Abstract
Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry assays were used to detect cell viability and apoptosis, respectively. The expression of relative proteins was measured using Western blot. The interaction between miR-320c and TUG1 or FUT4 was confirmed utilizing dual-luciferase reporter and RNA immunoprecipitation assays. In this study, levels of TUG1 and FUT4 were distinctly upregulated, but miR-320c level significantly decreased in OA tissues and chondrocytes derived from OA tissues as well as in IL-1β-stimulated C28/I2 cells. Mechanically, TUG1 sponged miR-320c and miR-320c targeted FUT4. In addition, TUG1 knockdown accelerated cell proliferation and repressed apoptosis and extracellular matrix (ECM) degradation in IL-1β-induced C28/I2 cells, whereas these effects of TUG1 deletion were rescued by either miR-320c inhibitor or FUT4 upregulation. Meanwhile, TUG1 sponged miR-320c to regulate FUT4 expression in IL-1β-induced C28/I2 cells. Collectively, TUG1 modulated cell proliferation, apoptosis and ECM degradation in IL-1β-induced C28/I2 cells via the miR-320c/FUT4 axis, providing a new insight into the OA treatment.
Highlights
Osteoarthritis (OA) is an extensively common degenerative joint disease, which is characterized by articular cartilage degradation along with joint inflammation [1]
The results showed that IL-1β could impede cell proliferation, while this inhibitory effect of IL-1β on cell proliferation was restored by taurine-upregulated gene 1 (TUG1) knockdown (Figure 2b)
Apoptotic cells were examined by flow cytometry, and the results uncovered that the promotion effect of IL-1β treatment on cell apoptosis was regained via TUG1 silencing (Figure 2c and d)
Summary
Osteoarthritis (OA) is an extensively common degenerative joint disease, which is characterized by articular cartilage degradation along with joint inflammation [1]. Previous investigations confirmed that chondrocyte viability, apoptosis and breakdown of extracellular matrix (ECM) degradation were considered to be related with the OA development [3,4,5]. LncRNAs, as a class of ncRNAs with longer than 200 nucleotides [7], have been revealed to possess critical regulatory functions in numerous pathological physiologies, such as cell proliferation, apoptosis and tumor formation [8,9,10]. TUG1 boosted chondrocyte ECM degradation through miR-195/ matrix metalloproteinase (MMP)-13 axis in OA [12]. These evidence suggested that TUG1 may have vital functions in the progression of OA
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