS in RKO cells was detected by flow cytometry. Results: The migration ability of RKO and SW480 cells after the treatment with G-1 was significantly reduced (all P<0.05). Additionally, G-1 treatment significantly increased the mRNA and protein expressions of E-cad and decreased the mRNA and protein expressions of FN in the cells (all P<0.05). G-1 treatment also stimulated the production of ROS in RKO cells. However, the protein expression changes of E-cad and FN caused by G-1 were partially reversed under the action of NAC. Conclusion: Speicific activation of GPER inhibits the migration of CRC cells by suppressing epithelial-mesenchymal transition (EMT). This inhibitory effect is likely mediated through the upregulation of ROS levels in CRC cells.
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