A host non-coding RNA, nc886, plays a pro-viral role by promoting virus trafficking to the nucleus

Cited 4 time in scopus
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Title
A host non-coding RNA, nc886, plays a pro-viral role by promoting virus trafficking to the nucleus
Author(s)
E Saruuldalai; J Park; D Kang; S P Shin; W R Im; H H Lee; J J Jang; Jong Lyul ParkSeon-Young Kim; J A Hwang; Y D Kim; J H Lee; E J Park; Y S Lee; I H Kim; S J Lee; Y S Lee
Bibliographic Citation
Molecular Therapy-Oncolytics, vol. 24, pp. 683-694
Publication Year
2022
Abstract
Elucidation of the interplay between viruses and host cells is crucial for taming viruses to benefit human health. Cancer therapy using adenovirus, called oncolytic virotherapy, is a promising treatment option but is not robust in all patients. In addition, inefficient replication of human adenovirus in mouse hampered the development of an in vivo model for preclinical evaluation of therapeutically engineered adenovirus. nc886 is a human non-coding RNA that suppresses Protein Kinase R (PKR), an antiviral protein. In this study, we have found that nc886 greatly promotes adenoviral gene expression and replication. Remarkably, the stimulatory effect of nc886 is not dependent on its function to inhibit PKR. Rather, nc886 facilitates the nuclear entry of adenovirus via modulating the kinesin pathway. nc886 is not conserved in mouse and, when xenogeneically expressed in mouse cells, promotes adenovirus replication. Our investigation has discovered a novel mechanism of how a host ncRNA plays a pro-adenoviral role. Given that nc886 expression is silenced in a subset of cancer cells, our study highlights that oncolytic virotherapy might be inefficient in those cells. Furthermore, our findings open future possibilities of harnessing nc886 to improve the efficacy of oncolytic adenovirus and to construct nc886-expressing transgenic mice as an animal model.
ISSN
2372-7705
Publisher
Elsevier-Cell Press
DOI
http://dx.doi.org/10.1016/j.omto.2022.02.018
Type
Article
Appears in Collections:
Aging Convergence Research Center > 1. Journal Articles
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