Long noncoding RNAs (lncRNAs) play pivotal roles in the pathogenesis, development, and treatment of atherosclerosis (AS). The endothelial cell injury is a feature of AS. However, the role and mechanism of lncRNA LINC00657 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell injury remain unclear. The serum samples were collected from 32 AS patients and normal volunteers. Ox-LDL-treated human umbilical vein endothelial cells (HUVEC) were used for the experiments in vitro. The levels of LINC00657, microRNA (miR)-30c-5p and Wnt family member 7B (Wnt7b) were measured by quantitative real-time polymerase chain reaction or western blot. The expression levels of proteins in Wnt7b/β-catenin pathway or endothelial-mesenchymal transition (EndMT) were detected by western blot. The secretion of inflammatory cytokine was examined by enzyme linked immunosorbent assay (ELISA). Cell viability and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, flow cytometry, and western blot. The target association of miR-30c-5p and LINC00657/Wnt7b was analyzed via dual-luciferase reporter assay and RNA pull-down assay. LINC00657 expression was increased in AS serum and ox-LDL-treated HUVEC cells. LINC00657 knockdown suppressed ox-LDL-induced Wnt7b/β-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. MiR-30c-5p was bound to LINC00657 and it knockdown reversed the role of LINC00657 inhibition in ox-LDL-induced HUVEC cell injury. MiR-30c-5p targeted Wnt7b to inhibit ox-LDL-induced Wnt7b/β-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. Silence of LINC00657 repressed ox-LDL-induced injury via inhibiting EndMT, inflammatory response, and apoptosis in HUVEC cells by regulating miR-30c-5p/Wnt7b/β-catenin, indicating a potential target for treatment of AS.

长链非编码RNA (lncRNA) 在动脉粥样硬化(AS) 的发病机制、发展和治疗中发挥着关键作用。内皮细胞损伤是AS的一个特征。然而，lncRNA LINC00657在氧化低密度脂蛋白（ox-LDL）诱导的内皮细胞损伤中的作用和机制仍不清楚。血清样本采集自 32 名 AS 患者和正常志愿者。 Ox-LDL 处理的人脐静脉内皮细胞 (HUVEC) 用于体外实验。通过定量实时聚合酶链反应或蛋白质印迹测量 LINC00657、microRNA (miR)-30c-5p 和 Wnt 家族成员 7B (Wnt7b) 的水平。 Western blot检测Wnt7b/β-catenin通路或内皮间质转化（EndMT）蛋白的表达水平。通过酶联免疫吸附测定（ELISA）检查炎症细胞因子的分泌。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基-四唑溴化物、流式细胞术和蛋白质印迹测定细胞活力和凋亡。通过双荧光素酶报告基因测定和 RNA Pull-down 测定分析 miR-30c-5p 和 LINC00657/Wnt7b 的靶标关联。 AS 血清和 ox-LDL 处理的 HUVEC 细胞中的 LINC00657 表达增加。 LINC00657 敲低可抑制 ox-LDL 诱导的 HUVEC 细胞中 Wnt7b/β-catenin 激活、EndMT、炎症反应和细胞凋亡。 MiR-30c-5p 与 LINC00657 结合，它的敲低逆转了 LINC00657 在 ox-LDL 诱导的 HUVEC 细胞损伤中的抑制作用。 MiR-30c-5p 靶向 Wnt7b，抑制 ox-LDL 诱导的 HUVEC 细胞中 Wnt7b/β-catenin 激活、EndMT、炎症反应和凋亡。 LINC00657 的沉默通过调节 miR-30c-5p/Wnt7b/β-catenin 来抑制 HUVEC 细胞中的 EndMT、炎症反应和细胞凋亡，从而抑制 ox-LDL 诱导的损伤，表明其是治疗 AS 的潜在靶点。