TUG1 knockdown promoted viability and inhibited apoptosis and cartilage ECM degradation in chondrocytes via the miR‑17‑5p/FUT1 pathway in osteoarthritis
- Zhichao Li
- Jin Wang
- Jing Yang
Affiliations: Department of Hand, Foot and Vascular Surgery, Hanyang Hospital, Wuhan University of Science and Technology, Wuhan, Hubei 430050, P.R. China, Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, Hubei 430060, P.R. China
- Published online on: October 6, 2020 https://doi.org/10.3892/etm.2020.9283
Copyright: © Li
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Osteoarthritis (OA) is a degenerative disease characterized by cartilage destruction. Previous research has demonstrated that long non‑coding RNAs serve a role in OA progression. The current study aimed to determine the function and mechanism of taurine upregulated gene (TUG) 1 in OA. The results of reverse transcription quantitative PCR revealed that TUG1 was elevated in OA cartilage tissues and interleukin (IL)‑1β‑induced chondrocytes. Cell Counting kit‑8 and flow cytometry analysis revealed that TUG1 knockdown promoted cell viability and inhibited cell apoptosis. Furthermore, matrix metalloprotein (MMP) 13, collagen II and aggrecan expression was determined by western blotting, of which the results demonstrated that TUG1 knockdown significantly decreased MMP13 expression and increased collagen II and aggrecan expression in IL‑1β‑stimulated chondrocytes, indicating that extracellular matrix (ECM) damage was inhibited. Additionally, using bioinformatics analysis, dual‑luciferase reporter and RNA immunoprecipitation assays, TUG1 was revealed to upregulate fucosyltransferase (FUT) 1 by targeting miR‑17‑5p. Furthermore, miR‑17‑5p was downregulated and FUT1 upregulated in OA cartilage tissues and IL‑1β‑induced chondrocytes. TUG1 overexpression reversed the aforementioned effects on cell viability, cell apoptosis and ECM degradation mediated by miR‑17‑5p in IL‑1β‑activated chondrocytes. Additionally, the effects of FUT1 knockdown on cell viability, apoptosis and ECM degradation mediated by FUT1 knockdown were reversed by miR‑17‑5p inhibition. In conclusion, TUG1 knockdown inhibited OA progression by downregulating FUT1 via miR‑17‑5p.