SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway

Figure 6 Serpin peptidase inhibitor clade H member 1 promoted colorectal cancer progression through the phosphatidylinositol 3-kinase/AKT/mechanistic target of rapamycin and phosphatidylinositol 3-kinase/AKT/FOXO1 signaling pathways. A: Western blotting analysis of p-AKT, total AKT, p-glycogen synthase kinase (GSK)-3β, total GSK-3β, p-mechanistic target of rapamycin (mTOR), total mTOR, p-FOXO1, and total FOXO1 in serpin peptidase inhibitor clade H member 1 (SERPINH1)-overexpressed cells or SERPINH1 siRNA-infected cells; B: HCT116/SERPINH1 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-E: The proliferation ability of HCT116/SERPINH1 cells were determined by cell counting kit 8 assay and 5-ethynyl-2’-deoxyuridine assay; F and G: The invasive and migratory abilities of HCT116/SERPINH1 cells were determined by transwell assays after treatment with rapamycin and DMSO; H and I: The G0/G1 ratio of HCT116/SERPINH1 cells were determined by flow assays after treatment with rapamycin and DMSO. All the data are presented as the mean ± SEM. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. SERPINH1: Serpin peptidase inhibitor clade H member 1.