Increasing expression of presenilin 1, β-catenin, and p-PTEN and its regulatory roles on cell invasion in gastric cancer

Figure 4 Presenilin-1 promoted gastric cancer cell invasion via β-catenin. A: The expression of total phosphorylation of tensin homolog deleted on chromosome ten, tensin homolog deleted on chromosome ten, and β-catenin were measured by western blot after transfection with β-catenin small interfering RNA and lentiviral presenilin-1 (PS-1); B: Decreasing expression of β-catenin reversed the enhanced invasion induced by upregulating PS-1. The quantifications were presented as mean ± SD on the right; C: The above proteins were measured after overexpression of β-catenin in stable knockdown PS-1 cell line MGC-803; D: Β-catenin increased the invasion ability of MGC-803 cells when PS-1 was downregulated. The quantifications were presented as mean ± SD on the right. ^bP < 0.01. NS: No significance; PS-1: Presenilin-1; p-PTEN: Phosphorylation of tensin homolog deleted on chromosome ten; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; Ctrl: Control; PTEN: Phosphorylation of tensin homolog deleted on chromosome ten.