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首页> 外文期刊>Advances in Rheumatology >Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis
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Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis

机译：长期非编码RNA KcNQ1OT1促进细胞活力和迁移，并通过调节miR-126-5P / TRPS1轴来抑制CHON-001细胞的降解

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Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. Relative expression of KCNQ1OT1, miR-126-5p and TRPS1 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. Western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic.
机译：骨关节炎（OA）定义为退行性疾病。广泛阐明了长期非编码RNA（LNCRNA）的长期非编码RNA（LNCRNA）的枢轴作用。在此，我们打算探讨LNCRNA KCNQ101中的CHON-001细胞的功能和分子机制。通过定量实时聚合酶链反应（QRT-PCR）测定KCNQ1OT1，miR-126-5p和TRPS1的相对表达。通过MTT测定检查细胞活力。通过Transwell测定评估软骨细胞的迁移能力。用于确定胶原II，MMP13和TRPS1的相对蛋白表达。施用双荧光素酶报告器（DLR）测定以测试LNCRNA KCNQ1OT1或miR-126-5P的靶标。降低了KCNQ1OT1和TRPS1和TRPS1的相对表达，而MIR-126-5P在创伤后OA患者的软骨组织中增加，而没有创伤后OA的受试者。增加KCNQ1OT1或降低MiR-126-5P增强的细胞活力和迁移，并在CHON-001细胞中抑制细胞外基质（ECM）降解。 MiR-126-5P是KCNQ1OT1的下游靶标，可以直接靶向TRPS1。 KCNQ1OT1和MIR-126-5P或MIR-126-5P和TRPS1之间存在反比相关性。同时，KCNQ1OT1和TRPS1之间存在正相关性。 KCNQ1OT1对细胞活力和迁移以及KCNQ1OT1对ECM降解的抑制作用的促进影响通过MIR-126-5P过表达或CHON-001细胞的TRPS 1敲低。 KCNQ1OT1的过度表达通过海绵MIR-126-5P瞄准TRPS来衰减OA的开发。我们的研究结果可以为临床中的人类OA提供可能的治疗策略。

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