It is increasingly evident that long non-coding RNAs (lncRNA) have causative roles in carcinogenesis. In this study, we report findings implicating a novel lncRNA in gastric cancer (GC), termed GAPLINC, based on the use of global microarray and in situ hybridization (ISH) analyses to identify aberrantly expressed lncRNA in human GC specimens. GAPLINC is a 924-bp long lncRNA that is highly expressed in GC tissues. GAPLINC suppression and with gene expression profiling in GC cells revealed alterations in cell migration pathways, with CD44 expression the most highly correlated. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effects of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression. Mechanistic investigations revealed that GAPLINC regulates CD44 as a molecular decoy for miR211-3p, a microRNA that targets both CD44 and GAPLINC. Tissue ISH analysis suggested that GAPLINC overexpression defines a subgroup of GC patients with very poor survival. Taken together, our results identify a non-coding regulatory pathway for the CD44 oncogene, shedding new light on the basis for GC cell invasiveness.