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. 2021 Jul 2;29(12):3449–3464. doi: 10.1016/j.ymthe.2021.06.023

Figure 7.

Figure 7

2-ME2 impairs glioma cell exosome production and exosomal miR-1246 expression

(A) Normoxic and hypoxic exosomes were isolated from glioma cell culture medium after 2-ME2 treatment and used to stimulate PBMCs. (B) MDSCs induced by the 4 types of GDEs in (A) were co-cultured with human CD8+ T cells. The proliferation of CD8+ T cells was measured by flow cytometry. (C) The expression of miR-1246 in the 4 types of GDEs in (A) was measured by quantitative real-time PCR. (D) The U87MG GDE concentration was measured with ZetaView after control (DMSO), 2-ME2, and vincristine (50 nM, MedChemExpress) treatment. (E) The expression of hnRNPA1 and POU5F1 in normoxic and hypoxic U87MG cells treated with 2-ME2 was measured by immunoblotting. (F) PD-L1 expression and T cell suppression assay of MDSCs isolated from GBM patient peripheral blood treated with hypoxia and 2-ME2 (n = 5 for each group). (G) Bioluminescence images and the corresponding quantification of U87MG glioma in mice treated with control (DMSO) or 2-ME2 (n = 5 for each group). (H) Plasma exosomal miR-1246 levels were measured with quantitative real-time PCR (n = 5 for each group). (I and J) The percentage of Cd11b+Ly6c+ M-MDSCs in the spleen and tumors of glioma-bearing mice was measured (n = 5 for each group). The data are presented as the mean ± SD; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.