FIGURE 3

Exosomal miR‐92b‐3p modulates tumor‐associated angiogenesis. (A) qRT‐PCR analysis on the relative expression of miR‐92b‐3p in HUVECs treated with IOSE‐80/exo, SKOV3/exo, and A2780/exo, respectively, for 48 h with or without 5,6‐dichlorobenzimidazole 1‐β‐D‐ribofuranoside (DRB) (20 μm/ml), compared to HUVECs treated with PBS (mean ± SD, n = 3). (B) qRT‐PCR analysis on the relative expressions of miR‐92b‐3p in SKOV3 cells, SKOV3‐92b cells, SKOV3/exo, and SKOV3‐92b/exo (mean ± SD, n = 3). (C) qRT‐PCR analysis on relative expression of miR‐92b‐3p in HUVECs treated with SKOV3/exo or SKOV3‐92b/exo (mean ± SD, n = 3). (D) qRT‐PCR analysis on the expression of miR‐92b‐3p in exosomes after enzyme digestion, with or without destroyed membranes by Triton X‐100 (mean ± SD, n = 3). (E) Representative images of tube formation and migration of HUVECs treated with SKOV3/exo and SKOV3‐92b/exo, respectively (scale bar = 100 μm). Total master segments length, number of master junctions, number of master nodes, and migration cell numbers were regarded as indicators of angiogenic ability in vitro and assessed by ImageJ (mean ± SD, n = 3). (F) Left: Representative confocal images of the trunk vasculature of zebrafish injected with SKOV3‐NC/exo or SKOV3‐92b/exo (scale bar = 100 μm). Right: Quantification of the number of ectopic sprouts observed per fish (mean ± SD) injected with SKOV3/exo (n = 14) or SKOV3‐92b/exo (n = 12), respectively. Data are shown by at least three independent experiments and the Student's t‐test was used to compare differences. *p < .05, **p < .01, ***p < .001, ****p < .0001