Long non-protein coding RNA DANCR functions as a competing endogenous RNA to regulate osteoarthritis progression via miR-577/SphK2 axis

Fan, Xiaochen; Yuan, Jian; Xie, Jun; Pan, Zhanpeng; Yao, Xiang; Sun, Xiangyi; Zhang, Pin; Zhang, Lei

doi:10.1016/j.bbrc.2018.04.130

Cited by 50 publications

(29 citation statements)

References 20 publications

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“…Some lncRNAs have been well documented to regulate the differentiation of osteoblasts via the lncRNA-miRNA ceRNA network [27]. Besides, Fan et al have found that DANCR can regulate the progression of OA via targeting miR-577 through ceRNA mechanism [32]. Moreover, the study by Mao et al shows the evidence that lncRNA HOTAIR is involved in OA pathogenesis by regulating synovial inflammation and proliferation and apoptosis of synoviocytes [33].…”

Section: Lncrna Ighcγ1 Promoted Inflammation Bymentioning

confidence: 99%

lncRNA IGHCγ1 Acts as a ceRNA to Regulate Macrophage Inflammation via the miR-6891-3p/TLR4 Axis in Osteoarthritis

Zhang

Sun²,

Liang

et al. 2020

Mediators of Inflammation

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Accumulating data have implicated that long noncoding RNA (lncRNA) plays an important role in osteoarthritis (OA), which may function as a competitive endogenous RNA (ceRNA) of microRNAs (miRNAs). lncRNA IGHCγ1 has been demonstrated to regulate inflammation and autoimmunity. Nonetheless, the altering effect of IGHCγ1 in OA remains unclear. This study is aimed at investigating the mechanism and function of lncRNA IGHCγ1 in OA. CCK-8, EdU, and transwell assays were used to estimate macrophage proliferation and migration. Fluorescence in situ hybridization (FISH) was performed to estimate the local expression of lncRNA IGHCγ1 in macrophages. Luciferase reporter assay was adopted to validate the ceRNA role of IGHCγ1 as miRNA sponge. lncRNA IGHCγ1 was primarily localized in macrophage cytoplasm and upregulated in OA. miR-6891-3p inhibited macrophage proliferation, migration, and inflammatory response by targeting TLR4, while lncRNA IGHCγ1 promoted TLR4 expression by functioning as a ceRNA for miR-6891-3p through the NF-κB signal in macrophages. This study strongly supports that lncRNA IGHCγ1 regulates inflammatory response via regulating the miR-6891-3p/TLR4/NF-κB axis in macrophages.

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Section: Lncrna Ighcγ1 Promoted Inflammation Bymentioning

confidence: 99%

lncRNA IGHCγ1 Acts as a ceRNA to Regulate Macrophage Inflammation via the miR-6891-3p/TLR4 Axis in Osteoarthritis

Zhang

Sun²,

Liang

et al. 2020

Mediators of Inflammation

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“…Zhu et al found that lncRNA FAS-AS1 promoted the degradation of extracellular matrix (ECM) of cartilage in OA [10]. Fan et al suggested that lncRNA DANCR functioned as a competing endogenous RNA to regulate OA progression via miR-577/SphK2 axis [11]. However, the roles and underlying mechanisms of lncRNAs in OA remain unclear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA FOXD2-AS1 induces chondrocyte proliferation through sponging miR-27a-3p in osteoarthritis

Wang

Cao

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Osteoarthritis (OA) is a common degenerative joint disease worldwide. Long non-coding RNAs (lncRNAs) have been widely confirmed to involve in the modulation of OA progression. However, the underlying mechanisms of lncRNA FOXD2-AS1 in OA remain unclear. In the present study, we showed FOXD2-AS1 expression was upregulated and positively associated with the severity of OA patients. IL-1b and/or TNF-a treatment could increase FOXD2-AS1 expression in chondrocytes. FOXD2-AS1 overexpression induced cell proliferation, inflammation and extracellular matrix (ECM) degradation in chondrocytes. Mechanistically, we found that FOXD2-AS1 upregulated the expression level of TLR4 by sponging miR-27a-3p. In addition, we revealed that miR-27a-3p mimics could abolish the effects of FOXD2-AS1 overexpression on cell proliferation, inflammation, and ECM degradation in chondrocytes. Therefore, we demonstrated that FOXD2-AS1 could play a crucial role in the progression of OA, at least partially, by regulating miR-27a-3p/TLR4 axis.

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“…There is only one cell type–chondrocytes in mature cartilage–which controls the degeneration progression of articular cartilage . Many experiments have proved that deregulation of genes in chondrocytes is linked to the synthesis and degradation of cartilage . Long noncoding RNAs (lncRNAs) with more than 200 nucleotides exert important regulation effects on gene expression .…”

Section: Introductionmentioning

confidence: 99%

Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR‐376‐3p/FGFR1 axis

Huang

Zhang

et al. 2019

J of Cellular Biochemistry

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Osteoarthritis (OA) is a common joint disease with high morbidity, but there is still no definitive treatment for it. Long noncoding RNAs (lncRNAs) have been confirmed to play key roles in OA progression. This work was done to investigate the roles and action mechanism of lncRNA TNFSF10 in OA. The messenger RNA levels of TNFSF10 in articular cartilage samples from patients or chondrocytes were detected by Quantitative real-time PCR assay (qRT-PCR).The effects of TNFSF10 on chondrocytes were evaluated on the basis of cell growth, apoptosis, and inflammation. Then, the interaction between TNFSF10 and miR-376-3p was explored by dual-luciferase reporter test, RNA-binding protein immunoprecipitation, and RNA pull-down assay. Finally, various cell experiments, Western blot analysis, and qRT-PCR were performed to study the interaction among TNFSF10, miR-376-3p, and fibroblast growth factor receptor 1 (FGFR1). It was found that TNFSF10 was upregulated in OA cartilages and stimulated cell proliferation, antiapoptosis, and inflammation for chondrocytes.In addition, TNFSF10 acted as a competing endogenous RNA to downregulate miR-376-3p, and the influence of TNFSF10 on chondrocytes was partly reversed by miR-376-3p. Moreover, FGFR1, as a target of miR-376-3p, had reversal functions on the outcomes mediated by miR-376-3p. The further analysis displayed that there was a negative relationship between TNFSF10 and miR-376-3p as well as miR-376-3p and FGFR1, while FGFR1 was positively related with TNFSF10. Altogether, TNFSF10 overexpression probably stimulated proliferation and inflammation, and inhibited apoptosis by regulating the miR-376-3p/FGFR1 axis, implying that its increase contributed to OA progression. Our study provided a new potential biomarker or therapeutic target-TNFSF10, which was helpful to develop an efficient approach to cure OA. K E Y W O R D Schondrocytes., FGFR1, long noncoding TNFSF10, miR-376-3p, osteoarthritis

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Long non-protein coding RNA DANCR functions as a competing endogenous RNA to regulate osteoarthritis progression via miR-577/SphK2 axis

Cited by 50 publications

References 20 publications

lncRNA IGHCγ1 Acts as a ceRNA to Regulate Macrophage Inflammation via the miR-6891-3p/TLR4 Axis in Osteoarthritis

lncRNA IGHCγ1 Acts as a ceRNA to Regulate Macrophage Inflammation via the miR-6891-3p/TLR4 Axis in Osteoarthritis

LncRNA FOXD2-AS1 induces chondrocyte proliferation through sponging miR-27a-3p in osteoarthritis

Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR‐376‐3p/FGFR1 axis

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