Fig. 5: B7-H3 promoted VEGFA expression and angiogenesis through the NF-κB pathway.

a The expression of p-STAT3, p-p65, p-AKT, p-JNK, and p-ERK1/2 in HCT116 (left) and RKO (right) stable cell lines with B7-H3 inhibition (shB7-H3) or their control cell lines (sh-NC) was analyzed by Western blot. β-actin was used as an internal control. b Relative mRNA level of VEGFA in B7-H3 CRC cells after treatment with perifosine, BAY11–7082 or cryptotanshinone were analyzed by RT-qPCR. c The protein expression of VEGFA in B7-H3 CRC cells after treatment with perifosine, BAY11–7082 or cryptotanshinone was analyzed by ELISA. d The protein expression of VEGFA in B7-H3 CRC cells after treatment with BAY11–7082 was detected by Western blot. e NF-κB activity in EV cells or B7-H3 cells was examined by luciferase reporter assay. f Schematic representation of the proposed B7-H3/NF-κB/VEGFA axis. g, h Cell migration (g) and invasion (h) in HUVECs were examined by transwell assays after HUVECs were co-treated with CM from EV cells or B7-H3 cells and BAY11–7082. Migrated and invaded HUVEC numbers are shown in the bar graph. i The tube formation of HUVECs co-treated with CM from EV cells or B7-H3 cells and BAY11–7082 was examined. The number of tubes counted is shown in the bar graph. The data represent the means ± SEM. NS no significant difference; *P < 0.05; **P < 0.01; ***P < 0.001.