Anti-silencing function 1B knockdown suppresses the malignant phenotype of colorectal cancer by inactivating the phosphatidylinositol 3-kinase/AKT pathway

Figure 4 Phosphatidylinositol 3-kinase activator reverses the inhibitory impact of anti-silencing function 1B down-regulation on proliferation, stemness and epithelial mesenchymal transition of colorectal cancer cells. A: Protein levels of p-phosphatidylinositol 3-kinase (PI3K), PI3K, p-AKT and AKT were detected by western blot in HCT116 and SW620 cells after transfection of sh-anti-silencing function 1B (ASF1B)#1 or sh-ASF1B#2; B: Protein levels of p-PI3K, PI3K, p-AKT and AKT were detected by western blot in HCT116 cells. Short hairpin RNA against ASF1B (sh-ASF1B#1) vs sh-negative control (NC), sh-ASF1B+740 Y-P vs sh-ASF1B#1; C: The proliferation of HCT116 cells was evaluated by the 5-Ethynyl-2’-Deoxyuridine assay; D: Protein levels of E-cadherin, N-cadherin, SOX2 and OCT4 were detected by western blot in HCT116 cells. sh-ASF1B#1 vs sh-NC, sh-ASF1B + 740 Y-P vs sh-ASF1B#1. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. Each experiment was repeated three times. ASF1B: Anti-silencing function 1B; NC: Negative control.