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. 2020 Feb 10;11(9):2518–2528. doi: 10.7150/jca.40055

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GluR2 antagonist decreases proliferation, migration and invasion of EC cells. (A-B) Ishikawa cells were treated with GluR2 agonist from 10nM to 100μM or antagonist from 0.1μM to 10μM for 0-96 h. CCK-8 assay was used to test the cell proliferation ability. (C-D) ISK cells treated with GluR2 agonist/antagonist (both at 10μM) and its control were subjected to wound-healing migration assay. Representative images of wounds at different time points (0, 24, 48 h) were displayed, and the percentage of wound closure was measured (percentage of wound healing: 0-24 h width of wound/0 h width of wound or 0-48 h width of wound/0 h width of wound). (E-G) Transwell migration/invasion assays were applied to evaluate the ISK cells while treated with GluR2 agonist or antagonist; scale bar, 50μm. Data are presented as the mean ± SD; *P< 0.05.