Fig. 8: TRPC1/NCX1 coupling induces AKT phosphorylation and promotes GC growth and metastasis.
From: NCX1 coupled with TRPC1 to promote gastric cancer via Ca2+/AKT/β-catenin pathway
A, D Inhibitory effects of either KB-R7943 (KB-R, 1 μM in MKN45, 8 μM in SGC7901), SKF96365 (SKF, 1 μM) or KB-R plus SKF on CaCl2 (2 mM)-induced AKT phosphorylation in GC cells. B, E Inhibitory effects of SKF, shNCX1 or shNCX1 plus SKF on CaCl2 (2 mM)-induced AKT phosphorylation in GC cells. C, F Inhibitory effects of either KB-R, shTRPC1 or shTRPC1 plus KB-R on CaCl2-induced AKT phosphorylation in GC cells. CaCl2 promoted growth of xenografted gastric tumors (G), which was attenuated by either KB-R7943 (H) or shNCX1 (I). J Inhibitory effects of shNCX1 on CaCl2-induced gastric tumor metastasis. K Immunohistochemical analysis and histological examination on expression of NCX1 and Ki67 proteins with or without NCX1 knockdown in GC tissues. Scale bar = 100 μm for each image. L, M Summary data comparing expression of NCX1 and Ki67 proteins analyzed by immunohistochemistry between with or without NCX1 knockdown in GC tissues. (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n = 3; ns, no significant differences). N The proposed oncogenic mechanisms of TRPC1/NCX1 coupling via Ca2+/AKT/β-catenin pathway in Hp-associated GC.
