Fig. 5

Mutation of CRM1 abolishes the anti-proliferative activity of S109 in glioma cells. a U87 cells expressing wild-type or C528S-mutant CRM1 were treated with the indicated doses of S109 for 12 h and evaluated by western blot analyses. b U87 cells expressing wild-type or C528S-mutant CRM1 were cultured in media with vehicle or S109 (2 μM) for 2 h. Fixed cells were stained for RanBP1 and DAPI and analyzed by fluorescence microscopy. c The cells were treated with vehicle or different concentrations of S109 for 72 h, and the cell viability was assessed through CCK-8 assays. d Quantitative analysis of the relative cell proliferation rate. The cell proliferation rate was measured using the EdU incorporation assay. e Assay of the colony formation ability of cells expressing wild-type or C528S-mutant CRM1. f Cell cycle distribution of U87 cells expressing wild-type or C528S-mutant CRM1 treated with S109 for 12 h