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10.2147/OV.S123292

http://scihub22266oqcxt.onion/10.2147/OV.S123292
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C5345992!5345992!28293547
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suck abstract from ncbi


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pmid28293547      Oncolytic+Virother 2017 ; 6 (ä): 21-30
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  • Proinflammatory response induced by Newcastle disease virus in tumor and normal cells #MMPMID28293547
  • Ginting TE; Suryatenggara J; Christian S; Mathew G
  • Oncolytic Virother 2017[]; 6 (ä): 21-30 PMID28293547show ga
  • 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-dimethylthiazol-2-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)-?, IFN-?, and IFN-? 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-? and IL-6 in the mechanism of tumor selectivity and oncolysis of NDV.
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