Fig. 6
IL-2 and sorafenib co-treatment regulated mitochondrial fission via the JNK-TAZ pathways. a–c JNK phosphorylation and TAZ expression were measured via western blotting. SP600125, an inhibitor of JNK, was used to inhibit the activity of the JNK-TAZ pathways. d, e Mitochondrial fission was observed via immunofluorescence, and the average length of the mitochondria was recorded. f–h The regulatory effects of IL-2 and sorafenib co-treatment on the JNK-TAZ pathways and mitochondrial fission were monitored via immunofluorescence. IL-2 and sorafenib co-treatment promoted the upregulation of JNK phosphorylation, which was accompanied by an increase in Drp1, a factor for mitochondrial fission. *P < 0.05 vs. control group; @P < 0.05 vs. IL-2+ sorafenib group. Cont control