The Biological Roles of lncRNAs and Future Prospects in Clinical Application.

Guohui Li,Fenyong Sun,Nan Huang,Liang Deng

doi:10.3390/diseases9010008

Guohui Li, Fenyong Sun + Show 2 more

Open Access

https://doi.org/10.3390/diseases9010008

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Abstract

Chemo and radiation therapies are the most commonly used therapies for cancer, but they can induce DNA damage, resulting in the apoptosis of host cells. DNA double-stranded breaks (DSBs) are the most lethal form of DNA damage in cells, which are constantly caused by a wide variety of genotoxic agents, both environmentally and endogenously. To maintain genomic integrity, eukaryotic organisms have developed a complex mechanism for the repair of DNA damage. Researches reported that many cellular long noncoding RNAs (lncRNAs) were involved in the response of DNA damage. The roles of lncRNAs in DNA damage response can be regulated by the dynamic modification of N6-adenosine methylation (m6A). The cellular accumulation of DNA damage can result in various diseases, including cancers. Additionally, lncRNAs also play roles in controlling the gene expression and regulation of autophagy, which are indirectly involved with individual development. The dysregulation of these functions can facilitate human tumorigenesis. In this review, we summarized the origin and overview function of lncRNAs and highlighted the roles of lncRNAs involved in the repair of DNA damage.

Highlights

DNA damage is constantly caused by various endogenous and exogenous factors, such as ionizing radiation, ultra-violet, reactive oxygen species (ROS), and genotoxic drugs [1,2]
Recent evidence showed that some long noncoding RNAs (lncRNAs) such as NORAD and GUARDIN could directly participate in the repair of DNA damage [9,10,11]
[13] reported that over 50,000 lncRNAs cou2ldofb1e2 generated in the human transcriptome from various tumors, normal tissues, and cell lines based on The Cancer Genome Atlas (TCGA; http://cancergenome.nih.gov/)

Summary

Introduction

DNA damage is constantly caused by various endogenous and exogenous factors, such as ionizing radiation, ultra-violet, reactive oxygen species (ROS), and genotoxic drugs [1,2]. It is generally accepted that DNA damage is a potential threat to human health. Human have evolved intricate mechanisms for the repair of DNA damage to sustain genome stability, and homologous recombination (HR) and nonhomologous end joining (NHEJ), as two major DSBs repair pathways, have been ubiquitously applied in cells [3,4]. Iyer et al (2015) [13] reported that over 50,000 lncRNAs (designated MiTranscriptome lncRNAs) could be generated in the human transcriptome from various tumors, normal tissues, Diseases 2021, 9, 8. [13] reported that over 50,000 lncRNAs (designated MiTranscriptome lncRNAs) cou2ldofb1e2 generated in the human transcriptome from various tumors, normal tissues, and cell lines based on The Cancer Genome Atlas (TCGA; http://cancergenome.nih.gov/). DDR and HR are the abbreviations for DNA damage response and homologous recombination.

Involvement in a Variety of Biological Functions

LncRNAs Participating in Transcription Regulation

Involvement of lncRNAs in the Repair of DNA Damage

Clinical Biomarkers in Cancer Patients

Regulation of Autophagy by lncRNAs

Expression Level of lncRNAs Regulated by m6A