LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation

Li, Shuiqi; Zhu, Xiaohua; Zhang, Na; Cao, Ruixiang; Zhao, Lei; Li, Xin; Jiang-an, Zhang

doi:10.1080/08916934.2021.1897976

Cited by 19 publications

(10 citation statements)

References 28 publications

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“…LncRNAs play crucial roles in regulating immune-mediated in ammatory and autoimmune diseases 14,31 . A previous study found that lncRNA NORAD promoted proliferation of psoriatic keratinocytes by targeting miR-26a 32 , furthermore another study revealed that lncRNA MEG3 represses proliferation while inducing apoptosis through serving as ceRNA of miR-21 for caspase-8 in psoriasis epidermal cells 33 . LncRNA TUG1 regulates prostate cancer cell proliferation, invasion, and migration via the Nrf2 signaling axis 34 .…”

Section: Discussionmentioning

confidence: 96%

845 Long non-coding RNA-GDA-1 regulates keratinocyte proliferation and psoriasis inflammation by regulating forkhead box m1 via the STAT3/NF-κB signaling pathway

Chen

Sun

2023

Journal of Investigative Dermatology

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Section: Discussionmentioning

confidence: 96%

845 Long non-coding RNA-GDA-1 regulates keratinocyte proliferation and psoriasis inflammation by regulating forkhead box m1 via the STAT3/NF-κB signaling pathway

Chen

Sun

2023

Journal of Investigative Dermatology

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“…Additionally, Trohatou et al verified that miR-26a mediates adipogenesis of amniotic fluid mesenchymal stem cells by interfering with CCNE1 [ 75 ], and Xin Zhang et al demonstrated that miR-26a/b can regulate DNA replication licensing, tumorigenesis, and prognosis by targeting CDC6 in lung cancer [ 33 ]. Interestingly, miR-26a was recently reported to reduce the expression of CDC6 by binding to the lncRNA NORAD (noncoding RNA activated by DNA damage), thereby inhibiting the proliferation of keratinocytes, which further enhances the development potential of miR-26a-5p as a therapeutic small nucleic acid drug [ 76 ]. We propose that dual interference of miR-26a-5p in the CDC6/CCNE1 axis may be a universal mechanism for inhibiting the proliferation of cells.…”

Section: Discussionmentioning

confidence: 99%

miR-26a-5p inhibits the proliferation of psoriasis-like keratinocytes in vitro and in vivo by dual interference with the CDC6/CCNE1 axis

Li,

Pang,

Zhou

et al. 2024

Aging

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Psoriasis is a chronic inflammatory proliferative dermatological ailment that currently lacks a definitive cure. Employing data mining techniques, this study identified a collection of substantially downregulated miRNAs (top 10). Notably, 32 targets were implicated in both the activation of the IL-17 signaling pathway and cell cycle dysregulation. In silico analysis revealed that one of these miRNAs, miR-26a-5p, is a highly conserved cross-species miRNA. Strikingly, the miR-26a-5p sequences in humans and mice are identical, and mmu-miR-26a-5p was found to target the same 7 cell cycle targets as its human counterpart, hsa-miR-26a-5p. Among these targets, CDC6 and CCNE1 were the most effective targets of miR-26a-5p, which was further validated in vitro using a dual luciferase reporter system and qPCR assay. The therapeutic assessment of miR-26a-5p revealed its remarkable efficacy in inhibiting the proliferation and G1/S transition of keratinocytes (HaCaT and HEKs) in vitro . In vivo experiments corroborated these findings, demonstrating that miR-26a-5p effectively suppressed imiquimod (IMQ)-induced psoriasis-like skin lesions in mice over an 8-day treatment period. Histological analysis via H&E staining revealed that miR-26a-5p treatment resulted in reduced keratinocyte thickness and immune cell infiltration into the spleens of IMQ-treated mice. Mechanistic investigations revealed that miR-26a-5p induced a cascade of downregulated genes associated with the IL-23/IL-17A axis, which is known to be critical in psoriasis pathogenesis, while concomitantly suppressing CDC6 and CCNE1 expression. These findings were corroborated by qPCR and Western blot analyses. Collectively, our study provides compelling evidence supporting the therapeutic potential of miR-26a-5p as a safe and reliable endogenous small nucleic acid for the treatment of psoriasis.

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“…In addition, the overexpression of NORAD reduced the concentration of miR-26a, and the elimination of NORAD accelerated the quantity of miR-26a. In psoriasis and head and neck squamous cell carcinoma, NORAD negatively manages miR-26a [ 28 , 29 ]. NORAD mediates hypertrophic scar formation by inhibiting the expression of miR-26a [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA NORAD Promotes Fracture Healing through Interacting with Osteoblast Differentiation via Targeting miR‐26a

Chen

et al. 2023

BioMed Research International

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The present study was designed to evaluate the dynamic expression of lncRNA NORAD in fracture healing of patients with brittle fractures and explore the function and mechanism of NORAD in regulating osteoblastic proliferation, differentiation, and apoptosis. The expression level of NORAD was detected by quantitative real-time PCR. The proliferation, differentiation, and apoptosis of osteoblasts were analyzed by MTT assay, ELISA, and flow cytometry. Luciferase report analysis was used to confirm the interaction between NORAD and its target ceRNA miR-26a. This study showed no significant differences in serum NORAD expression on the 7th day during fracture healing in patients, but increased expression of NORAD was certified on the 14, 21, and 28 days after fixation. Overexpression of NORAD promoted the proliferation and differentiation of osteoblasts and suppressed the apoptosis of osteoblasts. miR-26a proved to be the target gene of NORAD and was inhibited by overexpression of NORAD in osteoblasts. The enhanced expression of miR-26a was negatively linked to the lessened expression of NORAD. NORAD could accelerate the proliferation and differentiation of osteoblasts and inhibit apoptosis, thereby promoting fracture healing.

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LncRNA NORAD engages in psoriasis by binding to miR-26a to regulate keratinocyte proliferation

Cited by 19 publications

References 28 publications

845 Long non-coding RNA-GDA-1 regulates keratinocyte proliferation and psoriasis inflammation by regulating forkhead box m1 via the STAT3/NF-κB signaling pathway

845 Long non-coding RNA-GDA-1 regulates keratinocyte proliferation and psoriasis inflammation by regulating forkhead box m1 via the STAT3/NF-κB signaling pathway

miR-26a-5p inhibits the proliferation of psoriasis-like keratinocytes in vitro and in vivo by dual interference with the CDC6/CCNE1 axis

Long Noncoding RNA NORAD Promotes Fracture Healing through Interacting with Osteoblast Differentiation via Targeting miR‐26a

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