Background. Atherosclerosis (AS) is a common severe disease around the world. The merging paper reported that long noncoding RNAs (lncRNAs) took part in diversified pathological processes of AS, although the mechanism remains unknown. This study is aimed at uncovering the profile of lncRNA taurine-upregulated gene 1 (TUG1), which has biological function, and potential mechanism in AS progression in vitro. Methods. Oxidized low-density lipoprotein (ox-LDL) was used for AS model construction in vitro. Levels of lncRNA TUG1, miR-141-3p, and receptor tyrosine kinase-like orphan receptor 2 (ROR2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in AS tissues or in ox-LDL-treated vascular smooth muscle cells (HA-VSMCs). The biofunctional effects were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays. The expression of proliferation-related proteins (CyclinD1, Ki-67) and metastasis-associated proteins (β-catenin, Vimentin) and ROR2 in cells was determined by western blot analysis. The potential binding sites were predicted by starBase software online and confirmed by dual-luciferase reporter analysis. Results. The expression of TUG1 and ROR2 was promoted in AS tissues and ox-LDL-treated HA-VSMCs. While the low expression of miR-141-3p negatively correlated with that of TUG1 or ROR2 in AS tissues. Silencing of TUG1 inhibited the proliferation, migration, invasion, and metastasis in ox-LDL-treated HA-VSMCs. Moreover, the putative binding sites between miR-141-3p and TUG1 or ROR2 were predicted by starBase software online. Also, miR-141-3p deletion reversed the positive effects of TUG1 knockdown on cells. Besides, downregulation of miR-141-3p disrupted the biofunctional results from ROR2 silencing. Conclusion. TUG1 enhanced the progression of AS in vitro by regulating the miR-141-3p/ROR2 axis.

中文翻译：

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长链非编码 RNA TUG1 通过 miR-141-3p/ROR2 轴促进 ox-LDL 处理的 HA-VSMC 的功能。

背景。动脉粥样硬化（AS）是世界范围内常见的严重疾病。合并论文报告称，长链非编码 RNA (lncRNA) 参与了 AS 的多种病理过程，但其机制尚不清楚。本研究旨在揭示具有生物学功能的 lncRNA 牛磺酸上调基因 1 (TUG1) 的概况，以及体外 AS 进展的潜在机制。方法。氧化低密度脂蛋白 (ox-LDL) 用于体外AS 模型构建. 通过定量实时聚合酶链反应 (qRT-PCR) 在 AS 组织或 ox-LDL 处理的血管平滑肌中检测 lncRNA TUG1、miR-141-3p 和受体酪氨酸激酶样孤儿受体 2 (ROR2) 的水平肌肉细胞（HA-VSMC）。通过 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) 和 transwell 测定法检查了生物功能效应。通过蛋白质印迹分析确定细胞中增殖相关蛋白（CyclinD1，Ki-67）和转移相关蛋白（β-连环蛋白，波形蛋白）和ROR2的表达。通过starBase软件在线预测潜在的结合位点，并通过双荧光素酶报告基因分析确认。结果. 在 AS 组织和 ox-LDL 处理的 HA-VSMCs 中 TUG1 和 ROR2 的表达得到促进。而 miR-141-3p 在 AS 组织中的低表达与 TUG1 或 ROR2 的低表达呈负相关。TUG1 的沉默抑制了 ox-LDL 处理的 HA-VSMCs 的增殖、迁移、侵袭和转移。此外，通过starBase软件在线预测了miR-141-3p与TUG1或ROR2之间推定的结合位点。此外，miR-141-3p 缺失逆转了 TUG1 敲低对细胞的积极影响。此外，miR-141-3p 的下调破坏了 ROR2 沉默的生物功能结果。结论。TUG1通过调节 miR-141-3p/ROR2 轴促进体外AS 的进展。