Fig. 5

AKT and HIF1α are the downstream effectors of ROS in HCC. a RNA sequencing analysis of the transcriptional changes induced by MAP17 knockdown in HCC-LM3 cells; ClueGO analysis of the differentially expressed genes by CytoScape software. b The effect of MAP17 knockdown on the activity of ROS-associated signaling pathways (p38 MAPK, ERK1/2, AKT, STAT3, P70S6K, and HIF1α) in SMCC-7721 and HCC-LM3 cells was analyzed by western blotting. c The effect of MAP17 or MAP17-PDZm overexpression on AKT activity in the presence or absence of 10 mM N-acetyl cysteine (NAC) treatment was determined by western blotting. d Western blotting analysis of MAP17 or MAP17-PDZm overexpression on HIF1α protein in the presence or absence of 10 mM N-acetyl cysteine (NAC) treatment. e The effect of MAP17 or MAP17-PDZm overexpression on HIF1α transcriptional activity in MHCC-97H cells. f Western blotting analysis of HIF1α protein level in MAP17-overexprssing or vector control cells at indicated times upon 20 μg/ml CHX treatment. g Western blotting analysis of HIF1α protein level in MAP17 knockdown or overexpression cells treated with 10 μM MG132 under hypoxic conditions. *P < 0.05 and **P < 0.01