The role and mechanism of long non‐coding RNAs in homologous recombination repair of radiation‐induced DNA damage

Yu, Nanxi; Qin, Hongran; Zhang, Fangxiao; Liu, Tingting; Cao, Kun; Yang, Yanyong; Chen, Yuanyuan; Cai, Jianming

doi:10.1002/jgm.3470

Cited by 5 publications

(6 citation statements)

References 82 publications

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“…One of the stress factors for which a connection with and a role of lncRNAs was postulated or documented is DNA damage and its repair (reviewed in Fijen and Rothenberg 2021 ; Guiducci and Stojic 2021 ; Shaw and Gullerova 2021 ; Zhu et al . 2022 ; Yu et al . 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNAs contribute to DNA damage resistance in Arabidopsis thaliana

et al. 2023

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Efficient repair of DNA lesions is essential for faithful transmission of genetic information between somatic cells and for genome integrity across generations. Plants have multiple, partially redundant and overlapping DNA repair pathways, probably due to the less constricted germline and the inevitable exposure to light including higher energy wavelengths. Many proteins involved in DNA repair and their mode of actions are well described. In contrast, a role for DNA damage-associated RNA components, evident from many other organisms, is less well understood. Here, we have challenged young Arabidopsis thaliana plants with two different types of genotoxic stress and performed de novo assembly and transcriptome analysis. We identified three long non-coding RNAs (lncRNAs) that are lowly or not expressed under regular conditions but up-regulated or induced by DNA damage. We generated CRISPR/Cas deletion mutants and found that the absence of the lncRNAs impairs the recovery capacity of the plants from genotoxic stress. The genetic loci are highly conserved among world-wide distributed Arabidopsis accessions and within related species in the Brassicaceae group. Together, these results suggest that the lncRNAs have a conserved function in connection with DNA damage and provide a basis for a mechanistic analysis of their role.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNAs contribute to DNA damage resistance in Arabidopsis thaliana

et al. 2023

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“…BRCA2 also inhibits the ATPase activity of RAD51 and stabilizes the RAD51-ssDNA complex (10,79,83,84). Subsequently, a homology search and DNA repair through strand invasion take place (85).…”

Section: Lncrna Binding To Rbps Regulates Dna Dsb Repair In Cancer Cellsmentioning

confidence: 99%

Advances in the role of long non‑coding RNAs and RNA‑binding proteins in regulating DNA damage repair in cancer cells

Zou,

Gou,

Wen

2023

Int J Mol Med

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DNA damage and repair play a crucial role in the development, progression and treatment of cancer. In response to various types of DNA damage, the organism initiates a series of DNA damage responses that trigger post-DNA damage repair processes. Among the most severe forms of DNA damage are DNA double-strand breaks (DSBs), which can be repaired by the body through two pathways: Homologous recombination and non-homologous end joining. The repair of DNA damage, particularly DNA DSBs, significantly influences the sensitivity and resistance of cancer cells to chemotherapy and radiotherapy. Numerous studies have demonstrated that long non-coding RNAs (lncRNAs) can exert multiple regulatory effects on cancer cells by binding to RNA binding proteins (RBPs), thereby influencing DNA damage repair. Based on a comprehensive literature search, the existing research on the regulation of DNA damage repair by lncRNAs interacting with RBPs has primarily focused on the repair of DNA DSBs. Therefore, the present review discusses the regulatory effects of the interaction between lncRNAs and RBPs on DNA damage repair in cancer cells, with a specific focus on the repair of DNA DSBs and its implications in cancer. It is hoped that comprehensive analysis may enhance the current understanding of the molecular mechanisms underlying DNA damage repair in cancer and may lead to the identification of novel diagnostic biomarkers and potential therapeutic targets. Contents

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“…14,15 Long non-coding RNAs (lncRNAs), over 200 nucleotides lacking protein-coding capacity, are widely expressed and play critical roles in gene regulation. 16,17 Depending on their localization and interaction partners, lncRNAs can modulate chromatin conformation, modify cytoplasmic mRNA translation and interfere with signaling pathways. 18,19 Ultimately, these functions influence gene expression in various biological and pathological contexts.…”

Section: Introductionmentioning

confidence: 99%

“…A broad spectrum of non‐coding RNAs have been uncovered and shown to play an essential role in various biological processes 14,15 . Long non‐coding RNAs (lncRNAs), over 200 nucleotides lacking protein‐coding capacity, are widely expressed and play critical roles in gene regulation 16,17 . Depending on their localization and interaction partners, lncRNAs can modulate chromatin conformation, modify cytoplasmic mRNA translation and interfere with signaling pathways 18,19 .…”

Section: Introductionmentioning

confidence: 99%

GRIK1‐AS1 deficiency accelerates endometriosis progression by boosting DNMT1‐dependent SFRP1 promoter methylation in endometrial stromal cells

Liu

Wang

et al. 2023

The Journal of Gene Medicine

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BackgroundEndometriosis, a gynecological disease that affects up to 10% of women, is a major cause of pain and infertility. Deregulation of the epigenome is accountable for the onset and progression of endometriosis, although its exact mechanism is unknown. The purpose of the current study is to examine the role of the long non‐coding RNA (lncRNA) GRIK1‐AS1 in the epigenetic regulation of endometrial stromal cell proliferation and the development of endometriosis.MethodsEndometriosis datasets were screened to identify GRIKI‐AS1 as dramatically declining in endometriosis. Gain or loss of function endometrial stromal cell (ESC) models were established. The anti‐proliferation phenotype was investigated using in vitro and in vivo experiments. Epigenetic regulatory network analyses were conducted to suggest the intrinsic molecular mechanism.ResultsWith bioinformatic and clinical data, we observed that GRIK1‐AS1 and SFRP1 were expressed at low levels in endometriosis. Overexpressed GRIK1‐AS1 inhibited ESC proliferation, while SFRP1 knockdown rescued the antiproliferative ability of GRIK1‐AS1. Specifically, methylation‐dependent expression inhibition of SFRP1 was revealed in ESCs. Mechanistically, GRIK1‐AS1 hampers the occupancy of DNMT1 in SRFP1 promoter, leading to hypomethylation of SFRP1 and upregulated SFRP1 expression, thereby potentially suppressing Wnt signaling and its adverse proliferative effect. Therapeutically, lentivirus‐mediated upregulation of GRIK1‐AS1 inhibited endometriosis disease progression in vivo.ConclusionsOur study is a proof‐of‐concept demonstration for GRIKI‐AS1‐associated endometriosis pathogenesis and highlights a potential intervention target.

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The role and mechanism of long non‐coding RNAs in homologous recombination repair of radiation‐induced DNA damage

Cited by 5 publications

References 82 publications

Long noncoding RNAs contribute to DNA damage resistance in Arabidopsis thaliana

Long noncoding RNAs contribute to DNA damage resistance in Arabidopsis thaliana

Advances in the role of long non‑coding RNAs and RNA‑binding proteins in regulating DNA damage repair in cancer cells

GRIK1‐AS1 deficiency accelerates endometriosis progression by boosting DNMT1‐dependent SFRP1 promoter methylation in endometrial stromal cells

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