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. 2022 May 19;22:101451. doi: 10.1016/j.tranon.2022.101451

Fig. 4.

Fig. 4:

Targeting miR-9 in GSC-derived EVs for regulation of GBM cell growth. (A) The expression of miR-9 in GSC1/2 was significantly increased than U87 and U251 cell and showed strong enrichment in GSC-derived EVs than GSCs. (B) Exosomes isolated GSCs with or without miR-9 inhibitor treatment (termed as EXO and EXO-miR-9-inhibitor group) and then were co-incubated with U87 and U251 cells. The relative miR-9 expression was decreased after EXO-miR-9-inhibitor treatment and increased in EXO groups. (C) The cell growth was suppressed in EXO-miR-9-inhibitor groups while elevated in EXO groups both in U87 and U251cells. (D) Cell apoptosis was measured by flow cytometry. Cells treated with miR-9 inhibitor exosomes showed a higher apoptotic rate than control. The EdU positive cell rates was recorded. EXO groups showed increased tumor viability in U87 (E) and U251 (F) cells. (G and H) Intracranial xenograft model was employed. Inhibition of miR-9 impaired GBM growth and luciferase activity in vivo. (I) Kaplan-Meier analysis of overall survival of the sh-NC group and the sh-miR-9 group, n=6. (J)The expression of decreased in sh-miR-9 group. Data were represented as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 and #p < 0.05, ##p < 0.01, ###p < 0.001 versus corresponding NC groups.