Objective. We attempted to clarify the effect of lncRNA MSC-AS1 on carcinogenic and development of nasopharyngeal carcinoma (NPC) and the related mechanisms. Methods. The levels of MSC-AS1 and miR-429 were estimated in NPC tissues and cells using qRT-PCR. Correlation analysis, dual-luciferase report, and RNA pull down assay assessed the action association of MSC-AS1 and miR-429. MTT, colony formation, cell wound scratch, and transwell assays were used to assess the proliferation, invasion, and migration of C666-1 cells. Metastasis-related protein expressions and activation of the JAK1/STAT3 pathway were confirmed by western blot and immunohistochemistry. Results. The expression of MSC-AS1 presented significant upregulation, and miR-429 expression was markedly downregulated in NPC tissues and cells. The level of MSC-AS1 had negative relation to the miR-429 level. Knockdown of MSC-AS1 suppressed the proliferation, invasion, and migration of C666-1 cells. On the contrary, overexpressing of MSC-AS1 exerts the opposite effects on C666-1 cell growth and migration. miR-429 was determined as functional downstream of MSC-AS1. The suppressive function of MSC-AS1 knockdown was predominately abolished by the miR-429 inhibitor. miR-429 was an antitumor gene inhibiting NPC growth and metastasis through JAK1/STAT3 pathway. In C666-1 cells, the elevated cell growth and migration induced by the miR-429 inhibitor were significantly reversed by si-JAK1 transfection. Conclusions. High expression of MSC-AS1 exerted a carcinogenic effect on NPC cell growth and metastasis by inhibiting miR-429 and activating the JAK1/STAT3 pathway.

中文翻译：

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lncRNA MSC-AS1/miRNA-429轴通过JAK1/STAT3信号通路介导鼻咽癌的生长和转移

客观。我们试图阐明lncRNA MSC-AS1对鼻咽癌（NPC）的致癌和发展的影响及其相关机制。方法。使用 qRT-PCR 估计 NPC 组织和细胞中 MSC-AS1 和 miR-429 的水平。相关性分析、双荧光素酶报告和 RNA 下拉分析评估了 MSC-AS1 和 miR-429 的作用关联。MTT、集落形成、细胞伤口划痕和 transwell 测定用于评估 C666-1 细胞的增殖、侵袭和迁移。通过蛋白质印迹和免疫组织化学证实了转移相关蛋白的表达和 JAK1/STAT3 通路的激活。结果. MSC-AS1的表达显着上调，而miR-429的表达在NPC组织和细胞中显着下调。MSC-AS1水平与miR-429水平呈负相关。MSC-AS1 的敲低抑制了 C666-1 细胞的增殖、侵袭和迁移。相反，MSC-AS1 的过表达对 C666-1 细胞的生长和迁移产生相反的影响。miR-429 被确定为 MSC-AS1 的功能性下游。MSC-AS1 敲低的抑制功能主要被 miR-429 抑制剂消除。miR-429是一种通过JAK1/STAT3通路抑制NPC生长和转移的抗肿瘤基因。在 C666-1 细胞中，由 miR-429 抑制剂诱导的升高的细胞生长和迁移被 si-JAK1 转染显着逆转。结论. MSC-AS1 的高表达通过抑制 miR-429 和激活 JAK1/STAT3 通路对 NPC 细胞生长和转移发挥致癌作用。