Fig. 3

Lonidamine potentiates M1 virus-mediated ER stress-induced apoptosis. a–c GSEA of the unfolded protein response, response to ER stress, and intrinsic apoptotic signaling pathway gene sets in the HCT 116 cell line after treatment with M1 (MOI = 1 pfu/cell) or M1 (MOI = 1 pfu/cell) plus lonidamine (50 μM) for 24 h. NES, p and FDR values are shown in each box. d The HCT 116 cell line was treated with vehicle, lonidamine (50 μM), M1 virus (MOI = 1 pfu/cell), or M1 virus plus lonidamine for 24 h, and cellular morphology was observed by SEM. The red lines indicate the diameter of the ER. Scale bars, 1 μm. e–j The HCT 116 and HCT-8 cell lines were treated with vehicle, lonidamine (50 μM), M1 virus (MOI = 1 pfu/cell), or lonidamine plus M1 virus for 48 h, and caspase-8, caspase-9 and caspase-3/7 activity was assessed. n = 3. Statistical analysis was performed by one-way ANOVA with Dunnett’s tests for pairwise comparisons. The error bars indicate the mean ± SD values from three independent experiments with three technical replicates. ns nonsignificant; *p < 0.05, **p < 0.01, ***p < 0.001