Key messages
Loss of heterozygosity and stop-gain mutation of VPS52 were found in gastric cancer. Negative expression of VPS52 significantly correlated with poor prognosis. VPS52 inhibited viability and induced apoptosis of gastric cancer cells in vitro. VPS52 reduced tumor volume and tumor weight in vivo. VPS52 activated the apoptotic pathway through cathepsin D in gastric cancer cells.