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. 2011 May 27;108(24):9939–9944. doi: 10.1073/pnas.1105041108

Fig. 2.

Fig. 2.

Genetic ablation of endogenous angiogenesis inhibitors reveals functional roles as barriers to tumor growth but not angiogenic switching. (A) Deficiency in tumstatin (n = 6; RT2 only n = 6), endostatin (n = 2; RT2 only n = 2), or TSP1 (n = 5; RT2 only n = 5) did not significantly increase the frequency of angiogenic switching compared with RT2 mice. Deficiency in β3 integrin (n = 8; RT2 only n = 9), a functional receptor for tumstatin, also did not increase the frequency of angiogenic switching. (B) Enhanced tumor growth was observed in RT2 mice deficient in tumstatin (n = 5; RT2 only n = 6), endostatin (n = 3; RT2 only n = 9), TSP1 (n = 6; RT2 only n = 8), or β3 Integrin (n = 8; RT2 only n = 7). Additionally, a decreased lifespan was observed in RT2 mice deficient in tumstatin (n = 17; RT2 only n = 17) (C), endostatin (n = 6; RT2 only n = 16) (D), TSP1 (n = 21; RT2 only n = 17) (E), and β3 Integrin (n = 12; RT2 only n = 21) (F). Administration of the tumstatin peptide was able to improve survival of WT RT2 mice (n = 7) as shown in C. Results in A and B are shown as mean ± SEM; for C–F, significant differences are indicated by *P < 0.05, **P < 0.01.