Figure 3 | British Journal of Cancer

Figure 3

From: Cooperative stimulation of vascular endothelial growth factor expression by hypoxia and reactive oxygen species: the effect of targeting vascular endothelial growth factor and oxidative stress in an orthotopic xenograft model of bladder carcinoma

Figure 3

Increased VEGF production by thymidine-treated RT112-TP is due to TP activity in both normoxic and hypoxic conditions. During the same experiment as shown in Figure 2, triplicate wells of RT112-TP were also exposed to thymidine in the presence of 50 μ M TPI, a specific inhibitor of TP activity (Matsushita et al, 1999), under normoxic (A) and hypoxic (B) conditions. Mean VEGF production (+one standard error) is expressed as picogram VEGF/million cells/16 h of the culture. The data for the TPI-free wells are taken from Figure 2. (A) In normoxia, TPI abolished the thymidine-dependent increase in VEGF secretion by RT112-TP (P=0.0495, Kruskall–Wallis analysis), but had no effect upon baseline VEGF production (P=0.51, Kruskall–Wallis analysis). (B) In hypoxia, TPI abolished the thymidine-dependent increase in VEGF secretion by RT112-TP (P=0.0495, Kruskall–Wallis analysis), but had no effect upon baseline VEGF production (P=0.51, Kruskall–Wallis analysis). These results confirm that TP activity is responsible for the increased VEGF production observed in thymidine-treated RT112-TP. (NS=no significant difference by Kruskall–Wallis analysis. *=significant difference by Kruskall–Wallis analysis).

Back to article page