Cargando…

Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis

Newcastle disease virus (NDV) strongly induces both type I and III antiviral interferons (IFNs-α/-β and IFN-λ, respectively) in tumor cells while it induces mainly type III IFN in normal cells. Impairment of antiviral type I IFN signaling in tumor cells is thought to be the reason for effective onco...

Descripción completa

Detalles Bibliográficos
Autores principales: Ginting, Teridah Ernala, Christian, Salomo, Larasati, Young Othiwi, Suryatenggara, Jeremiah, Suriapranata, Ivet Marita, Mathew, George
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806003/
https://www.ncbi.nlm.nih.gov/pubmed/31641164
http://dx.doi.org/10.1038/s41598-019-51465-6
_version_ 1783461527624351744
author Ginting, Teridah Ernala
Christian, Salomo
Larasati, Young Othiwi
Suryatenggara, Jeremiah
Suriapranata, Ivet Marita
Mathew, George
author_facet Ginting, Teridah Ernala
Christian, Salomo
Larasati, Young Othiwi
Suryatenggara, Jeremiah
Suriapranata, Ivet Marita
Mathew, George
author_sort Ginting, Teridah Ernala
collection PubMed
description Newcastle disease virus (NDV) strongly induces both type I and III antiviral interferons (IFNs-α/-β and IFN-λ, respectively) in tumor cells while it induces mainly type III IFN in normal cells. Impairment of antiviral type I IFN signaling in tumor cells is thought to be the reason for effective oncolysis. However, there is lack of clarity why lentogenic strain NDV can also induce oncolysis. NDV infection caused apoptosis in normal and tumor cells as demonstrated with the caspase-3 enzyme activation and annexin-V detection. The apoptosis response was inhibited by B18R protein (a type I IFN inhibitor) in tumor cells i.e. A549 and U87MG, and not in normal cells i.e. NB1RGB and HEK293. Similarly, UV-inactivated medium from NDV infection was shown to induce apoptosis in corresponding cells and the response was inhibited in A549 and U87MG cells with the addition of B18R protein. Treatment with combination of IFNs-α/-β/-λ or IFNs-α/-β or IFN-λ in NB1RGB, HEK293, A549 and U87MG showed that caspase activity in IFNs-α/-β/-λ group was the highest, followed with IFN-α/-β group and IFN-λ group. This suggests that tumor-selectivity of NDV is mainly because of the cumulative effect of type I and III in tumor cells that lead to higher apoptotic effect.
format Online
Article
Text
id pubmed-6806003
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Nature Publishing Group UK
record_format MEDLINE/PubMed
spelling pubmed-68060032019-10-24 Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis Ginting, Teridah Ernala Christian, Salomo Larasati, Young Othiwi Suryatenggara, Jeremiah Suriapranata, Ivet Marita Mathew, George Sci Rep Article Newcastle disease virus (NDV) strongly induces both type I and III antiviral interferons (IFNs-α/-β and IFN-λ, respectively) in tumor cells while it induces mainly type III IFN in normal cells. Impairment of antiviral type I IFN signaling in tumor cells is thought to be the reason for effective oncolysis. However, there is lack of clarity why lentogenic strain NDV can also induce oncolysis. NDV infection caused apoptosis in normal and tumor cells as demonstrated with the caspase-3 enzyme activation and annexin-V detection. The apoptosis response was inhibited by B18R protein (a type I IFN inhibitor) in tumor cells i.e. A549 and U87MG, and not in normal cells i.e. NB1RGB and HEK293. Similarly, UV-inactivated medium from NDV infection was shown to induce apoptosis in corresponding cells and the response was inhibited in A549 and U87MG cells with the addition of B18R protein. Treatment with combination of IFNs-α/-β/-λ or IFNs-α/-β or IFN-λ in NB1RGB, HEK293, A549 and U87MG showed that caspase activity in IFNs-α/-β/-λ group was the highest, followed with IFN-α/-β group and IFN-λ group. This suggests that tumor-selectivity of NDV is mainly because of the cumulative effect of type I and III in tumor cells that lead to higher apoptotic effect. Nature Publishing Group UK 2019-10-22 /pmc/articles/PMC6806003/ /pubmed/31641164 http://dx.doi.org/10.1038/s41598-019-51465-6 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Ginting, Teridah Ernala
Christian, Salomo
Larasati, Young Othiwi
Suryatenggara, Jeremiah
Suriapranata, Ivet Marita
Mathew, George
Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title_full Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title_fullStr Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title_full_unstemmed Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title_short Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis
title_sort antiviral interferons induced by newcastle disease virus (ndv) drive a tumor-selective apoptosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806003/
https://www.ncbi.nlm.nih.gov/pubmed/31641164
http://dx.doi.org/10.1038/s41598-019-51465-6
work_keys_str_mv AT gintingteridahernala antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis
AT christiansalomo antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis
AT larasatiyoungothiwi antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis
AT suryatenggarajeremiah antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis
AT suriapranataivetmarita antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis
AT mathewgeorge antiviralinterferonsinducedbynewcastlediseasevirusndvdriveatumorselectiveapoptosis