Fig. 5

IMPDH2 promoted CRC progression through the PI3K/AKT/mTOR and PI3K/AKT/FOXO1 signaling pathways. (a) Western blotting analysis of p-AKT, total AKT, p-GSK-3β, total GSK-3β, p-mTOR, total mTOR, p-FOXO1, and total FOXO1 in IMPDH2-overexpressed cells or IMPDH2 shRNA-infected cells. (b) SW480/IMPDH2 and LoVo/IMPDH2 cells were treated with the AKT inhibitor LY294002 (20IM) and DMSO for 24 h, then harvested to examine the expression levels of the indicated proteins by Western blotting. (c) Colony formation assay after treatment with LY294002 and DMSO. Mean ± SD (n = 3). (d) The proliferation ability of SW480/IMPDH2 and LoVo/IMPDH2 cells were determined by CCK8 assay. *P < 0.05; **P < 0.01. (e and f) The invasive and migratory abilities of SW480/IMPDH2 and LoVo/IMPDH2 cells were determined by transwell and wound healing assays after treatment with rapamycin and DMSO. Mean ± SD (n = 3). *P < 0.05; **P < 0.01. (g) Inhibition of the mTOR activity induced upregulation of E-cadherin and downregulation of Vimentin and Snail in IMPDH2-overexpressed CRC cells