Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 63, 5224-5229, September 1, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Matrix Metalloproteinases (MMP9 and MMP2) Induce the Release of Vascular Endothelial Growth Factor (VEGF) by Ovarian Carcinoma Cells

Implications for Ascites Formation1

Dorina Belotti2, Paola Paganoni, Luigi Manenti, Angela Garofalo, Sergio Marchini, Giulia Taraboletti and Raffaella Giavazzi

Laboratory of Biology and Therapy of Metastasis [D. B., P. P., L. M., A. G., G. T., R. G.] and Laboratory of Molecular Pharmacology [S. M.], Department of Oncology, Mario Negri Institute for Pharmacological Research, 24125 Bergamo, Italy

This study investigated the functional interplay between vascular endothelial growth factor (VEGF) and metalloproteinases (MMPs) in ovarian carcinomas. Levels of MMP9 (pro and activated form) and proMMP2 in ascites correlated with VEGF and with the ascitic volume in nude mice bearing human ovarian carcinoma xenografts (HOC22 and HOC8). The MMP inhibitor batimastat (BB-94) reduced VEGF release and ascitic fluid formation. Exogenous, activated MMP9, and, to a lesser extent, MMP2, increased VEGF release by SKOV3 and OVCAR3 ovarian carcinoma cells. The effect was dose and time dependent and inhibited by BB-94. MMP9-released VEGF was biologically active, because it induced endothelial cell motility, and its activity was prevented by the VEGF inhibitor SU5416. Our results indicate that MMPs, mainly MMP9, play a role in the release of biologically active VEGF and consequently in the formation of ascites.




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