Background: Long non-coding RNAs (lncRNAs) have become an essential factor in gastric cancer (GC) initiation and metastasis. This study aimed to uncover the functional significance of lncRNA EBLN3P in GC. Method: The potential role of lncRNA EBLN3P in GC was analyzed through Starbase database and RT-qPCR. Cell transfections were utilized to regulate target gene, including lncRNA EBLN3P, miR-589-5p and HIF3A. Cell viability, colony formation, migration and invasion were respectively estimated via MTT, colony formation, and transwell assays. Subsequently, Starbase database and luciferase reporter assay were utilized for studying the binding of lncRNA EBLN3P and miR-589-5p, as well as miR-589-5p and HIF3A. To further investigate this molecular mechanism of lncRNA EBLN3P/miR-589-5p/HIF3A axis, bioinformatics analysis and rescue experiments were performed. Results: In GC, lncRNA EBLN3P and HIF3A was significantly increased. In contrast, miR-589-5p was decreased. Localization assay revealed that EBLN3P primarily localized in the cytoplasm rather than the nucleus. Starbase database and luciferase reporter assays were utilized to predict and confirm that lncRNA EBLN3P could directly bind to miR-589-5p, which might bind to HIF3A. In MKN28 and SGC7901 cells, lncRNA EBLN3P knockdown suppressed cell viability, colony formation, migration, and invasion. On the contrary, overexpression of lncRNA EBLN3P facilitated these cellular processes. Interestingly, such negative modulation of lncRNA EBLN3P knockdown on these cellular processes could be reversed by miR-589-5p suppression or HIF3A excessive expression. Furthermore, lncRNA EBLN3P knockdown induced a reduction of HIF3A in GC cells. Conclusion: The lncRNA EBLN3P/miR-589-5p/HIF3A axis is identified to play crucial functions in GC mechanistic progression.