Fig. 5: Inhibition of mitochondrial fission alleviates oxidative stress and UPR in cancer cells.

A Mitochondrial morphology of TSCCs was visualized by fluorescent dye MitoTracker Red CMXRos (Mito: red). B Oxidation of cardiolipin in TSCC was assessed by fluorescent dye NAO (NAO: green). DAPI, nuclear staining. Scale bars, 2 μm. C, D Assessment of intracellular ROS by flow cytometry in TSCCs (mean ± s.e.m; n = 9; p = 0.0104, 0.0012 for SCC-9 Mdivi-1 treatment group and 0.0136, 0.0059 for CAL-27 Mdivi-1 treatment group; p < 0.0001, p < 0.0001 and p = 0.0004 for SCC-9; p = 0.0008, 0.0002 and 0.049 for CAL-27; ^#p < 0.05, *p < 0.01, **p < 0.001). E Immunoblotting for associated ER stress markers in TSCCs. MW molecular weight. GAPDH, loading control. F, G Flow cytometric analysis of MHC-I membrane expression after depicted treatments in TSCCs (mean ± s.e.m; n = 4; the upper panel, p = 0.0001, 0.0001 and 0.4341 for SCC-9; p < 0.0001, <0.0001 and 0.0944 for CAL-27; the lower panel, p < 0.0001, p < 0.0001 and p = 0.8971 for SCC-9; p = 0.0004, <0.0001 and 0.6033 for CAL-27; *p < 0.01, **p < 0.001, DN IRE1α compared with vector 1 and IRE1α+XBP-1s, XBP-1s compared with vector 2 and IRE1α+XBP-1s; siDRP-1 compared with NC and siDRP-1+XBP-1s, XBP-1s compared with vector and siDRP-1+XBP-1s). M indicates mean fluorescence intensity. For experiments that were conducted at different time points, the isotype tubes were adjusted to ensure that their fluorescence intensity was at similar levels.