<scp>LncRNA SNHG14</scp> contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the <scp>miR</scp>‐17‐5p/<scp>MINK1‐JNK</scp> pathway

Zhang, Jihui; Lei, Hongwei; Li, Xiu

doi:10.1002/tox.23361

Cited by 20 publications

(11 citation statements)

References 38 publications

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“…Moreover, similar to the key roles of miRNAs in human pathology ( 34 – 40 ), deregulated lncRNA expression has been documented in many kinds of diseases, such as degenerative diseases, tumors, cardiovascular disease, and autoimmune/inflammatory diseases ( 41 – 48 ). Recently, an increasing amount of evidence suggested that lncRNAs also actively take part in development of orthopedic diseases, including scoliosis, intervertebral disc herniation, arthritis and AS ( 49 – 51 ).…”

Section: Introductionmentioning

confidence: 99%

Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis

et al. 2022

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Ankylosing spondylitis (AS) is a chronic systemic autoimmune disease characterized by inflammation, bone erosion, spur formation of the spine and the sacroiliac joints. However, the etiology and molecular pathogenesis of AS remain largely unclear. Recently, a growing number of studies showed that long non-coding RNAs (lncRNAs) played critical roles in the development and progression of autoimmune and orthopedic conditions, including AS. Studies demonstrated that a myriad of lncRNAs (e.g. H19, MEG3, LOC645166) pertinent to regulation of inflammatory signals were deregulated in AS. A number of lncRNAs might also serve as new biomarkers for the diagnosis and predicting the outcomes of AS. In this review, we summarize lncRNA profiling studies on AS and the functional roles and mechanism of key lncRNAs relevant to AS pathogenesis. We also discuss their potential values as biomarkers and druggable targets for this potentially disabling condition.

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Section: Introductionmentioning

confidence: 99%

Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis

et al. 2022

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“…However, we suggest MINK1 as a novel candidate gene for autism, congenital cataract, epilepsy and osteoporosis. Although we report the first patient with disruption of MINK1 , the gene has already been implicated in a variety of disorders based on cohort studies in humans, in silico models and work on model organisms, including congenital heart disease in humans [ 20 ] and skeletal and neuronal phenotypes in mice [ 21 , 22 ], as well as cancer [ 23 , 24 ], platelet formation [ 25 ], Alzheimer disease [ 26 , 27 ] and arthritis [ 28 ]. As such, it appears that MINK1 is part of a diverse set of biological processes, which is expected as MINK1 is highly expressed in a variety of tissues ( Figure 2 B) and interacts with a diversity of proteins ( Table S3 ).…”

Section: Discussionmentioning

confidence: 99%

Multi-Omic Investigations of a 17–19 Translocation Links MINK1 Disruption to Autism, Epilepsy and Osteoporosis

Eisfeldt

Schuy

Stattin

et al. 2022

IJMS

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Balanced structural variants, such as reciprocal translocations, are sometimes hard to detect with sequencing, especially when the breakpoints are located in repetitive or insufficiently mapped regions of the genome. In such cases, long-range information is required to resolve the rearrangement, identify disrupted genes and, in symptomatic carriers, pinpoint the disease-causing mechanisms. Here, we report an individual with autism, epilepsy and osteoporosis and a de novo balanced reciprocal translocation: t(17;19) (p13;p11). The genomic DNA was analyzed by short-, linked- and long-read genome sequencing, as well as optical mapping. Transcriptional consequences were assessed by transcriptome sequencing of patient-specific neuroepithelial stem cells derived from induced pluripotent stem cells (iPSC). The translocation breakpoints were only detected by long-read sequencing, the first on 17p13, located between exon 1 and exon 2 of MINK1 (Misshapen-like kinase 1), and the second in the chromosome 19 centromere. Functional validation in induced neural cells showed that MINK1 expression was reduced by >50% in the patient’s cells compared to healthy control cells. Furthermore, pathway analysis revealed an enrichment of changed neural pathways in the patient’s cells. Altogether, our multi-omics experiments highlight MINK1 as a candidate monogenic disease gene and show the advantages of long-read genome sequencing in capturing centromeric translocations.

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“…Zhang et al. showed that lncSNHG14 can promote misshapen-like kinase 1 (MINK1) expression through a ceRNA mechanism, ultimately increasing pro-inflammatory cytokine expression in rheumatoid arthritis ( 104 ).In LPS induced acute lung injury, lncSNHG14 was reported to be induced and mediate Wnt1 inducible signaling pathway protein 1 (WISP1) expression by sponging miR-34c-3p, thus promoting proinflammatory proteins IL-18, IL-1β, TNF-α and IL-6 ( 105 ).…”

Section: Lncsnhg-mediated Anti-tumor Immune Responsesmentioning

confidence: 99%

SnoRNA and lncSNHG: Advances of nucleolar small RNA host gene transcripts in anti-tumor immunity

et al. 2023

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The small nucleolar RNA host genes (SNHGs) are a group of genes that can be transcript into long non-coding RNA SNHG (lncSNHG) and further processed into small nucleolar RNAs (snoRNAs). Although lncSNHGs and snoRNAs are well established to play pivotal roles in tumorigenesis, how lncSNHGs and snoRNAs regulate the immune cell behavior and function to mediate anti-tumor immunity remains further illustrated. Certain immune cell types carry out distinct roles to participate in each step of tumorigenesis. It is particularly important to understand how lncSNHGs and snoRNAs regulate the immune cell function to manipulate anti-tumor immunity. Here, we discuss the expression, mechanism of action, and potential clinical relevance of lncSNHGs and snoRNAs in regulating different types of immune cells that are closely related to anti-tumor immunity. By uncovering the changes and roles of lncSNHGs and snoRNAs in different immune cells, we aim to provide a better understanding of how the transcripts of SNHGs participate in tumorigenesis from an immune perspective.

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LncRNA SNHG14 contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the miR‐17‐5p/MINK1‐JNK pathway

Cited by 20 publications

References 38 publications

Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis

Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis

Multi-Omic Investigations of a 17–19 Translocation Links MINK1 Disruption to Autism, Epilepsy and Osteoporosis

SnoRNA and lncSNHG: Advances of nucleolar small RNA host gene transcripts in anti-tumor immunity

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