RETRACTED: Long noncoding RNA LINC00671 exacerbates osteoarthritis by promoting ONECUT2-mediated Smurf2 expression and extracellular matrix degradation

Chen, Cheng-Wei; Xu, Yaozeng

doi:10.1016/j.intimp.2020.106846

Cited by 10 publications

(12 citation statements)

References 39 publications

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“…Chen et al . have shown that ONECUT2 and Smurf2 were highly expressed in OA cartilage tissue 21 . Our results found that IL‐1β induced ONECUT2/Smurf2 expression in hFSCs, which indicated ONECUT2 might also be closely related to the function of hFSCs in OA.…”

Section: Methodssupporting

confidence: 64%

“…Smurf2‐mediated up‐regulation of β‐catenin by inducing proteasome degradation of GSK‐β in chondrocytes might activate articular chondrocyte maturation and associated gene expression changes, an early event of OA 29 . It has been confirmed that ONECUT2 could bind Smurf2 21 . Bioinformatics analysis demonstrated that ONECUT2 and Smurf2 genes were remarkably elevated in the OA group compared with the control group.…”

Section: Discussionmentioning

confidence: 96%

“…ONECUT2, as a transcription factor, consists of two DNA‐binding domains, a homeobox domain and a cleaved domain; MAPK was thought to be highly expressed in various diseases, including lung and prostate cancer 20 . As previously described, LncRNA LINC00671 exacerbates OA by promoting ONECUT2‐mediated Smurf2 expression and ECM degradation in chondrocytes 21 . Circ_0084615 promotes colon cancer cell proliferation, migration, and invasion through miR‐599/ONECUT2 axis 22 .…”

Section: Introductionmentioning

confidence: 93%

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LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

