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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/50317
Title: Protein kinase R and its cellular regulators in cancer: An active player or a surveillant?
Authors: Yong Sun Lee
Nawapol Kunkeaw
Yeon Su Lee
National Cancer Center, Gyeonggi
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Jan-2019
Citation: Wiley Interdisciplinary Reviews: RNA. (2019)
Abstract: © 2019 Wiley Periodicals, Inc. Protein kinase R (PKR), originally known as an antiviral protein, senses various stresses as well as pathogen-driven double-stranded RNAs. Thereby activated PKR provokes diverse downstream events, including eIF2α phosphorylation and nuclear factor kappa-light-chain-enhancer of activated B cells activation. Consequently, PKR induces apoptosis and inflammation, both of which are highly important in cancer as much as its original antiviral role. Therefore, cellular proteins and RNAs should tightly control PKR activity. PKR and its regulators are often dysregulated in cancer and it is undoubted that such dysregulation contributes to tumorigenesis. However, PKR's precise role in cancer is still in debate, due to incomprehensible and even contradictory data. In this review, we introduce important cellular PKR regulators and discuss about their roles in cancer. Among them, we pay particular attention to nc886, a PKR repressor noncoding RNA that has been identified relatively recently, because its expression pattern in cancer can explain interesting yet obscure oncologic aspects of PKR. Based on nc886 and its regulation of PKR, we have proposed a tumor surveillance model, which reconciles contradictory data about PKR in cancer. This article is categorized under: Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA Interactions with Proteins and Other Molecules > Protein–RNA Interactions: Functional Implications.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/50317
metadata.dc.identifier.url: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85068031803&origin=inward
ISSN: 17577012
17577004
Appears in Collections:Scopus 2019

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