Figure 1.

Role of NF‐κB in glioma angiogenesis under a hypoxic microenvironment. Hypoxia‐induced NF‐κB is conducive to the upregulation of the HIF‐1α, VEGF, gal‐3 and MMP genes, which are released by tumour cells to induce EC chemotaxis and motility and stimulate angiogenesis. Hypoxia activated TNFR2 and VEGFR induced NF‐κB to upregulate the expression of antiapoptotic genes, such as Bcl‐2, Bcl‐XL, survivin and XIAP in ECs. NDRG1 induced the upregulation of anti‐angiogenesis gene TNFSF15 by the activation of NF‐κB and AP‐1 in the TNFSF15 promoter region. TNFSF: tumour necrosis factor super family; TNFR: tumour necrosis factor receptor; NF‐κB: nuclear factor‐κB; VEGF: vascular endothelial growth factor; VEGFR: vascular endothelial growth factor receptor; PI3K: phosphatidylinositol 3‐kinase; Gal‐3: galectin‐3; XIAP: X‐chromosome‐linked inhibitor of apoptosis protein; HIF: hypoxia‐inducible factor; MMP: matrix metalloproteinase; AP: activator protein; ECM: extracellular matrix; NDRG1: N‐myc downstream‐regulated gene‐1