p73 Overexpression and angiogenesis in human colorectal carcinoma

Solid tumors requires neovascularization for growth and metastasis. Angiogenesis depends on the local balance between positive and negative effectors, the production of which can be regulated by oncogenes and tumor suppressor genes. The aim of this study was to investigate expression of p73, a gene homologous to the tumor suppressor gene p53, in colorectal cancer and its relationship to angiogenesis.

p73 expression was examined by immunohistochemistry and western blot analysis on 56 primary colon carcinomas with matched normal mucosas. Vascular endothelial growth factor (VEGF) and microvessels were highlighted using a monoclonal antibody specific to VEGF and von Willebrand factor (vWF).

The immunoexpressions of p73 were significantly higher in the primary colorectal carcinomas than that in the matched normal mucosa (P < 0.001). Western blotting showed that 85% patients have a high level of p73 expression (more than double the normal level). A close association between p73 and VEGF expression level was observed (P = 0.016). Colorectal adenocarcinoma that expressed p73 showed significantly greater vascularity than p73-negative tumors (P = 0.012). However, no association between immunoexpression of p73 and tumor stage or differentiation was observed.

These findings suggest a potential role of p73 in tumor angiogenesis.