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

Figure 1 CALD1 overexpression in gastric cancer: Correlation with epithelial-mesenchymal transition type, prognostic implications, and enhanced protein expression in tissues. A: Bioinformatics results showed that CALD1 was highly expressed in gastric cancer (GC), and CALD1 in GC tissues of epithelial-mesenchymal transition (EMT) type was significantly higher than that in GC tissues of other types; B and C: Patients with high expression of CALD1 had a poorer prognosis than those with low expression, and a prognostic model was constructed and evaluated; D: Validation experiment showed that the protein expression of CALD1 in GC tissues was enhanced compared with that in paracancerous tissues (60 cases); E: CALD1 mRNA (qPCR) and protein (Western blot) in EMT-type GC tissues were significantly higher than those of other types (20 cases); F: Patients with high CALD1 expression had a poorer prognosis than those with low expression (60 cases). ^cP < 0.001.