Fig. 3
From: Efficient RNA drug delivery using red blood cell extracellular vesicles
RBCEVs deliver ASOs to leukemia and breast cancer cells for miR-125b inhibition. a Experimental scheme of ASOs delivery to cancer cells using RBCEVs. b Percentage of anti-miR-125b ASOs (125b-ASOs) associated with 6.2 × 1011 unelectroporated or 125b-ASO-electroporated RBCEVs after a treatment with RNase If for 30 min. c Copy number of 125b-ASO in MOLM13 cells treated with 12.4 × 1011 RBCEVs unelectroporated (UE-EVs) or RBCEVs electroporated with NC-ASOs or with 125b-ASOs for 72 h. d Expression fold change of miR-125b in MOLM13 cells that were incubated with 125b-ASOs alone, 16.8 × 1011 unelectroporated RBCEVs (UE-EVs), 16.8 × 1011 NC-ASOs-loaded RBCEVs, or 4.2 to 16.8 × 1011 125b-ASOs loaded RBCEVs. miR-125b expression was determined using Taqman qRT-PCR normalized to U6b RNA and presented as average fold change relative to the untreated control. e Expression fold change of BAK1 in MOLM13 cells treated as in d, determined using SYBR Green qRT-PCR, normalized to GAPDH and presented as average fold change relative to the untreated control. f Proliferation of MOLM13 cells treated with 12.4 × 1011 unelectroporated or NC/125b-ASO-electroporated EVs, determined using cell counts. g Viability of breast cancer CA1a cells (%) treated as in f, determined by crystal violet staining. In all panels, the experiments were repeated three or four times with 3 or 4 cell passages. Bar graphs present mean ± SEM. P values were calculated using one-way ANOVA test (d, e) or student’s one-tail t-test relative to the untreated controls (b, f, g) *P < 0.05, **P < 0.01
