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.

中文翻译：

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长非编码RNA TUG1通过miR-320c / MMP-13轴调节骨关节炎中软骨细胞胞外基质的降解

骨关节炎（OA）是一种常见的慢性关节疾病。这项研究旨在探讨长非编码RNA牛磺酸上调基因1（TUG1）在OA的进展和起始中的功能。通过定量逆转录酶聚合酶链反应（qRT-PCR）检测了TUG1，microRNA-320c（miR-320c）和岩藻糖基转移酶4（FUT4）的水平。使用3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2-H-四唑溴化物和流式细胞术分别检测细胞活力和凋亡。使用蛋白质印迹法测量相对蛋白的表达。miR-320c与TUG1或FUT4之间的相互作用已通过双荧光素酶报告基因和RNA免疫沉淀测定法得以证实。在这项研究中，TUG1和FUT4的水平明显上调，但是在OA组织和来自OA组织的软骨细胞以及IL-1β刺激的C28 / I2细胞中，miR-320c水平显着降低。在机械上，TUG1用海绵将miR-320c和miR-320c靶向FUT4。此外，在IL-1β诱导的C28 / I2细胞中，TUG1敲低可促进细胞增殖，并抑制细胞凋亡和细胞外基质（ECM）降解，而miR-320c抑制剂或FUT4上调可挽救TUG1缺失的这些作用。同时，TUG1使miR-320c发挥作用，以调节IL-1β诱导的C28 / I2细胞中FUT4的表达。总的来说，TUG1通过miR-320c / FUT4轴调节IL-1β诱导的C28 / I2细胞中的细胞增殖，凋亡和ECM降解，为OA治疗提供了新的见识。TUG1用海绵将miR-320c和miR-320c靶向FUT4。此外，在IL-1β诱导的C28 / I2细胞中，TUG1敲低可促进细胞增殖，并抑制细胞凋亡和细胞外基质（ECM）降解，而miR-320c抑制剂或FUT4上调可挽救TUG1缺失的这些作用。同时，TUG1使miR-320c发挥作用，以调节IL-1β诱导的C28 / I2细胞中FUT4的表达。总的来说，TUG1通过miR-320c / FUT4轴调节IL-1β诱导的C28 / I2细胞中的细胞增殖，凋亡和ECM降解，为OA治疗提供了新的见识。TUG1用海绵靶向miR-320c和miR-320c靶向FUT4。此外，在IL-1β诱导的C28 / I2细胞中，TUG1敲低可促进细胞增殖，并抑制细胞凋亡和细胞外基质（ECM）降解，而miR-320c抑制剂或FUT4上调可挽救TUG1缺失的这些作用。同时，TUG1使miR-320c发挥作用，以调节IL-1β诱导的C28 / I2细胞中FUT4的表达。总的来说，TUG1通过miR-320c / FUT4轴调节IL-1β诱导的C28 / I2细胞中的细胞增殖，凋亡和ECM降解，为OA治疗提供了新的见识。而通过miR-320c抑制剂或FUT4上调可以挽救TUG1缺失的这些作用。同时，TUG1使miR-320c发挥作用，以调节IL-1β诱导的C28 / I2细胞中FUT4的表达。总的来说，TUG1通过miR-320c / FUT4轴调节IL-1β诱导的C28 / I2细胞中的细胞增殖，凋亡和ECM降解，为OA治疗提供了新的见识。而通过miR-320c抑制剂或FUT4上调可以挽救TUG1缺失的这些作用。同时，TUG1使miR-320c发挥作用，以调节IL-1β诱导的C28 / I2细胞中FUT4的表达。总的来说，TUG1通过miR-320c / FUT4轴调节IL-1β诱导的C28 / I2细胞中的细胞增殖，凋亡和ECM降解，为OA治疗提供了新的见识。