Tensin4 promotes invasion and migration of gastric cancer cells via regulating AKT/GSK-3β/snail signaling pathway

Gastric cancer (GC) remains one of the most lethal human malignancies, and exploring novel therapeutic targets for the treatment has been a major focus. The molecular mechanism of invasion and migration of GC cells remains unclear. The present study aimed to investigate the role of Tensin 4 and the associated molecular signaling pathways in the process of invasion and metastasis of GC. The expression of Tensin 4 protein and phosphorylated AKT (p-AKT) were evaluated in GC and normal adjacent tissues of 80 patients using immunohistochemistry staining. The expression of Tensin4 mRNA was analyzed in 10 GC tissues and 3 GC cell lines (SGC7901, MKN45, and MKN28) by qPCR. Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays in the Tensin 4 siRNA transfected SGC7901 cells and Tensin 4 plasmid transfected MKN28 cells. Additionally, protein expressions of Tensin 4, E-cadherin, vimentin, AKT, p-AKT, GSK-3 beta, p-GSK-3 beta, and Snail were analyzed by western blotting. The results demonstrated that the expression of Tensin 4 was significantly up-regulated in the GC tissues and cell lines, especially in the SGC7901 cells. The expression of Tensin 4 positively correlated with p-AKT in GC tissues and with GC progression, and was an independent risk factor for the prognosis of GC. Tensin 4 promoted the invasion and migration abilities of GC cells, but had no significant effect on GC cell proliferation. Tensin 4 promoted the occurrence of epithelial mesenchymal transition (EMT) through up-regulating the expression of p-AKT, p-GSK-3 beta, and snail. Overall, this study suggests that the activation of AKT/GSK-3 beta/Snail signaling pathway promoted by Tensin 4 plays an important role in the progression of GC. Therefore, Tensin 4 may serve as a potential target in GC treatment.