Abstract：
:Tumor growth is an angiogenesis-dependent process and therapeutic strategies aimed at inhibiting angiogenesis are theoretically attractive. Angiostatin has been shown to potently inhibit endothelial proliferation in vitro and tumor growth in vivo. We now show that a shift in the balance of tumor angiogenesis by gene transfer of a cDNA coding for mouse angiostatin into mouse squamous cell carcinoma NRS-1 and SCC-VII cells suppresses tumor growth in vivo. The inhibition of an angiostatin-transfected tumor was accompanied by a marked reduction in vascularity and the presence of many apoptotic tumor cells. However, transfected-angiostatin cDNA does not affect the expression of the vascular endothelial growth factor (VEGF) and VEGF-R2 in the vascular endothelium. The inhibition mechanisms of neovascularization may be mediated independent of VEGF:VEGF-R2 complex. Our data may provide a useful approach for human oral cancer therapy by gene therapy with angiostatin.
journal_name
Oral Oncoljournal_title
Oral oncologyauthors
Matsumoto G,Ohmi Y,Shindo Jdoi
10.1016/s1368-8375(00)00100-7subject
Has Abstractpub_date
2001-06-01 00:00:00pages
369-78issue
4eissn
1368-8375issn
1879-0593pii
S1368-8375(00)00100-7journal_volume
37pub_type
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