CALD1 facilitates epithelial-mesenchymal transition progression in gastric cancer cells by modulating the PI3K-Akt pathway

Figure 4 Effects of CALD1 modulation and PI3K-Akt inhibition on tumor cell activity, migration, and EMT-related gene expression. A: Up-regulation of CALD1 enhanced the expression of PI3K, p-AKT, and p-mTOR, members of the PI3K-Akt pathway, whereas PTEN expression was weakened; the addition of a PI3K-Akt inhibitor attenuated the expression of PI3K, p-AKT, and p-mTOR, while the expression of PTEN was enhanced; B: CCK-8 results showed that showed that the effect of CALD1 on tumour cell activity was weakened after adding a PI3K-Akt inhibitor (blank group-moderate activity, negative group-moderate activity, CALD1 overexpression group-high activity, CALD1 overexpression + inhibitor group-moderate activity or slightly high activity); C: Scratch and Transwell assay results showed that the effect of CALD1 on tumour cell migration and invasion was weakened after adding a PI3K-Akt inhibitor (blank group-moderate, negative group-moderate, CALD1 overexpression group-strong, CALD1 overexpression + inhibitor group-moderate or slightly strong); D: CALD1 overexpression, alone or in combination with PI3K-Akt inhibition, resulted in corresponding changes in EMT-related genes and proteins in AGS and MKN45 cells. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001.