Artículo
Bortezomib enhances the antitumor effects of interferon-β gene transfer on melanoma cells
Fecha de publicación:
05/2017
Editorial:
Bentham Science Publishers
Revista:
Anti-cancer Agents In Medicinal Chemistry
ISSN:
1871-5206
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
We evaluated the cytotoxic effects of the combination of bortezomib (BTZ) and interferon-β (IFNβ) gene lipofection on cultured melanoma cells. Four canine mucosal (Ak, Br, Bk and Ol) and two human dermal (A375 and SB2) melanoma cell lines were assayed. BTZ sub-pharmacological concentrations (5 nM) enhanced the cytotoxic effects of IFNβ transgene expression on melanoma cells monolayers and spheroids. The combination was also more effective than the single treatments when assayed for clonogenic survival and cell migration. The combined treatment produced a significant raise of apoptosis evidenced by DNA fragmentation as compared to either BTZ or IFNβ gene lipofection single treatments. Furthermore, BTZ significantly increased the intracellular reactive oxygen species (ROS) generation induced by IFNβ gene transfer in melanoma cells, an effect that was reversed by the addition of the ROS inhibitor N-acetyl-L-cystein. The present work encourages further studies about the potential of the combination of interferon gene transfer with proteasome inhibitors as a new combined therapy for malignant melanoma, both in veterinary and/or human clinical settings.
Palabras clave:
Bortezomib
,
Canine
,
Human
,
Interferon-Β
,
Lipofection
,
Melanoma
,
Ros
,
Spheroids
Archivos asociados
Licencia
Identificadores
Colecciones
Articulos(OCA HOUSSAY)
Articulos de OFICINA DE COORDINACION ADMINISTRATIVA HOUSSAY
Articulos de OFICINA DE COORDINACION ADMINISTRATIVA HOUSSAY
Citación
Rossi, Ursula Amaranta; Finocchiaro, Liliana Maria Elena; Glikin, Gerardo Claudio; Bortezomib enhances the antitumor effects of interferon-β gene transfer on melanoma cells; Bentham Science Publishers; Anti-cancer Agents In Medicinal Chemistry; 17; 5; 5-2017; 754-761
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