〔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 gas- tric 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/# -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），transform- ing growth factor-#（ 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/# -catenin pathway—Wnt family member 3a（Wnt3a）， glycogen synthase kinase-3#（GSK-3#）， and # -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 prolifera- tion，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 #-catenin proteins in cells increased（P<0. 05）， and the expression level of GSK-3# protein decreased（P<0. 05）. However，co-treatment with IWR-1 markedly reversed the promoting effects of LINC02086 overexpression on the expression of M2 polariza- tion markers，including CD206，IL⁃10，and TGF⁃β mRNA，in macrophages（P<0. 05），as well as its activation of the Wnt/#-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 of IWR-1 significantly reversed the promotion of LINC02086 overex- pression on the proliferation，migration and invasion of HGC-27 cells（P<0. 05）. Conclusion LINC02086 overex- pression promotes the proliferation，migration and invasion of gastric cancer cells by activating Wnt/#-catenin path- way to mediate M2 polarization of macrophages.