Gastric cancer (GC) is among the most common types of human cancer and is associated with recurrence and metastasis, despite comprehensive surgical and medical treatment. Previous studies observed downregulation of T-cadherin expression in GC tissues, suggesting that this protein may act as an oncosuppressor. The current study investigated the activity of T-cadherin in GC tissues. In a follow-up study of 81 patients with GC, a Kaplan-Meier analysis of overall survival revealed a strong association of T-cadherin overexpression with increased overall survival (P<0.01). Furthermore, stable T-cadherin-overexpressing cell lines were established from HGC-27 cells via transfection of a pcDNA3.1-T-cadherin plasmid and in vitro growth and cell cycle of these cells were measured using MTT and flow cytometry assays, respectively. MTT assays revealed that proliferation of engineered T-cadherin-overexpressing cells was significantly inhibited and flow cytometry demonstrated that T-cadherin overexpression in HGC-27 cells induced cell cycle arrest in the G 0/G 1 phase. Transwell assays demonstrated that T-cadherin-overexpressing HGC-27 cells exhibited reduced invasiveness and metastatic potential. Phosphorylated (p)-protein kinase B (AKT) and p-mammalian target of rapamycin (mTOR) protein levels were reduced in T-cadherin overexpressing HGC-27 cells, suggesting that the AKT/mTOR signaling pathway was involved in the gastric tumor inhibitory effect of T-cadherin. Administration of AKT-activator, insulin-like growth factor-1, to T-cadherin-overexpressing HGC-27 cells significantly affected the proliferation phenotype. In conclusion, the current study provided clinical evidence and revealed a potential mechanism supporting that T-cadherin inhibits gastric tumorigenesis through inhibition of the AKT/mTOR signaling pathway.