Abstract
Protection of genome integrity is vital for all living organisms, particularly when DNA double-strand breaks (DSBs) occur. Eukaryotes have developed two main pathways, namely Non-Homologous End Joining (NHEJ) and Homologous Recombination (HR), to repair DSBs. While most of the current research is focused on the role of key protein players in the functional regulation of DSB repair pathways, accumulating evidence has uncovered a novel class of regulating factors termed non-coding RNAs. Non-coding RNAs have been found to hold a pivotal role in the activation of DSB repair mechanisms, thereby safeguarding genomic stability. In particular, long non-coding RNAs (lncRNAs) have begun to emerge as new players with vast therapeutic potential. This review summarizes important advances in the field of lncRNAs, including characterization of recently identified lncRNAs, and their implication in DSB repair pathways in the context of tumorigenesis.
Highlights
An intact genome is vital for the survival of living organisms as it ensures normal homeostasis [1]
We focus on the role that long non-coding RNAs play as versatile tools in the various damage response and repair (DDRR) pathways, and in the detection and repair of DNA double-strand breaks (DSBs), the most deleterious type of DNA damage [1,4]
According to the function that they exert, long non-coding RNAs (lncRNAs) are categorized into the following groups: (a) Transcriptional regulation. This group involves lncRNAs that are implicated in chromatin remodeling and transcriptional interference, including enhancer lncRNAs that are transcribed from enhancers; (b) Posttranscriptional regulation
Summary
An intact genome is vital for the survival of living organisms as it ensures normal homeostasis [1]. Known as DNA damage response and repair (DDRR) pathways, these circuits represent an intense field of investigation, especially from the perspective of pathological conditions, as their failure results in the accumulation of genetic alterations that are disease-causing factors [1,2]. Mounting evidence has revealed an unexpected new class of players to participate in genome surveillance pathways. These new factors constitute a subset of RNA molecules defined as non-coding RNAs (ncRNAs) [1,3]. We focus on the role that long non-coding RNAs (lncRNAs) play as versatile tools in the various DDRR pathways, and in the detection and repair of DNA double-strand breaks (DSBs), the most deleterious type of DNA damage [1,4]. We examine how deregulation of these factors relates to human pathology, cancer onset and progression
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