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Downmodulation of bFGF-binding protein expression following restoration of p53 function
Z A Sherif1, S Nakai, K F Pirollo
1Department of Oncology, Lombardi Cancer Center, Georgetown University Medical Center, Washington, District of Columbia 20007, USA.
Abstract:
Angiogenesis is a requirement for solid tumor growth. Therefore, inhibition of this neovascularization is one mechanism by which restoration of wtp53 function may lead to tumor regression. Here we report that adenoviral vector-mediated wild-type p53 transduction results in growth inhibition of squamous cell carcinoma of the head and neck tumor cells both in vitro and in a xenograft mouse model. This growth inhibition is associated with the down-regulation of the expression of fibroblast growth factor binding protein, a secreted protein required for the activation of angiogenic factor basic FGF. These findings suggest that wtp53-induced tumor regression is due, at least in part, to antiangiogenesis mediated by the downmodulation of fibroblast growth factor binding protein.
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