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

Figure 2 Presenilin-1 enhanced the expression of phosphorylation of tensin homolog deleted on chromosome ten in gastric cancer cells. A and B: Western blot analysis testing the expression of presenilin-1 (PS-1), β-catenin, phosphorylation of tensin homolog deleted on chromosome ten (PTEN), and PTEN by upregulating and downregulating PS-1. Glyceraldehyde-3-phosphate dehydrogenase was used as a loading control. The quantified analysis of the expression of PS-1 and phosphorylation of PTEN is presented. The values were shown as mean ± SD of three independent experiments. ^bP < 0.01. 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.