Journal
ONCOLYTIC VIROTHERAPY
Volume 6, Issue -, Pages 21-30Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OV.S123292
Keywords
Newcastle disease virus; oncolytic virus; interferons; cytokines
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Funding
- Mochtar Riady Institute for Nanotechnology
- Ethics Committee (EC) of the Mochtar Riady Institute for Nanotechnology (MRIN) [011/MRIN-EC/01/2014]
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Purpose: To investigate the specific role of immune responses induced by lentogenic Newcastle disease virus (NDV) for its antitumor effect. Materials and methods: NDV LaSota strain was used to infect the following human cells: non-small cell lung carcinoma (A549), glioblastoma (U87MG and T98G), mammary gland adenocarcinoma (MCF7 and MDA-MB-453), hepatocellular carcinoma (Huh7), transformed embryonic kidney cells (HEK293), primary monocytes, lung fibroblast (HF19), skin fibroblast (NB1RGB) and rat astroglia (RCR-1) at 0.001 multiplicity of infection. NDV-induced cytotoxicity and expression of proinflammatory cytokines were analyzed using 3-(4,5-dimethylthiazol2- Yl)-2,5-diphenyltetrazolium bromide assay and multiplex enzyme-linked immunosorbent assay, respectively. Results: Tumor cells (A549, U87MG, T98G, Huh7, MDA-MB-453, and MCF7) showed viability of < 44%, while normal cell lines HEK293, NB1RGB, and RCR-1 showed 84%, 73%, and 69% viability at 72 hours postinfection, respectively. Proinflammatory cytokine profiling showed that NDV mainly induced the secretion of interferon (IFN)-alpha, IFN-beta, and IFN-lambda in tumor cells and only IFN-. in normal cells. In addition, NDV infection induced the production of interleukin (IL)-6 in most cells. Conclusion: Our findings suggest a new perspective regarding the role of IFN-lambda and IL-6 in the mechanism of tumor selectivity and oncolysis of NDV.
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