Over-Expression of Gastrin Inhibits Apoptosis of Gastric Cancer Cells via Reactive Oxygen Species and Annexin A2-Mediated Mitochondrial Dysfunction

Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated GC tissues several cell lines. Yet, underlying mechanism remains to be investigated. Here, we aim investigate gastrin proliferation. Gastrin-overexpressing model was constructed using SGC7901 cells. Then differentially expressed proteins were identified by iTRAQ analysis. Next, use flow cytometry immunofluorescence study effect on mitochondrial potential mitochondria-derived ROS production. Finally, studied regulating function Co-IP, mass spectrometry immunofluorescence. Overexpression promoted proliferation vitro vivo. A total 173 differently between controls gastrin- overexpression cells most these involved tumorigenesis Among them, Cox17, Cox5B ATP5J that all localized respiratory chain down-regulated gastrin-overexpression Furthermore, led decrease increase. Additionally, gastrin-induced generation resulted inhibition apoptosis via activating NF-kB, inhibiting Bax promoting Bcl-2 expression. found interacted with membrane protein Annexin A2 Co-IP spectrometry. Overexpr ession inhibits inducing dysfunction through interacting A2, then up-regulating production activate NF-kB further leading Bax/Bcl-2 ratio decrease.