Abstract
Osteoarthritis (OA) is one of the most common chronic joint disease. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in a variety of diseases including OA. However, the underlying mechanism of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) in OA has not been well elucidated. The expression of DANCR in cartilage tissues from OA patients was detected using quantitative real-time PCR. After cell transfection, the effects of DANCR inhibition on the proliferation, apoptosis and inflammatory factors of OA chondrocytes were detected using Cell Counting Kit-8 assay and flow cytometry assay. Novel target of DANCR was then identified through bioinformatics analysis and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The expression of DANCR was significantly increased in OA patients. Function assays demonstrated that DANCR suppression inhibited the proliferation, inflammation, and promoted apoptosis of chondrocytes cells. Additionally, DANCR regulated survival of OA chondrocytes through acting as a competitive endogenous RNA for miR-216a-5p. Furthermore, JAK2 was a direct target of miR-216a-5p, and DANCR regulated the JAK2/STAT3 signal pathway through miR-216a-5p in OA chondrocytes. In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.
Highlights
Osteoarthritis (OA) is a common chronic joint disease, which is mainly characterized by proteolytic degradation of the cartilage and synovial inflammation [1]
Results showed that IL-6 and IL-8 were significantly inhibited in chondrocytes by down-regulation of differentiation antagonizing non-protein coding RNA (DANCR) (Figure 2B, P
Several Long non-coding RNAs (lncRNAs) were identified to participate in OA progression, including HOTAIR [17], FAS-AS1 [18], SNHG5 [19] and MEG3 [20]
Summary
Osteoarthritis (OA) is a common chronic joint disease, which is mainly characterized by proteolytic degradation of the cartilage and synovial inflammation [1]. The incidence rate of OA increases with age, so it has become the main cause of pain, disability, and shortening of adult working life around the world [2]. Current therapeutic options for OA are aimed at pain reduction and symptom control. To improve the therapeutic options available for patients with OA, it is necessary to explore the pathophysiology and regulatory mechanism of OA. In recent years, increasing evidences have demonstrated that dysregulation of lncRNA is closely associated with diverse diseases including OA [8,9,10]. LncRNA-CIR was significantly up-regulated in OA patients and overexpression of lncRNA-CIR promoted the degradation of the extracellular matrix of chondrocyte in OA [11]
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