Biological roles of A-to-I editing: implications in innate immunity, cell death, and cancer immunotherapy

Adenosine-to-inosine (A-to-I) editing, a key RNA modification widely found in eukaryotes, is catalyzed by adenosine deaminases acting on RNA (ADARs). Such RNA editing destabilizes endogenous dsRNAs, which are subsequently recognized by the sensors of innate immune and other proteins as autologous ds...

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Published in:Journal of experimental & clinical cancer research 2023-06, Vol.42 (1), p.149-149, Article 149
Main Authors: Yuan, Jing, Xu, Li, Bao, Hai-Juan, Wang, Jie-Lin, Zhao, Yang, Chen, Shuo
Format: Article
Language:English
Subjects:
A-to-I editing
Adenosine
Apoptosis
Biochemistry
Biological response modifiers
Cancer
Cancer immunotherapy
Care and treatment
Cell death
DNA methylation
Drug therapy
Enzymes
Genes
Health aspects
Immunotherapy
Innate immunity
Interferon
Kinases
Localization
Messenger RNA
MicroRNAs
Mutation
Proteins
Review
Sensors
Targeted therapy
Tumorigenesis
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Summary:Adenosine-to-inosine (A-to-I) editing, a key RNA modification widely found in eukaryotes, is catalyzed by adenosine deaminases acting on RNA (ADARs). Such RNA editing destabilizes endogenous dsRNAs, which are subsequently recognized by the sensors of innate immune and other proteins as autologous dsRNAs. This prevents the activation of innate immunity and type I interferon-mediated responses, thereby reducing the downstream cell death induced by the activation of the innate immune sensing system. ADARs-mediated editing can also occur in mRNAs and non-coding RNAs (ncRNAs) in different species. In mRNAs, A-to-I editing may lead to missense mutations and the selective splicing of coding regions. Meanwhile, in ncRNAs, A-to-I editing may affect targeting and disrupt ncRNAs maturation, leading to anomalous cell proliferation, invasion, and responses to immunotherapy. This review highlights the biological functions of A-to-I editing, its role in regulating innate immunity and cell death, and its potential molecular significance in tumorigenesis and cancer targeted therapy and immunotherapy.
ISSN:1756-9966
0392-9078
1756-9966
DOI:10.1186/s13046-023-02727-9