Background Glioblastoma has been seen as the most common malignancy of brain tumor. Emerging reports has claimed that SNHG29 (LRRC75A-AS1) was involved in several biological processes via modulation of signaling pathway, and served as an malignant facilitatorin osteosarcoma. However, the specific role of SNHG29 in glioblastoma remains unknown. Methods RT-qPCR and microarray were operated to measure genes expression. Western blot was performed to examine protein expression. CCK-8 and colony formation assays were used to evaluate cell proliferation. Cell migration was tested by transwell assay. Nuclear-cytoplasmic fractionation was conducted to locate SNHG29. The binding capacity of miR-223-3p to SNHG29 or CTNND1 3'UTR was verified by RIP and luciferase reporter assay. Results SNHG29 presented high expression in glioblastoma to boost cell proliferation, migration and EMT process. In addition, miR-223-3p was validated to bind with SNHG29 after prediction and screening. Furthermore, miR-223-3p was proved to be a negative regulator for its target CTNND1. Then, the inhibition on cell proliferation, migration and EMT process resulted from SNHG29 knockdown was recovered by CTNND1 overexpression. At last, the inhibitive impacts on cell proliferation, migration and EMT process of CTNND1 deficiency was abrogated by LiCl. Conclusions In conclusion, SNHG29 regulates miR-223-3p/CTNND1 axis to promote glioblastoma progression via Wnt/β-catenin signaling pathway, offering a potential therapeutic point for glioblastoma patients.

中文翻译：

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SNHG29 通过 Wnt/β-catenin 信号通路调节 miR-223-3p/CTNND1 轴促进胶质母细胞瘤进展。

背景 胶质母细胞瘤已被视为脑肿瘤中最常见的恶性肿瘤。新的报道声称 SNHG29 (LRRC75A-AS1) 通过信号通路的调节参与了多个生物学过程，并作为一种恶性促进骨肉瘤。然而，SNHG29 在胶质母细胞瘤中的具体作用仍然未知。方法采用RT-qPCR和微阵列检测基因表达。进行蛋白质印迹以检查蛋白质表达。CCK-8 和集落形成测定用于评估细胞增殖。通过transwell测定测试细胞迁移。进行核质分离以定位 SNHG29。miR-223-3p 与 SNHG29 或 CTNND1 3'UTR 的结合能力通过 RIP 和荧光素酶报告基因测定进行验证。结果SNHG29在胶质母细胞瘤中高表达，促进细胞增殖、迁移和EMT过程。此外，经过预测和筛选，验证了 miR-223-3p 与 SNHG29 结合。此外，miR-223-3p 被证明是其靶标 CTNND1 的负调节因子。然后，通过 CTNND1 过表达恢复了 SNHG29 敲低对细胞增殖、迁移和 EMT 过程的抑制作用。最后，LiCl消除了CTNND1缺陷对细胞增殖、迁移和EMT过程的抑制作用。结论综上所述，SNHG29通过Wnt/β-catenin信号通路调控miR-223-3p/CTNND1轴促进胶质母细胞瘤进展，为胶质母细胞瘤患者提供潜在的治疗点。在预测和筛选后，验证了 miR-223-3p 与 SNHG29 结合。此外，miR-223-3p 被证明是其靶标 CTNND1 的负调节因子。然后，通过 CTNND1 过表达恢复了 SNHG29 敲低对细胞增殖、迁移和 EMT 过程的抑制作用。最后，LiCl消除了CTNND1缺陷对细胞增殖、迁移和EMT过程的抑制作用。结论综上所述，SNHG29通过Wnt/β-catenin信号通路调控miR-223-3p/CTNND1轴促进胶质母细胞瘤进展，为胶质母细胞瘤患者提供潜在的治疗点。在预测和筛选后，验证了 miR-223-3p 与 SNHG29 结合。此外，miR-223-3p 被证明是其靶标 CTNND1 的负调节因子。然后，通过 CTNND1 过表达恢复了 SNHG29 敲低对细胞增殖、迁移和 EMT 过程的抑制作用。最后，LiCl消除了CTNND1缺陷对细胞增殖、迁移和EMT过程的抑制作用。结论综上所述，SNHG29通过Wnt/β-catenin信号通路调控miR-223-3p/CTNND1轴促进胶质母细胞瘤进展，为胶质母细胞瘤患者提供潜在的治疗点。CTNND1过表达恢复了由SNHG29敲低引起的迁移和EMT过程。最后，LiCl消除了CTNND1缺陷对细胞增殖、迁移和EMT过程的抑制作用。结论综上所述，SNHG29通过Wnt/β-catenin信号通路调控miR-223-3p/CTNND1轴促进胶质母细胞瘤进展，为胶质母细胞瘤患者提供潜在的治疗点。CTNND1过表达恢复了由SNHG29敲低引起的迁移和EMT过程。最后，LiCl消除了CTNND1缺陷对细胞增殖、迁移和EMT过程的抑制作用。结论综上所述，SNHG29通过Wnt/β-catenin信号通路调控miR-223-3p/CTNND1轴促进胶质母细胞瘤进展，为胶质母细胞瘤患者提供潜在的治疗点。