Journal
ANNALS OF ONCOLOGY
Volume 19, Issue 9, Pages 1584-1591Publisher
OXFORD UNIV PRESS
DOI: 10.1093/annonc/mdn167
Keywords
angiogenesis; apoptosis; cisplatin-resistant; ovarian cancer; vesicular stomatitis virus matrix protein (VSVMP)
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Funding
- National Basic Research Program of China [2004CB518800, 2004CB518800, 2004CB518706]
- 863 Hi-tech Research and Development Program of China [2007AA021106]
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Background: The vesicular stomatitis virus matrix protein (VSVMP) has been receiving attention as an anticancer agent because of its ability of inducing apoptosis. Materials and methods: Nude mice bearing A2780s and A2780cp ovarian tumors were treated twice weekly with i.v. administration of 50 mu g VSVMP/250 mu g liposome complex, 50 mu g empty plasmid/250 mu g liposome complex, 0.9% NaCl solution or weekly with i.p. administration of cisplatin (5 mg/kg) for 3 weeks. Tumor volume and survival time were observed. TUNEL assay and CD34 vessel staining were conducted in tumor tissue. Antiangiogenesis in vivo were determined by sponge assay. Antiproliferative and apoptosis-inducing activities of VSVMP in vitro were tested on MS1murine endothelial cells and four human ovarian cancer cell lines: A2780s, A2780cp, HO8910 and COC1. Results: Administration of VSVMP resulted in significant inhibition (87%-98% maximum inhibition relative to controls) in the growth of A2780s and A2780cp tumor xenografts, and prolonged the survival of the treated mice. Complete tumor regression happened in VSVMP-treated mice in both tumor models. These antitumor responses were associated with marked increases in tumor apoptosis and reductions in intratumoral microvessel density. Conclusions: Our data indicate that VSVMP may provide an effective approach to inhibit both cisplatin-sensitive and -resistant human ovarian cancer growth with minimal side-effects.
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