Abstract: Objective To investigate the effects of LINC00987 activated by STAT1 on M2-type polarization of human glioblastoma (GBM) associated macrophages. Methods LncRNAs with dysregulated expression in GBM were screened by GEO analysis. The expression of LINC00987, miR-223-3p and FZD4 was detected by RT-qPCR. THP-1 cells were induced into M0, M1, and M2 macrophages, and GBM cells were co-cultured with THP-1 cells. The proportion of CD14⁺/CD206⁺ macrophages was detected by flow cytometry, The expression of M2-type macrophage-related factors (VEGF, TGF-β1) was detected by ELISA. Over-expression of LINC00987 promoted the M2-type polarization of GBM-related macrophages (P<0.05). FZD4 knockdown inhibited M2-type polarization of GBM-related macrophages, but this effect was partially reversed by over expression of LINC00987(P<0.05). Results Compared with paracancerous tissues and HEB cells, the expressions of LINC00987 and FZD4 in GBM tissues and cells were up-regulated while the expression of miR-223-3p was down-regulated(P<0.05). In GBM cells, STAT1 activated LINC00987 and affected miR-223-3p/FZD4 axis. LINC00987 knockdown inhibited M2-type polarization of GBM-related macrophages, but this effect was partially reversed by miR-223-3p inhibitors(P<0.05). Conclusions STAT1 activated LINC00987 regulates miR-223-3p/FZD4 axis to induce M2-type polarization of GBM-related macrophages.

Key words: glioblastoma, LINC00987, miR-223-3p, polarization of M2 type macrophages