Fig. 6

Cadmium inhibits KIF5B-RhoT1-driven mitochondrial transfer and increases lipid accumulation. AML12 cells were treated with 2.5, 5, and 10 μM Cd for 6 h. Levels of KIF5B and RhoT1 were determined using western blotting (A). Results are shown as the mean ± SD (n = 3). Compared with the control group, *P < 0.05, **P < 0.01. RhoT1 and phalloidin were co-stained to observe RhoT1 intracellular localization (B). Scale bar = 25 μm. Based on treatment with KIF5B siRNA or KIF5B OE plasmid for 24 h, AML12 cells were treated with or without Cd for 6 h. TOMM20 and Tubulin-Tracker-Red co-staining to detect mitochondrial transfer (C). Scale bar = 25 μm. AML12 cells were treated with 5 μM Cd for 6 h. Co-immunoprecipitation detection of KIF5B and RhoT1 interactions (D). Based on treatment with KIF5B OE plasmid for 24 h, AML12 cells were treated with or without Cd for 6 h. Oil red O (E) and BODIPY (F) were used to observe intracellular lipid droplets. Scale bar = 200 μm. Scale bar = 25 μm. TG and TC contents were detected (G, H). Levels of CPT1and ACSL1 were determined using western blotting (I). Results are shown as the mean ± SD (n = 3). Compared with the control group, *P < 0.05, **P < 0.01. Compared with the Cd group, ^#P < 0.05, ^##P < 0.01