BackgroundGastric cancer (GC) is one of the most common malignancies around the world. Recently, the role of long non-coding RNA (lncRNA) in cancer biology has become a hot research topic. This work aimed to explore the biological function and underlying mechanism of LINC01089 in GC.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was employed to investigate the expression of LINC01089 in GC tissues and cells. The relationship between the expression level of LINC01089 and the clinicopathological parameters of GC was assessed. Cell models of LINC01089 overexpression, LINC01089 knockdown, miR-27a-3p overexpression, and miR-27a-3p inhibition were established by transfection. CCK-8 assay, BrdU assay, and Transwell assay were utilized to investigate the malignant biological behaviors of GC cell lines after transfection. Dual luciferase activity reporter assay, Pearson’s correlation analysis, and Western blot were utilized to the regulatory relationships among LINC01089, miR-27a-3p and tet methylcytosine dioxygenase 1 (TET1).ResultLINC01089 down-regulation was observed in GC tissues and cell lines. Low expression level of LINC01089 in GC tissues was markedly linked to larger tumor size, higher T stage, as well as lymphatic metastasis of the patients. Functional experiments implied that LINC01089 overexpression impeded the proliferation, migration, as well as invasion of GC cells, whereas LINC01089 knockdown promoted the above malignant phenotypes. Additionally, up-regulation of miR-27a-3p was also observed in GC tissues. Functional experiments also showed that, miR-27a-3p overexpression boosted the malignant biological behaviors of GC cells; on the contrast, these phenotypes were impeded by miR-27a-3p inhibition. Moreover, LINC01089 interacted with and repressed miR-27a-3p, and miR-27a-3p antagonized the impact of LINC01089 on GC cells. Additionally, TET1 was verified as a target gene of miR-27a-3p, and could be positively regulated by LINC01089.ConclusionLINC01089 impedes the proliferation, migration, and invasion of GC cells by adsorbing miR-27a-3p and up-regulating the expression of TET1.