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From the Molecular Biology Laboratory and the Tumor Progression
Section,*
Istituto Nazionale per la Ricerca sul Cancro, the
Centro di Biotecnologie Avanzate,
Genova; the
Department of Experimental Medicine, Anatomy
Section,
Università di Genova, Genova;
the Istituto Superiore di Sanità,§
Rome;
and the Servizio di Anatomia, Istologia e Citologia
Patologica,¶
Ospedale San Martino, Genova, Italy
We developed an in vivo gene therapy
approach to characterize and optimize the anti-angiogenic activity of
class I interferons (IFNs), using packaging cell lines
producing an amphotropic LXSN-based retrovirus expressing either
IFN-
1 (1Am12), IFN-ß (ßAm12) murine cDNAs, or
the vector alone (neoAm12). Pretreatment of endothelial-like Eahy926
cells in vitro with conditioned media (CM) from
1Am12 or ßAm12 cells for 48 hours significantly inhibited their
migration and invasion as compared to neoAm12-CM-treated cells.
ßAm12-CM also inhibited the formation of capillary-like
structures on Matrigel by EAhy926 cells. In
vivo, inclusion of the ßAm12 cells strongly
inhibited, and 1Am12 partially inhibited, the
angiogenic response in the Matrigel sponge model in both
immune-competent and athymic nude mice. Electron microscopy showed a
reduction of host cell infiltration in 1Am12- and ßAm12-containing
sponges and reduction of invading tubular clefts of host cells as
compared to controls. Finally, inoculation of either 1Am12
or ßAm12 cells (10%) along with a highly angiogenic Kaposi’s
sarcoma cell line (90%) resulted in a powerful reduction of tumor
growth in nude mice in vivo, as did infection with the
interferon--producing retroviruses. These data suggest that a gene
therapy approach using class I interferons can effectively inhibit
tumor angiogenesis and growth of vascular tumors.
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