Fig. 6
bFGF was critical for Gli1 mediated enhancement effect on angiogenesis and pericyte coverage. A-D Anti-bFGF treatment abolished the simulative effect of CM from A549Gli1 vector or NCI-H460Gli1 vector cells on the migration, invasion and tube formation of endothelial cells, indicating by wound healing (A), Transwell migration (B) and Transwell invasio (C), and tube formation assays (D). E Anti-bFGF attenuated the enhancement effect of CM from A549Gli1 vector or NCI-H460Gli1 vector cells on vessel sprouting. F, G bFGF neutralizing antibody weaken Gli1-mediated enhancement effect on the adhesion (F) and recruitment of HBVP (G). H–K bFGF supplement rescued CM from Gli1-knockdown NSCLC cells mediated inhibitory effect on the migration (H and I), invasion (J) and tube formation (K) of endothelial cells. L bFGF rescued the vessel sprouting of aortic ring educated by CM of NCI-H1299sh Gli1 and NCI-H1703sh Gli1 cells. M–N bFGF treatment enhanced the adhesion (M) and recruitment (N) of HBVP that were treated with CM from NCI-H1299sh Gli1 or NCI-H1703sh Gli1 cells. All the data were showed as mean ± SD, n = 3. ***p < 0.001 vs NC vector group or shNC group; ###p < 0.001 vs Gli1 vector group or shGli1 group