Fig. 6

Exosomal CLEC3B decreased VEGF via activating phosphorylation of AMPK in ECs. a mRNA expression of VEGF in ECs treated with Exo-3B (no CC, P = 0.0065; CC, P = 0.7226; among groups, P < 0.0001) or Exo-3B-KD (no CC, P = 0.0063; CC, P = 0.7087; among groups, P < 0.0001). b Protein level changes in ECs treated with CC or not and Exo-3B or Exo-3B-KD, which were isolated from tumor cells. c The secretion of VEGF from ECs treated with Exo-3B (no CC, P = 0.0320; CC, P = 0.5765; among groups, P = 0.0021) or Exo-3B-KD (no CC, P = 0.0105; CC, P = 0.5004; among groups, P < 0.0001). d Tube formation of ECs treated with CC, Sunitinib and Exo-3B (no CC, no Sunitinib, P = 0.0204; CC, no Sunitinib, P = 0.0240; CC, Sunitinib, P = 0.0573; group no CC and CC, P < 0.0001; group no Sunitinib and Sunitinib, P < 0.0001) or Exo-3B-KD (no CC, no Sunitinib, P = 0.0017; CC, no Sunitinib, P = 0.0087; CC, Sunitinib, P = 0.3094; group no CC and CC, P < 0.0001; group no Sunitinib and Sunitinib, P < 0.0001). e Schematic graph for the functions of CLEC3B in HCC. *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., not significant