Fig. 2: mTOR attenuates sorafenib-mediated ROS accumulation and oxidative stress in liver cancer cells.

A Viability of HCCLM3 cells treated with sorafenib (10 μM) in the presence or absence of specific inhibitors for 24 h, n = 3. Ferrostatin-1 (Fer-1, 10 μM), N-acetylcysteine (NAC, 1 mM), deferoxamine (DFO, 10 μM), necrostatin-1 (Nec-1, 20 μM) and chloroquine (CQ, 10 μM). B–D HCCLM3 cells were treated with sorafenib (10 μM) for 24 h, n = 3. The intracellular ROS (B) and lipid peroxidation (C) were measured with flow cytometry. Cytosolic Fe²⁺ levels were assayed by PGSK probe, fluorescence intensity was observed under the fluorescence microscope, scale bar=50 μm (D). E, F HCCLM3 cells were transfected with vector or mTOR plasmid and treated with sorafenib (10 μM) for 24 h, n = 3. The intracellular ROS were measured with flow cytometry (E). Relative total antioxidant capacity, GSH level, and NADPH/NADP+ ratio were measured (F). G, H SNU886 cells were transfected with control or mTOR shRNA and treated with sorafenib (10 μM) for 24 h, n = 3. The intracellular ROS were measured with flow cytometry (G). Relative total antioxidant capacity, GSH level, and NADPH/NADP+ ratio were measured (H). Data are displayed as mean ± SD (error bars). **p < 0.01, ***p < 0.001. Sora: sorafenib.