Downmodulation of bFGF-binding protein expression following restoration of p53 function.

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.

journal_name

Cancer Gene Ther

journal_title

Cancer gene therapy

authors

Sherif ZA,Nakai S,Pirollo KF,Rait A,Chang EH

doi

10.1038/sj.cgt.7700361

subject

Has Abstract

pub_date

2001-10-01 00:00:00

pages

771-82

issue

10

eissn

0929-1903

issn

1476-5500

journal_volume

8

pub_type

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