Fig. 3: mTOR-enhanced SESN3 promotes sorafenib resistance.

A Volcano plot exhibits the differentially expressed genes (DEGs) of Tsc2^−/− MEFs vs WT MEFs from GSE21755 dataset in GEO database. The thresholds were set as false discovery rate (FDR) < 0.01 and fold change >1.5. B Schematic delineation of flows and results of screening for potential candidates. C, D mRNA and protein levels of SESN3 in HCCLM3 or HepG2 cells (C) transfected with vector or mTOR plasmid, and SNU886 or SNU398 cells (D) transfected with control or mTOR shRNA. E, F Immunoblotting of HCCLM3 cells (E) transfected with vector or SESN3 plasmid, and SNU886 cells (F) transfected with control or SESN3 shRNA. G, H HCCLM3 cells were transfected with vector or SESN3 plasmid, n = 3.The intracellular ROS of cells treated with sorafenib (10 μM) for 24 h (G). Viability of cells treated with different concentrations of sorafenib for 24 h (H). I, J SNU886 cells were transfected with control or SESN3 shRNA, n = 3. The intracellular ROS of cells treated with sorafenib (10 μM) for 24 h (I). Viability of cells treated with different concentrations of sorafenib for 24 h (J). K, L SNU886/shmTOR cells were transfected with vector or SESN3 plasmid. Immunoblotting of cells (K). Viability of cells treated with different concentrations of sorafenib for 24 h, n = 3 (L). Data are displayed as mean ± SD (error bars). **p < 0.01, ***p < 0.001. Sora: sorafenib.