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. 2023 Apr 17;22(6):100551. doi: 10.1016/j.mcpro.2023.100551

Fig. 5.

Fig. 5

Sulconazole triggers mitochondrial oxidative stress and inhibits glycolysis.A, transmission electron microscopy (TEM) images of KYSE30 cells subjected to the indicated treatments for 24 h. White arrows indicate mitochondria. Scale bars represent left, 1 μm; right, 500 nm. B; PI, propidium iodideD, mitochondrial membrane potential analysis (B), ROS level analysis (C), and glucose uptake analysis (D) in KYSE30 and KYSE150 cells after sulconazole treatment for 24 h. E, heat map of 19 glycolysis-related enzymes that were differentially expressed in KYSE30 and KYSE150 cells with or without sulconazole treatment. F and G, the mRNA expression of glycolysis pathway enzymes by quantitative RT-PCR in KYSE30 (F) and KYSE150 (G) cells. H, Western blot analyses of glycolysis-related enzymes after sulconazole treatment for 24 h in KYSE30 (left panel) and KYSE150 (right panel) cells. Quantification of the blots is shown below. I, Western blot analyses for the expression of p-AKT, AKT, p-MEK, MEK, p-ERK, ERK, p-STAT3, and STAT3 after sulconazole treatment for 24h in KYSE30 (left panel) and KYSE150 (right panel) cells. The data in (B–D, F and G) are representative of three independent experiments and presented as the mean ± SD. p-values were calculated by two-way ANOVA. ∗∗p < 0.01, ∗∗∗p < 0.001. ROS, reactive oxygen species.