LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway

Zhuo, Qin; Lü, Wei; Yin, Xietian; Li, Huiling; Qin, Guifu; Li, Siqi; Peng, Ting; Liu, Bo; Zhao, Shusen; Ye, Zhiqin

doi:10.1080/08916934.2021.1966770

Cited by 17 publications

(11 citation statements)

References 34 publications

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“…Similarly, ZNF667-AS1 was downregulated in LPS stimulated chondrocytes. The inhibition of the expression of ZNF667-AS1 can significantly promote the expression of TNF-in chondrocytes and thereby increase the angiogenic activity (54). some of the pathways in which LncRNAs participate in the migration or invasion of FLSs.…”

Section: Lncrnas Regulate Angiogenesismentioning

confidence: 99%

“…Once β-catenin has reached the nucleus, it can initiate the expression of genes that promote cell division, such as cellular myelocytomatosis oncogene (c-myc) and cyclin D1, which promotes cell proliferation. In contrast, the LncRNA ZNF667-AS1 was significantly downregulated in RA tissues and FLSs compared to normal tissues and cells ( 54 ). LncRNA ZNF667-AS1 acts as a competitive sponge for miR-523-3p in RA lesions and thereby inhibits the activation of miR-523-3p on the Janus kinase (JAK)/STAT signaling pathway.…”

Section: The Relationship Between Lncrnas and The Pathological Features Of Ramentioning

confidence: 99%

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LncRNAs and Rheumatoid Arthritis: From Identifying Mechanisms to Clinical Investigation

Huang

et al. 2022

Front. Immunol.

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Rheumatoid arthritis (RA) is a systemic chronic autoinflammatory disease, and the synovial hyperplasia, pannus formation, articular cartilage damage and bone matrix destruction caused by immune system abnormalities are the main features of RA. The use of Disease Modifying Anti-Rheumatic Drugs (DMARDs) has achieved great advances in the therapy of RA. Yet there are still patients facing the problem of poor response to drug therapy or drug intolerance. Current therapy methods can only moderate RA progress, but cannot stop or reverse the damage it has caused. Recent studies have reported that there are a variety of long non-coding RNAs (LncRNAs) that have been implicated in mediating many aspects of RA. Understanding the mechanism of LncRNAs in RA is therefore critical for the development of new therapy strategies and prevention strategies. In this review, we systematically elucidate the biological roles and mechanisms of action of LncRNAs and their mechanisms of action in RA. Additionally, we also highlight the potential value of LncRNAs in the clinical diagnosis and therapy of RA.

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Section: Lncrnas Regulate Angiogenesismentioning

confidence: 99%

Section: The Relationship Between Lncrnas and The Pathological Features Of Ramentioning

confidence: 99%

LncRNAs and Rheumatoid Arthritis: From Identifying Mechanisms to Clinical Investigation

Huang

et al. 2022

Front. Immunol.

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“…LncRNA MEG3 and lncRNA ZNF667-AS1 were down-regulated in LPS-stimulated chondrocytes. These two lncRNAs could protect chondrocytes from LPS-induced damage and inhibit the secretion of inflammatory factors by chondrocytes ( Li et al, 2019 ; Zhuo et al, 2021 ).…”

Section: Lncrnas In Joint Destruction Of Ramentioning

confidence: 99%

The effect of long non-coding RNAs in joint destruction of rheumatoid arthritis

Zhao

et al. 2022

Front. Cell Dev. Biol.

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Rheumatoid arthritis (RA) is a systemic autoimmune disease accompanied with joint destruction. Serious joint destruction will eventually lead to disability and the decline of life quality in RA patients. At present, the therapeutic effect of drugs to alleviate joint destruction in RA is limited. Recently, accumulating evidences have shown that long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of joint diseases. Therefore, this paper reviews the expression change and the action mechanism of lncRNAs in joint destruction of RA in recent years. A more comprehensive understanding of the role of lncRNAs in joint destruction will help the treatment of RA.

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“…LncRNA LERFS (lowly expressed in rheumatoid fibroblast-like synoviocytes) could promote synovial aggression and joint destruction by interacting with heterogeneous nuclear ribonucleoprotein Q (hnRNP Q) ( 108 ). LncRNA ZNF667-AS1 was reported to be down-regulated in RA-FLS, and its overexpression could play a protective role in RA by sponging miR-523-3p, thus inactivating the JAK/STAT signaling pathway ( 109 ). The down-regulated expression of the lncRNA X-inactive specific transcript (XIST) was found to inhibit the proliferation of synovial fibroblasts (SFs) by promoting the miR-126-3p/NF-κB pathway, thereby playing a protective role in RA ( 110 ).…”

Section: Lncrna and Ramentioning

confidence: 99%

LncRNA Expression Profiles in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Emerging Biomarkers and Therapeutic Targets

Chen

et al. 2021

Front. Immunol.

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Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two common multisystem autoimmune diseases that share, among others, many clinical manifestations and serological features. The role of long non-coding RNAs (lncRNAs) has been of particular interest in the pathogenesis of autoimmune diseases. Here, we aimed to summarize the roles of lncRNAs as emerging novel biomarkers and therapeutic targets in SLE and RA. We conducted a narrative review summarizing original articles on lncRNAs associated with SLE and RA, published until November 1, 2021. Based on the studies on lncRNA expression profiles in samples (including PBMCs, serum, and exosomes), it was noted that most of the current research is focused on investigating the regulatory mechanisms of these lncRNAs in SLE and/or RA. Several lncRNAs have been hypothesized to play key roles in these diseases. In SLE, lncRNAs such as GAS5, NEAT1, TUG1, linc0949, and linc0597 are dysregulated and may serve as emerging novel biomarkers and therapeutic targets. In RA, many validated lncRNAs, such as HOTAIR, GAS5, and HIX003209, have been identified as promising novel biomarkers for both diagnosis and treatment. The shared lncRNAs, for example, GAS5, may participate in SLE pathogenesis through the mitogen-activated protein kinase pathway and trigger the AMP-activated protein kinase pathway in RA. Here, we summarize the data on key lncRNAs that may drive the pathogenesis of SLE and RA and could potentially serve as emerging novel biomarkers and therapeutic targets in the coming future.

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LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway

Cited by 17 publications

References 34 publications

LncRNAs and Rheumatoid Arthritis: From Identifying Mechanisms to Clinical Investigation

LncRNAs and Rheumatoid Arthritis: From Identifying Mechanisms to Clinical Investigation

The effect of long non-coding RNAs in joint destruction of rheumatoid arthritis

LncRNA Expression Profiles in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Emerging Biomarkers and Therapeutic Targets

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