Background: Gastric cancer (GC) is one of most common malignancies worldwide. Long noncoding RNA insulin growth factor 2 antisense (IGF2-AS) is associated with the progression of various cancers. Here, we further explore the detailed molecular mechanism of IGF2-AS in GC. Materials and Methods: The expression of IGF2-AS, microRNA-937 (miR-937), and enhancer of zeste homolog 2 (EZH2) was gauged by quantitative real-time polymerase chain reaction or western blot, respectively. The role of IGF2-AS in the GC prognosis was analyzed by the Kaplan-Meier method. The proliferation, migration, and invasion abilities were measured by using cell counting kit-8 (CCK-8) or transwell assay, respectively. The interaction between miR-937 and lncIGF2-AS or EZH2 was confirmed by luciferase reporter assay or RNA immunoprecipitation (RIP) assay. Murine xenograft model was established by using SGC-7901 cells stably transfected with sh-IGF2-AS. Results: The expression of IGF2-AS was elevated in GC tissues and cell lines, and highly expressed IGF2-AS predicted poor prognosis. Knockdown of IGF2-AS inhibited cells proliferation, migration, and invasion in vitro as well as tumor growth in vivo. IGF2-AS directly interacted with miR-937 and regulated GC progression by sponging miR-937. EZH2 was a target of miR-937 and miR-937 exerted antitumor effects in GC through downregulating EZH2 cells. Besides that, IGF2-AS indirectly regulated EZH2 expression by sponging miR-937. Conclusions: IGF2-AS promotes cell proliferation, migration, and invasion in GC via the miR-937/EZH2 axis, indicating that IGF2-AS works as an oncogene and may be a promising therapeutic and prognostic biomarker for GC.