Activation of P2RY2 activated AKT/GSK-3beta/VEGF signal to promote the proliferation of GC cells, and the P13/AKT signaling pathway LY294002 reversed the corresponding phenomenon, but no synergistic pharmacological properties of AR-C118925XX and LY294002 have been found. In vivo experiments showed that ATP induced tumor growth, while AR-C118925XX inhibited ATP-induced tumor growth. Our conclusion is that P2RY2 activated the AKT/GSK-3beta/VEGF signal to promote the proliferation and migration of GC, suggesting that P2RY2 may be a new potential target for the treatment of GC.
The PI3K/AKT signaling pathway was blocked by Src or EGFR inhibitor. Extracellular ATP activates the PI3K/AKT pathway through the P2Y2-Src-EGFR axis to promote OSCC invasion and migration, and thus, P2Y2 may be a potential novel target for antimetastasis therapy.