AIM: To investigate the mechanism by which mi R-19 a is up-regulated in gastric cancer(GC), which plays an oncogenic role.METHODS: In the present study, we investigated the role of mi R-19 a in gastric tissues as well as two GC cell lines. In vivo, we detected the basal expression level of mi R-19 a using real-time reverse transcription-PCR(RTPCR), and the relevance between expression of mi R-19 a and clinicopathological information was analyzed.In vitro, mi R-19 a was ectopically expressed using overexpression and knock-down strategies.RESULTS: Overexpression of mi R-19 a was significantly associated with metastasis of GC and inferior overall prognosis. However, no significant correlation was f o u n d b e t w e e n m i R- 1 9 a e x p r e s s i o n a n d o t h e r characteristics such as age, gender, tobacco, alcohol or tumor size. Cell proliferation, migration and invasion assays showed that overexpression of mi R-19 a promoted the proliferation, migration and invasion, and that overexpression of mi R-19 a promoted the epithelialmesenchymal transition through activating the PI3K/AKT pathway. Blocking the PI3K/AKT pathway could cancel the effect of mi R-19 a.CONCLUSION: All together, our results suggest that mi R-19 a could be used as a promising therapeutic target in the treatment of GC. To investigate the mechanism by which mi R-19 a is up-regulated in gastric cancer (GC), which plays an oncogenic role. METHODS: In the present study, we investigated the role of mi R-19 a in gastric tissues In vivo, we detected the basal expression level of mi R-19 a using real-time reverse transcription-PCR (RTPCR), and the relevance between the expression of mi R-19 a and clinicopathological information was analyzed in vitro, mi R-19 a was ectopically expressed using overexpression and knock-down strategies .RESULTS: Overexpression of mi R-19 a was significantly associated with metastasis of GC and inferior overall prognosis. However, no significant correlation was found between miR - 1 9 aexpressionandother characteristics such as age, gender, tobacco, alcohol or tumor size. Cell proliferation, migration and invasion assays showed that overexpression of mi R-19 a promoted the proliferation, migration and invasion, and that over expression of mi R-19 a promoted the epithelialmesenchymal transition through activating the PI3K / AKT pathway. Blocking the PI3K / AKT pathway could cancel the effect of mi R-19 a.CONCLUSION: All together, our results suggest that mi R-19 a could be used as a promising therapeutic target in the treatment of GC.