LINC01268 promotes epithelial-mesenchymal transition, invasion and metastasis of gastric cancer via the PI3K/Akt signaling pathway and targeting MARCKS

Figure 7 The relationship between LINC01268 and PI3K/Akt signaling pathway and epithelial-mesenchymal transition in gastric cancer. A: The expression level of PIK3CA in the LINC01268^high gastric cancer (GC) tissues was significantly higher than that in the LINC01268^low cancer tissues; B: The expression level of Akt in the LINC01268^high GC tissues was higher than that in the LINC01268^low cancer tissues, but there was no statistical difference. Expression levels were normalized to ACTB levels. The results were shown as the mean ± SEM; C-E: After knocking down LINC01268, the p-MARCKS, p-PI3K, p-Akt and p-β-catenin protein levels were down-regulated in MGC80-3 and AGS cells, but the protein level of MARCKS had no significant change. Expression levels were normalized to GAPDH levels; F-H: Knocking down LINC01268 reduced vimentin, MMP-9 and N-cadherin protein levels, and increased E-cadherin protein levels in MGC80-3 and AGS cells. Expression levels were normalized to GAPDH levels. The results were shown as the mean ± SD. ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001, ^eP > 0.05. MARCKS: Myristoylated alanine rich protein kinase C substrate; sh-NC: sh-negative control.