On page 1826, two incorrect images were used in Figure 5B for representing “TGF-β + 4 (10 nM)” and “TGF-β + 1 (50 nM)” groups, and another two incorrect images were used in Figure 5C for representing “Control, 0h” and “Oxaliplatin 50 nM, 0h” groups. The corrected Figure 5 is shown below. Figure 5. Effects of the tested compounds on transwell migration (A,D), invasion (B,E), and lateral migration (C,F) of HCT-116 cells. (A) HCT-116 cells were seeded on chambers and incubated with the compounds for 48 h. Cells that migrated through the chambers were stained with crystal violet, and representative images were captured. (B) HCT-116 cells were seeded on chambers and incubated with the indicated factors for 48 h. Cells that migrated through the Matrigel-coated chambers were stained with crystal violet, and representative images were captured. (C) HCT-116 cells were seeded on 48-well plates. After 24 or 48 h incubation with the indicated factors, representative images of the wound were captured. (D) Cells that migrated through the chambers were counted from three independent experiments. (E) Cells that migrated through the Matrigel-coated chambers were counted from three independent experiments. (F) Rate of lateral migration is presented. Experiment was confirmed for three independent times. All the data in D–F were expressed as the means ± SD of each group of cells. *P < 0.05, **P < 0.01, ***P < 0.001 vs respective TGF-β group; #P < 0.05, ###P < 0.001. Scale bars: 100 μm. On pages 1827 and 1828, three incorrect WB images were used in Figure 8A for representing MMP-9, Snail, and Twist groups. The corrected Figures 8 and 9 are shown below (Figures 8 and 9 were involved in one experiment). Figure 8. Treatment with 4 reverses the TGF-β-induced EMT process in HCT-116 cells. HCT-116 cells were treated with or without TGF-β (10 ng/mL) for 48 h in the presence or absence of 1 or 4 at the indicated concentrations. The relative levels of E-cadherin, Vimentin, MMP-9, Snail, and Twist to the control β-actin expression were determined by Western blotting. Data are representative images or expressed as the mean ± SD of each group of cells from three independent experiments. (A) Western blot analysis. (B) Levels of E-cadherin. (C) Levels of Vimentin. (D) Levels of MMP-9. (E) Levels of Snail. (F) Levels of Twist. *P < 0.05, **P < 0.01 vs TGF-β group; #P < 0.05. Figure 9. Treatment with 4 inhibits the AKT and Wnt/β-catenin signaling induced by TGF-β in HCT-116 cells. HCT-116 cells were treated with or without TGF-β (10 ng/mL) for 48 h in the presence or absence of 1 or 4 at the indicated concentrations. The relative levels of Akt and GSK-3β phosphorylation and cytoplasm and nuclear β-catenin expression in HCT-116 cells were determined by Western blot assays. Data are representative images or expressed as the mean ± SD of each group of cells from three independent experiments. (A) Western blot analysis. (B) Levels of AKT and GSK-3β phosphorylation. (C) Western blot analysis of cytoplasm and nuclear β-catenin expression. (D) Levels of cytoplasm and nuclear β-catenin expression. *P < 0.05, **P < 0.01 vs TGF-β group; #P < 0.05. This article has not yet been cited by other publications. Figure 5. Effects of the tested compounds on transwell migration (A,D), invasion (B,E), and lateral migration (C,F) of HCT-116 cells. (A) HCT-116 cells were seeded on chambers and incubated with the compounds for 48 h. Cells that migrated through the chambers were stained with crystal violet, and representative images were captured. (B) HCT-116 cells were seeded on chambers and incubated with the indicated factors for 48 h. Cells that migrated through the Matrigel-coated chambers were stained with crystal violet, and representative images were captured. (C) HCT-116 cells were seeded on 48-well plates. After 24 or 48 h incubation with the indicated factors, representative images of the wound were captured. (D) Cells that migrated through the chambers were counted from three independent experiments. (E) Cells that migrated through the Matrigel-coated chambers were counted from three independent experiments. (F) Rate of lateral migration is presented. Experiment was confirmed for three independent times. All the data in D–F were expressed as the means ± SD of each group of cells. *P < 0.05, **P < 0.01, ***P < 0.001 vs respective TGF-β group; #P < 0.05, ###P < 0.001. Scale bars: 100 μm. Figure 8. Treatment with 4 reverses the TGF-β-induced EMT process in HCT-116 cells. HCT-116 cells were treated with or without TGF-β (10 ng/mL) for 48 h in the presence or absence of 1 or 4 at the indicated concentrations. The relative levels of E-cadherin, Vimentin, MMP-9, Snail, and Twist to the control β-actin expression were determined by Western blotting. Data are representative images or expressed as the mean ± SD of each group of cells from three independent experiments. (A) Western blot analysis. (B) Levels of E-cadherin. (C) Levels of Vimentin. (D) Levels of MMP-9. (E) Levels of Snail. (F) Levels of Twist. *P < 0.05, **P < 0.01 vs TGF-β group; #P < 0.05. Figure 9. Treatment with 4 inhibits the AKT and Wnt/β-catenin signaling induced by TGF-β in HCT-116 cells. HCT-116 cells were treated with or without TGF-β (10 ng/mL) for 48 h in the presence or absence of 1 or 4 at the indicated concentrations. The relative levels of Akt and GSK-3β phosphorylation and cytoplasm and nuclear β-catenin expression in HCT-116 cells were determined by Western blot assays. Data are representative images or expressed as the mean ± SD of each group of cells from three independent experiments. (A) Western blot analysis. (B) Levels of AKT and GSK-3β phosphorylation. (C) Western blot analysis of cytoplasm and nuclear β-catenin expression. (D) Levels of cytoplasm and nuclear β-catenin expression. *P < 0.05, **P < 0.01 vs TGF-β group; #P < 0.05.