Capacity of wild-type and chemokine-armed parvovirus H-1PV for inhibiting neo-angiogenesis

Abstract Anti-angiogenic therapy has been recognized as a powerful potential strategy for impeding the growth of various tumors. However no major therapeutic effects have been observed to date, mainly because of the emergence of several resistance mechanisms. Among novel strategies to target tumor v...

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Published in:Virology (New York, N.Y.) N.Y.), 2013-12, Vol.447 (1), p.221-232
Main Authors: Lavie, Muriel, Struyf, Sofie, Stroh-Dege, Alexandra, Rommelaere, Jean, Van Damme, Jo, Dinsart, Christiane
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
ANGIOGENESIS
Animals
Biological Therapy - methods
Cancer therapy
CAPACITY
Cell Survival - drug effects
Cells, Cultured
Chemokine
Chemokines - metabolism
Endothelial Cells - drug effects
Humans
Infectious Disease
Kaposi sarcoma
Mice
Neoplasms - therapy
Neovascularization, Pathologic - prevention & control
Parvovirus
Parvovirus - physiology
RODENTS
SARCOMAS
Survival Analysis
THERAPY
TOXICITY
Treatment Outcome
TUMOR CELLS
VALIDATION
VIRUSES
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Summary:Abstract Anti-angiogenic therapy has been recognized as a powerful potential strategy for impeding the growth of various tumors. However no major therapeutic effects have been observed to date, mainly because of the emergence of several resistance mechanisms. Among novel strategies to target tumor vasculature, some oncolytic viruses open up new prospects. In this context, we addressed the question whether the rodent parvovirus H-1PV can target endothelial cells. We show that cultures of human normal (HUVEC) and immortalized (KS-IMM) endothelial cells sustain an abortive viral cycle upon infection with H-1PV and are sensitive to H-1PV cytotoxicity. H-1PV significantly inhibits infected KS-IMM tumor growth. This effect may be traced back by the virus ability to both kill proliferating endothelial cells and inhibit VEGF production Recombinant H-1PV vectors can also transduce tumor cells with chemokines endowed with anti-angiogenesis properties, and warrant further validation for the treatment of highly vascularized tumors.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2013.09.019