〔Abstract〕 To investigate the effect and mechanism of long intergenic non-coding RNA02086 (LINC02086) overexpression mediated macrophage polarization on the proliferation, migration and invasion of gastric cancer cells. Methods The expression levels of LINC02086 in the human gastric epithelial cell line GES-1 and human gastric cancer cell lines HCG-27, NCI-N87, and AGS were determined by qRT-PCR. Human acute monocytic leukemia cells (THP-1) were induced to differentiate into M0 macrophages using phorbol 12-myristate 13-acetate (PMA). HGC- 27 cells were infected with either LINC02086 overexpression lentivirus (OE-LINC02086) or its negative control lentivirus (Vector), and the culture supernatants were collected as conditioned medium (CM1). M0 macrophages were co-cultured with the infected HGC-27 cells, and the resulting supernatants were designated as conditioned medium 2 (CM2). M0 macrophages were treated with CM1 alone or in combination with Wnt/β-catenin pathway inhibitor IWR-1, forming the Vector+CM1, OE-LINC02086+CM1, and OE-LINC02086+CM1+IWR-1 groups, respectively. Flow cytometry was used to detect mannose receptor C-type 1 (CD206) expression, and qRT-PCR was employed to measure mRNA levels of interleukin-10 (IL-10), transforming growth factor-β (TGF-β), vascular endothelial growth factor (VEGF), and chemokine ligand 22 (CCL22). Western blot was performed to evaluate protein expression of CD206, VEGF, and key components of the Wnt/β-catenin pathway—Wnt family member 3a (Wnt3a), glycogen synthase kinase-3β (GSK-3β), and β-catenin. HGC-27 cells were treated with CM2 alone or combined with IWR-1, establishing the Vector+CM2, OE-LINC02086+CM2, and OE-LINC02086+CM2+IWR-1 groups. CCK-8 assay was used to evaluate cell proliferation, and Transwell assays were conducted to assess migration and invasion capabilities. Results Compared with GES-1 cells, the expression levels of LINC02086 were upregulated in HCG-27, NCI-N87, and AGS cells (P < 0.05), with the smallest increase observed in HCG-27 cells. Compared with Vector+CM1 group, the level of CD206 and the expression levels of IL-10, TGF-β, VEGF and CCL22 mRNA in macrophages stimulated by OE- LINC02086+CM1 increased (P<0.05). Meanwhile, the expression levels of Wnt3a and β-catenin proteins in cells increased (P<0.05), and the expression level of GSK-3β protein decreased (P<0.05).However, co-treatment with IWR-1 markedly reversed the promoting effects of LINC02086 overexpression on the expression of M2 polarization markers, including CD206, IL-10, and TGF-β mRNA, in macrophages (P<0.05), as well as its activation ofthe Wnt/β-catenin signaling pathway (P<0.05). Compared with Vector+CM2 group, HGC-27 cells infected with OE-LINC02086+CM2 had increased proliferation activity and increased number of migration and invasion cells (P<0.05). However, the combined intervention ofIWR-1 significantly reversed the promotion of LINC02086 overexpression on the proliferation, migration and invasion of HGC-27 cells (P<0.05). Conclusion LINC02086 overexpression promotes the proliferation, migration and invasion of gastric cancer cells by activating Wnt/β-catenin pathway to mediate M2 polarization of macrophages.