Yang

et al. 2022

Orthopaedic Surgery

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Objective This study explores LncRNA TM1‐3P effects on the proliferation, apoptosis, and inflammatory response of fibroblasts in osteoarthritis (OA) and its underlying mechanism. Methods Bioinformatics was performed to analyze OA disease‐related genes, miRNA profiles, and function. The targeted regulation of LncRNA TM1‐3P and miR‐144‐3p, ONECUT2 and miR‐144‐3p were analyzed by dual luciferase reporter gene assay, RNA Binding Protein Immunoprecipitation (RIP), and RNA pull down. Histopathological morphology of the knee joint was observed by hematoxylin–eosin (HE) and Annona Red O/Fast Green. The expressions of mRNAs and proteins were detected by RT‐qPCR, Western blot, and immunohistochemistry. Unpaired T test was used between groups, and the one‐way analysis of variance of repeated measurement data was applied for multi‐group comparison, following Tukey's post‐test. Results ONECUT2 and Smurf2 genes were significantly elevated in the osteoarthritis group compared with the normal group (P < 0.001, P < 0.001). Expressions of ONECUT2 and LncRNA TM1‐3P were increased, and expression of miR‐144‐3p was decreased in interleukin (IL)‐1β‐induced human fibroblast synovial cells (hFSCs) (mRNA: 1.06 ± 0.24 vs. 3.29 ± 0.73, proteins: 0.22 ± 0.03 vs. 0.46 ± 0.22, 1.23 ± 0.22 vs. 3.76 ± 0.73, 1.06 ± 0.25 vs. 0.37 ± 0.13, P < 0.01, P < 0.001, P < 0.01, P < 0.05). Overexpression of miR‐144‐3p down‐regulated the ONECUT2 expression, reduced cell proliferation, promoted apoptosis in hFSCs induced by IL‐1β (mRNA: 0.89 ± 0.14 vs. 0.15 ± 0.01, P < 0.05; proteins: 0.46 ± 0.01 vs. 0.23 ± 0.01, P < 0.001; CCK8: 1.88 ± 0.07 vs. 1.65 ± 0.07; P < 0.05; EDU: 55.82 ± 1.44 vs 40.57 ± 2.24, P < 0.05; apoptosis: 10.57 ± 0.79 vs 16.36 ± 0.35, P < 0.0001). Overexpression of LncRNA TM1‐3P up‐regulated the expression of ONECUT2, promoted cell proliferation, and inhibited apoptosis (mRNA: 0.9 ± 0.09 vs 1.94 ± 0.12, P < 0.05; proteins: 0.61 ± 0.05 vs 0.76 ± 0.03, P > 0.05; CCK8: 2.07 ± 0.05 vs 2.47 ± 0.06; P < 0.01; EDU: 52.67 ± 1.17 vs 60.06 ± 3.24, P < 0.05; apoptosis: 10.57 ± 0.79 vs 16.36 ± 0.35, P < 0.001), which were reversed by the overexpression of miR‐144‐3p treatment (mRNA: 1.82 ± 0.07 vs 0.31 ± 0.07, P < 0.0001; proteins: 0.74 ± 0.02 vs 0.35 ± 0.01, P < 0.01; CCK8: 2.41 ± 0.01 vs 1.67 ± 0.02; P < 0.0001; EDU: 66.85 ± 2.86 vs 44.68 ± 1.97, P < 0.0001; apoptosis: 7.19 ± 0.19 vs 13.36 ± 0.53, P < 0.0001). Silencing LncRNA TM1‐3P attenuated the injury of knee joint tissue, down‐regulated the expression of ONECUT2, Smurf2, IL‐1β, IL‐6, TNF‐α, and improved the expression of Rap1 in rats (0.71 ± 0.04 vs 0.48 ± 0.02, 0.68 ± 0.06 vs 0.36 ± 0.02, 0.74 ± 0.03 vs 0.49 ± 0.04, 0.78 ± 0.01 vs 0.54 ± 0.03, 0.68 ± 0.02 vs 0.4 ± 0.04, 0.24 ± 0.01 vs 0.4 ± 0.03, P < 0.05, P < 0.05, P < 0.05, P < 0.01, P < 0.01, P < 0.05). Conclusion LncRNA TM1‐3P improved inflammation and damage of knee joints in OA rats through miR‐144‐3p/ONECUT2 axis, providing a new theoretical basis for gene therapy of OA.

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Section: Methodssupporting

confidence: 64%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 93%

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LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

Yang

et al. 2022

Orthopaedic Surgery

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“…Mechanically, its inhibition may enhance endochondral ossification and mitochondrial oxidative stress, increase cell death and β-catenin expression and ultimately lead to ECM remodelling. 29 Defects of the TGFβ signalling pathway may make cartilage more susceptible to damage. The typical TGFβ signalling pathway is activated by three TGFβ subtypes, including type II serine/threonine kinase receptors (TGFBR2).…”

Section: Role Of Lncrnas In Ecm Degradation In Oamentioning

confidence: 99%

LncRNAs as a new regulator of chronic musculoskeletal disorder

et al. 2021

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Musculoskeletal disorders are a group of conditions that affect the motor system, including bones, muscles, tendons, ligaments and joints. 1 People with multiple disorders are particularly vulnerable, especially in the context of an ageing population. Musculoskeletal disorders include a variety of conditions such as osteoarthritis (OA), rheumatoid arthritis (RA), osteopenia, osteoporosis, fractures, sarcopenia, etc. 2 Non-protein-coding RNA makes up 98% of the whole human genome. 3,4 These functional RNAs can be divided into two groups according to the threshold of 200 nucleotides (NTS): small and long non-coding RNAs (lncRNAs). 5,6 LncRNAs regulate the activities of both nearby and distant genes by multiple mechanisms. It could act as a scaffold for transcription factors and other molecules involved in transcription initiation. 7 Moreover, it could serve as protein and microRNA decoys to interfere with cell division by regulating a series of key genes. 8 For those mainly located in the cytoplasm, it could directly target mRNA and induce translation. 9 Currently, an increased number of lncRNAs are found to be involved in the regulation of development and homeostasis of skeletal muscle system. 10,11 It is notable that lncRNAs take key roles in musculoskeletal disorders.

