Background: Numerous previous studies have revealed that many long non-coding RNAs (lncRNAs) are upregulated in gastric cancer (GC) and are associated with tumor onset and progression in GC. ADPGK-AS1, a novel IncRNA, has been discovered as an oncogenic IncRNA in pancreatic cancer while its function in GC remains unclear. Materials and Methods: The expression of ADPGK-ASI and miR-3196 was determined by RT-qPCR. The expression of KDM1B was assessed by RT-qPCR and WB. The association between ADPGK-AS1 and overall survival of GC patients was explored using Kaplan-Meier curves. The function of ADPGK-AS1 in GC was examined through CCK-8, EdU, transwell as well as flow cytometry analysis. The interaction of miR-3196 and ADPGK-AS1 or KDM1B was confirmed by RIP, RNA pull down and luciferase reporter assay.Materials and Methods Results: ADPGK-ASI was increased in GC tissues and cell lines. GC patients with an increased expression of ADPGK-AS1 had a poor prognosis compared to those with a reduced expression. ADPGK-AS1 knockdown led to inhibition of GC cell proliferation and migration. The suppressive effect of ADPGK-AS1 silence on GC progression was abolished by KDM1B upregulation.Results Conclusions: We unveiled that ADPGK-AS1 could promote GC progression via sponging miR-3196 and therefore upregulating KDM1B, providing a novel prognostic biomarker and therapeutic target for GC patients.Conclusions (C) 2019 Elsevier Inc. All rights reserved.