Research Paper Volume 13, Issue 15 pp 19243—19259

Glioma stem cell-derived exosomal miR-944 reduces glioma growth and angiogenesis by inhibiting AKT/ERK signaling


Figure 7. Exosomal miR-944 derived from GSCs suppresses angiogenesis of HUVECs by targeting VEGFC. (A) Targetscan analysis results show miR-944 binding sites in the 3’UTR of VEGFC. The mutated miR-944 binding site in the 3’UTR of VEGFC is also shown. (B) Dual luciferase reporter assay results show relative luciferase activity in HUVECs co-transfected with agomiR-NC or agomiR-944 plus luciferase vector with VEGFC-3’UTR-WT or VEGFC-3’UTR-MUT. A blank control was also included. **P < 0.01 vs. the agomir-ctrl group. (C) RT-qPCR analysis shows VEGFC levels in HUVECs transfected with agomiR-NC or agomiR-944. **P < 0.01 vs. the agomiR-NC group. (DF) Western blot analysis shows expression levels of p-Akt, Akt, p-ERK, and ERK in HUVECs co-cultured with GSC/agomiR-NC-Exo and GSC/agomiR-944-Exo for 24 h. The relative expression levels of p-Akt and p-ERK in HUVECs were normalized to total Akt and total ERK levels, respectively. **P < 0.01 vs. the GSC/agomiR-NC-Exo group. NC, negative control; GSCs, glioma stem cells; HUVECs, human umbilical vein endothelial cells.