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“…A substantial portion of this "genomic dark matter" is long non-coding RNA (lncRNA), de ned as ncRNA greater than ~200 nucleotides in length, accounting for 68% of RNA molecules [11; 12]. Recently, the functions of lncRNAs and their associations with human diseases have attracted much attention from researchers because increasing evidences indicated that lncRNAs play critical roles in the development of various autoimmune diseases, such as ankylosing spondylitis (AS) [13], osteoarthritis (OA) [14]and systemic lupus erythematosus (SLE) [15]with the complete mechanism. LncRNAs can crosstalk with immune cells and mediate immunological and in ammatory response through phosphoinositide-3-kinase (PI3K) / protein kinase B (AKT) signaling pathway [16].…”

Section: Introductionmentioning

confidence: 99%

LINC02085 Regulates Cell Growth and Inflammatory Response in Rheumatoid Arthritis by Regulating PI3K/ AKT Signaling Pathway

Wen¹,

Liu²,

Wang³

et al. 2020

Preprint

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Background: The present study explored the possible functions and the underlying mechanism of long Non-coding RNA LINC02085 in rheumatoid arthritis (RA). Methods: Primary fibroblast-like synoviocytes (FLS) were separated from synovial tissues and was established cell lines, then cultured for subsequent cell experiments by transfecting different vectors. Rat with AA were injected with sh-LINC02085. The progression of AA was explored by measuring arthritis score and histologic analysis. ELISA analysis was employed to detect the levels of inflammatory cytokines. CCK8 assay, migration and invasion assays were used to evaluate the proliferation, migration and invasion abilities of cells, respectively. Besides, the levels of the the PI3K/AKT pathway-related proteins were measured by WB and IF. Results: The expression level of LINC02085 was significant high in patients with RA, and positively associated with clinical indexes. We found that LINC02085 was upregulated in RA -FLS and TNF-αstimulated. And overexpression of LINC02085 could promote proliferation, migration and invasion induced by TNF-α, through upregulating the levels of TNF-αand TNFAIP2 and promoting the activation of PI3K/AKT pathway. Whereas downexpression of LINC02085 received the opposite results. Knockdown of LINC02085 significantly ameliorated the progression of AA reflected by decreased arthritis score and cartilage destruction. Conclusion: The present study revealed that LINC02085 could regulate cell growth and inflammatory response of RA-FLS by activating the PI3K/ AKT signaling pathway, subsequently playing important roles in promoting the occurrence and development of RA.

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RETRACTED: Long noncoding RNA LINC00671 exacerbates osteoarthritis by promoting ONECUT2-mediated Smurf2 expression and extracellular matrix degradation

Cited by 10 publications

References 39 publications

LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

LncRNAs as a new regulator of chronic musculoskeletal disorder

LINC02085 Regulates Cell Growth and Inflammatory Response in Rheumatoid Arthritis by Regulating PI3K/ AKT Signaling Pathway

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RETRACTED: Long noncoding RNA LINC00671 exacerbates osteoarthritis by promoting ONECUT2-mediated Smurf2 expression and extracellular matrix degradation

Cited by 10 publications

References 39 publications

LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

LncRNA TM1‐3P Regulates Proliferation, Apoptosis and Inflammation of Fibroblasts in Osteoarthritis through miR ‐144‐3p/ ONECUT2 Axis

LncRNAs as a new regulator of chronic musculoskeletal disorder

LINC02085 Regulates Cell Growth and Inflammatory Response in Rheumatoid Arthritis&nbsp;by Regulating PI3K/ AKT Signaling Pathway

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LINC02085 Regulates Cell Growth and Inflammatory Response in Rheumatoid Arthritis by Regulating PI3K/ AKT Signaling Pathway