Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance

Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cel...

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Detalles Bibliográficos
Autores principales: Li, Weike, Turaga, Ravi Chakra, Li, Xin, Sharma, Malvika, Enadi, Zahra, Dunham Tompkins, Sydney Nicole, Hardy, Kyle Christian, Mishra, Falguni, Tsao, Jun, Liu, Zhi-ren, Fan, Daping, Luo, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society of Gene & Cell Therapy 2019
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610632/
https://www.ncbi.nlm.nih.gov/pubmed/31312717
http://dx.doi.org/10.1016/j.omto.2019.05.006
Descripción
Sumario:Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis.

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