Fig. 3

UBE2CP3 in HCC cells promoted EC proliferation, migration, and tube formation by enhancing the secretion of VEGFA into the supernatant via activation of the ERK/HIF-1α signalling pathway. a, b The levels of VEGFA in HepG2 concentrated supernatant were analysed by ELSIA (a) and western blot (b). For western blot, β-actin served as the internal control, β-Actin in the cell supernatant served as the quantity control. c, d, e Using VEGFA neutralizing antibody markedly reduce the effects of UBE2CP3 in HCC cells on EC proliferation (c), migration (d) and tube formation (e) in the co-culture system, IgG antibodies were used for negative control. f The levels of ERK1/2, p-ERK, p70S6K, p-p70S6K, HIF-1α, and VEGFA were examined by Western blot analysis in HepG2 cells overexpressing UBE2CP3 and in HepG2 cells with UBE2CP3 expression silenced. g Treatment with p-ERK inhibitor (PD98059) markedly reduce the levels of p-ERK, p-p70S6K, HIF-1α and VEGFA in UBE2CP3 overexpressing HepG2 cells. The data are expressed as the means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001