Accumulating evidence indicates that long noncoding RNAs (LncRNAs) are involved in tumorigenesis and tumor development. LncRNA GACAT3 (GACAT3) has been reported to be upregulated in gastric cancer (GC); however, the biological function and underlying mechanisms of GACAT3 remain largely unknown. Here, we found that GACAT3 showed a higher expression in GC tissues and cell lines. Increased GACAT3 level was significantly associated with a shorter overall survival of patients with GC. Functionally, we demonstrated that knockdown of GACAT3 significantly inhibited proliferation, colony formation, migration, and invasion of GC cells in vitro. Moreover, underexpression of GACAT3 decreased tumorigenesis in vivo. Mechanistically, we proved that GACAT3 directly binds to microRNA-497 (miR-497), and GACAT3 expression was inversely correlated with miR-497 expression. Taken together, we demonstrate that GACAT3 may function as an oncogene that promotes GC progression, and may serve as a potential target for GC therapy in the future.