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. 2023 Apr 3;55(4):779–793. doi: 10.1038/s12276-023-00961-x

Fig. 5. SAMHD1 regulates Rac1 activity and enhances ccRCC cell migration.

Fig. 5

a GO analysis was performed, and subcategories in the molecular function category were highly correlated with the high expression of SAMHD1. b, c Subcategories of the molecular function category related to cell migration. **p < 0.01. d A G-LISA-based assay was performed to measure GTP-bound Rac1 activity in SAMHD1-knockdown SN12C cells and SAMHD1-overexpressing Caki-1 cells. Data are presented as the mean ± SD. The data shown are representative of three independent experiments. **p < 0.01. e GTP-bound-cdc42 activity in SAMHD1-knockdown SN12C cells and SAMHD1-overexpressed Caki-1 cells. Data are presented as the mean ± SD. The experiments were independently performed three times. *p < 0.05; ***p < 0.001. f Wound-healing assay of cell migration ability with FAK inhibitor (PF573228), Rho A inhibitor (fasudil), Rac1 inhibitor (NSC23766), and cdc42 inhibitor (ML141). SAMHD1-knockdown SN12C cells were treated with each corresponding inhibitor at 10 μM over 24 h. The relative wound-healing area was normalized to that of the controls. Data are presented as the mean ± SD. The data shown are representative of three independent experiments. ***p < 0.001. g A wound healing assay was performed as in (f) in SAMHD1-overexpressing Caki-1 cells. The relative wound-healing area was normalized to that of DMSO-treated controls. *p < 0.05; ***p < 0.001. Data are presented as the mean ± SD of three independent experiments.