Fig. 2: TNFAIP2 promotes angiogenesis in vitro by upregulating the HIF1α expression.
A Overexpressing TNFAIP2 in HCC1806 cells increased HIF1α protein expression. Following stable overexpression of TNFAIP2, the cells were exposed to 1% O2. Cell lysates were harvested for WB analysis. B Overexpression of TNFAIP2 in HCC1806 cells increased the mRNA levels of HIF1α, GLUT-1 and VEGFA. Following stable overexpression of TNFAIP2, the cells were exposed to 1% O2 for 48 h. Cell lysates were harvested for real-time PCR. C Overexpressing TNFAIP2 in HCC1806 cells increased the secreted VEGFA protein levels. The cells were exposed to 1% O2 for 24 h. D Overexpression of TNFAIP2 and knockdown of HIF1α in HCC1806 cells, as detected by WB. E HIF1α knockdown abolished TNFAIP2-induced VEGFA transcription upregulation. HCC1806 cells with stable TNFAIP2 overexpression were transfected with HIF1α siRNA. After 48 h of transfection, cell lysates were harvested for real-time PCR analysis. F, G Knockdown of HIF1α impeded the TNFAIP2 overexpression-induced migration of HUVECs by the wound-healing assay. Representative images are shown. H, I Knockdown of HIF1α impeded the TNFAIP2 overexpression-induced tube formation of HUVECs. Representative images are shown. Scale bar, 200 μm, in the histogram, the bars represent the mean ± SD (n = 3), *P < 0.05, **P < 0.01 and ***P < 0.001; ns not significant.
