Abstract: Gastric cancer (GC) remains one of the most common malignancy globally, with high incidence and mortality rates. The dysregulation of miR-768-3p has been observed in several types of tumors, and it is involved in the carcinogenesis of GC. This present study aimed to determine the regulatory mechanisms of miR-768-3p in GC progression. First of all, we found that miR-768-3p expression was downregulated in human GC tissues and cell line MGC803. Furthermore, Ectopic expression of miR-768-3p mimics interfering RNA resulted in a decrease in cell proliferation and G1/S transition, as well as promotion of apoptosis. Further investigation in the present study indicated that the expression of eIF4E protein and mRNA were decreased following upregulation of the expression of miR-768-3p.... Moreover, eIF4E was demonstrated to be a target gene of miR-768-3p, according to the results of bioinformatics analysis and identified by dual luciferase assays. Collectively, these data suggest that miR-768-3p functions as a tumor suppressor in GC by targeting eIF4E. Therefore, miR-768-3p may be a novel biomarker and potential therapeutic target for GC.