Skip to main content
. 2006 Oct 20;103(44):16266–16271. doi: 10.1073/pnas.0608017103

Fig. 3.

Fig. 3.

p53 status modifies the angiogenic response of tumors upon MYC inactivation. (A Left) p53 status does not affect the angiogenic response of tumor onset upon MYC activation. p53 wild-type (p53+), p53 negative (p53−) and p53 restored (p53− to +) transplanted tumors were examined by immunofluorescence for microvessel density (CD31) and TSP-1 expression (MYC on). (A Right) The loss of p53 decreases TSP-1 levels despite MYC inactivation. p53 wild-type (p53+), p53 negative and p53 restored (p53− to +) transplanted tumors were examined by immunofluorescence for microvessel density (CD31) and TSP-1 expression 6 days after MYC inactivation (MYC Off). Whereas there was no significant difference in the level of TUNEL reactivity, there were significantly more TUNEL-positive endothelial cells (white arrow) in p53 wild-type (p53+) and p53 restored (p53− to +) tumors as compared with p53 negative (p53−) tumors. Specificity of staining was ensured by immunostaining of serial tumor sections with isotype matched control antibodies. (B) Western blot analysis of p53 wild-type (p53+) and p53 negative (p53−) transplanted tumors were performed for TSP-1 expression upon MYC activation and 6 days after MYC inactivation. Densitometric analysis demonstrated significantly higher TSP-1 expression in p53 wild-type (p53+) tumor cells relative to β-actin as compared with p53 negative (p53−) tumor cells. (C) Quantification of microvessel density (MVD) per high power field (hpf) demonstrated significantly increased MVD/hpf in p53 negative (p53−) tumors 6 days after MYC inactivation as compared with p53 wild-type (p53+) tumors. At least five fields were counted in representative tumor sections, and at least two different transplanted tumors were analyzed. Values are represented as means ± standard deviation.

HHS Vulnerability Disclosure