Bladder cancer (BCa) is one of the most common urinary malignancies in the world. Growing evidence suggests that epithelial-to-mesenchymal transition (EMT) is a major contributor for BCa metastasis. lncRNA small nucleolar RNA host gene 16 (SNHG16) has been reported as a tumor promoter in many cancers. This study aims to investigate the function and mechanism of SNHG16 on EMT in BCa. Quantitative RT-PCR (qRT-PCR) was used to determine the expression of SNHG16 in human BCa tissues and TGF-β-induced cells. Western blot (WB) was performed to evaluate the expression of EMT-related proteins. Transwell assay was exerted to assess the migration and invasion ability of SNHG16 in BCa. RNA pull-down assay was conducted to confirm the RNA–RNA interaction. The precise mechanism by which SNHG16 regulated EMT process in BCa was also explored. SNHG16 was found up-regulated in TGF-β-induced BCa cells and BCa tissues. Transwell assay showed that overexpression of SNHG16 significantly promoted the migration and invasion of BCa cells, whereas knock-down of SNHG16 caused the opposite effects. Then, the interaction between SNHG16 and miR-200a-3p was verified by dual-luciferase reporter assay and RNA pull-down assay. And the effects of knock-down or overexpression of SNHG16 on migration and invasion were reversed by co-transfecting miR-200a-3p inhibitors or mimics. This study first demonstrated that SNHG16 was responsible for EMT of BCa cells via miR-200a-3p/ ZEB1/ZEB2 axis. These results provided a potential therapeutic strategy for BCa treatment, especially in metastatic BCa.

中文翻译：

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SNHG16通过诱导上皮到间质转化来调节膀胱癌的侵袭和迁移。

膀胱癌（BCa）是世界上最常见的泌尿系统恶性肿瘤之一。越来越多的证据表明，上皮到间质转化（EMT）是BCa转移的主要因素。lncRNA小核仁RNA宿主基因16（SNHG16）已被报道为许多癌症中的肿瘤启动子。本研究旨在探讨SNHG16对BCa EMT的作用和机制。定量RT-PCR（qRT-PCR）用于测定人BCa组织和TGF-β诱导的细胞中SNHG16的表达。进行蛋白质印迹（WB）评估EMT相关蛋白的表达。用Transwell分析法评估SNHG16在BCa中的迁移和侵袭能力。进行RNA下拉测定以确认RNA-RNA相互作用。还探讨了SNHG16调控BCa中EMT过程的精确机制。SNHG16在TGF-β诱导的BCa细胞和BCa组织中被上调。Transwell分析表明，SNHG16的过表达显着促进了BCa细胞的迁移和侵袭，而敲除SNHG16则引起了相反的作用。然后，通过双荧光素酶报告基因测定和RNA下拉测定验证了SNHG16与miR-200a-3p之间的相互作用。通过共转染miR-200a-3p抑制剂或模拟物可以逆转SNHG16的敲低或过表达对迁移和侵袭的影响。这项研究首先证明SNHG16通过miR-200a-3p / ZEB1 / ZEB2轴负责BCa细胞的EMT。这些结果为BCa治疗提供了潜在的治疗策略，尤其是在转移性BCa中。Transwell分析表明，SNHG16的过表达显着促进了BCa细胞的迁移和侵袭，而敲除SNHG16则引起了相反的作用。然后，通过双荧光素酶报告基因测定和RNA下拉测定验证了SNHG16与miR-200a-3p之间的相互作用。通过共转染miR-200a-3p抑制剂或模拟物可以逆转SNHG16的敲低或过表达对迁移和侵袭的影响。这项研究首先证明SNHG16通过miR-200a-3p / ZEB1 / ZEB2轴负责BCa细胞的EMT。这些结果为BCa治疗提供了潜在的治疗策略，尤其是在转移性BCa中。Transwell分析表明，SNHG16的过表达显着促进了BCa细胞的迁移和侵袭，而敲除SNHG16则引起了相反的作用。然后，通过双荧光素酶报告基因测定和RNA下拉测定验证了SNHG16与miR-200a-3p之间的相互作用。通过共转染miR-200a-3p抑制剂或模拟物可以逆转SNHG16的敲低或过表达对迁移和侵袭的影响。这项研究首先证明SNHG16通过miR-200a-3p / ZEB1 / ZEB2轴负责BCa细胞的EMT。这些结果为BCa治疗提供了潜在的治疗策略，尤其是在转移性BCa中。SNHG16与miR-200a-3p之间的相互作用通过双荧光素酶报告基因分析和RNA下拉分析进行了验证。通过共转染miR-200a-3p抑制剂或模拟物可以逆转SNHG16的敲低或过表达对迁移和侵袭的影响。这项研究首先证明SNHG16通过miR-200a-3p / ZEB1 / ZEB2轴负责BCa细胞的EMT。这些结果为BCa治疗提供了潜在的治疗策略，尤其是在转移性BCa中。SNHG16与miR-200a-3p之间的相互作用通过双荧光素酶报告基因分析和RNA下拉分析进行了验证。通过共转染miR-200a-3p抑制剂或模拟物可以逆转SNHG16的敲低或过表达对迁移和侵袭的影响。这项研究首先证明SNHG16通过miR-200a-3p / ZEB1 / ZEB2轴负责BCa细胞的EMT。这些结果为BCa治疗提供了潜在的治疗策略，尤其是在转移性BCa中。