Fig. 4: NF1 and DUSP9 loss reactivate PI3K/AKT and MAPK/ERK signaling pathways.
From: Genome-scale CRISPR-Cas9 knockout screening in hepatocellular carcinoma with lenvatinib resistance
The expression levels of phosphorylated AKT, ERK, FOXO3 were assayed by WB analysis in Huh7 and PLC/PRF/5 cells after NF1 (A) and DUSP9 (B) were knocked out or knocked down. The expression levels of phosphorylated AKT, ERK, FOXO3 were significantly increased after NF1 were knocked out or knocked down, however, depletion of DUSP9 only increased the expression levels of phosphorylated ERK and FOXO3. C NF1 and DUSP9 overexpression reversed the expression levels of phosphorylated AKT, ERK, FOXO3 enhanced by NF1 and DUSP9 loss. Error bars represent mean ± SEM for triplicate experiments, *P < 0.05, **P < 0.01, ***P < 0.001, ns no significantly changed.
