RGS4 promotes the progression of gastric cancer through the focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and epithelial-mesenchymal transition

Figure 5 Knocking down regulator of G protein signaling 4 in gastric cancer cells inhibited tumor growth in vivo. A-F: Tumors from MGC-803 cells with regulator of G protein signaling 4 (RGS4) knockdown and AGS cells with RGS4 overexpression and their controls (n = 5/groups) (A and D), tumor growth curves (B and E), tumor weight of each group (C and F); G: The expression of focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and epithelial mesenchymal transition related proteins in MGC-803 cells and AGS cells in vivo were validated by western blot. β-actin was used as a loading control; H: The expression of RGS4, Ki67 and p-AKT in these xenografts via immunohistochemistry staining; I: Schematic diagram of the mechanism of RGS4 promoting gastric cancer progression. ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001. FAK: Focal adhesion kinase; PI3K: Phosphatidyl-inositol-3-kinase; AKT: Protein kinase B; RGS4: Regulator of G protein signaling 4; PIP: Prolactin-induced protein; mTOR: Mechanistic target of rapamycin.