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Yuqing Ji,Man Wang,Xueshen Li,Fusheng Cui 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.4
Purpose: Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been deemed an oncogene in many humancancers. However, the underlying mechanism of NEAT1 in nasopharyngeal carcinoma (NPC) progression remains largelyunclear. Materials and Methods: Quantitative real-time PCR assay was performed to assess the expression of NEAT1 and miR-34a-5p inNPC tissues and cells. Western blot analysis was used to observe cell epithelial to mesenchymal transition (EMT) and the activationof Wnt/β-catenin signaling in 5-8F cells. MiRNA directly interacting with NEAT1 were verified by dual-luciferase reporter assayand RNA immunoprecipitation. Cell proliferation ability was determined by CCK-8 assay, and cell migration and invasion capacitieswere assessed by transwell assays. An animal model was used to investigate the regulatory effect of NEAT1 on tumorgrowth in vivo. Results: Our data revealed that NEAT1 is upregulated, while miR-34a-5p is downregulated in NPC tissues and cell lines. NEAT1knockdown repressed tumor growth in vitro and in vivo. Additionally, we discovered that NEAT1 directly binds to miR-34a-5pand suppresses miR-34a-5p expression. Moreover, NEAT1 knockdown exerted suppression effects on cell proliferation, migration,invasion, and EMT by miR-34a-5p. NEAT1 knockdown blocked Wnt/β-catenin signaling via miR-34a-5p. Conclusion: Our study demonstrated that NEAT1 targets miR-34a-5p at least partly to drive NPC progression by regulating Wnt/β-catenin signaling, suggesting a potential therapeutic target for NPC.