Fig. 2: Depletion of NF1 or DUSP9 can reverse the inhibitory effect of lenvatinib on Huh7 cell.
From: Genome-scale CRISPR-Cas9 knockout screening in hepatocellular carcinoma with lenvatinib resistance
A Cell viability assessed by CCK8 assay for 14 candidate genes. Depletion of NF1 and DUSP9 showed a significant proliferative advantage relative to the other candidate genes under lenvatinib treatment. The 14 candidate genes were separated as three groups (There are two sgRNA for BBs7, NF1, CRYAB, OR51V1, respectively. NC-, Negative control, without drug.NC + , Negative control, under drug treatment). B NF1 and DUSP9 knockout expression levels were confirmed by western blotting in Huh7 cell. Expression of NF1 or DUSP9 is undetectable in Huh7 cell after knocked out by NF1 or DUSP9 sgRNA, respectively. C Clone formation capacity of Huh7 cells was assessed by the clone formation assay. Lenvatinib significantly inhibited Huh cells proliferation compared with NC-, however, the number of clones significantly increased again after NF1 or DUSP9 knockout. D CCK8 assay for NF1 and DUSP9 knockout. E Cell number counting for NF1 and DUSP9 knockout. F Transwell migration assay and transwell invasion assay were performed in Huh 7 cell. Error bars represent mean ± SEM for triplicate experiments, *P < 0.05, **P < 0.01, ***P < 0.001 or the values were shown in the figures.
