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Nuclear paraspeckle assembly transcript 1 promotes the metastasis and epithelial-mesenchymal transition of hepatoblastoma cells by inhibiting miR-129-5p

机译:核旁散组装转录本1通过抑制miR-129-5p促进肝母细胞瘤细胞的转移和上皮-间质转化

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摘要

The abnormal expression of nuclear paraspeckle assembly transcript 1 (NEAT1) may serve critical functions for the development and progression of various types of human tumor. However, the expression and biological function of NEAT1 in hepatoblastoma (HB) and the underlying mechanisms for the function of NEAT1 in HB remain largely uncharacterized. In the present study, the results of reverse transcription-quantitative polymerase chain reaction revealed that the expression of NEAT1 was significantly elevated in HB tissues. HB tissues with metastasis also exhibited significantly increased levels of NEAT1 compared with tissues without metastasis. The biological functions of NEAT1 were then assessed using gain-/loss-of-function studies. The results of in vitro assays revealed that inhibiting NEAT1 expression reduced the migration and invasion of HepG2 cells. By contrast, the induced expression of NEAT1 exhibited the opposite effect. The present study also demonstrated that the inhibition of NEAT1 expression prevented the epithelial-mesenchymal transition of HepG2 cells, whereas forced expression of NEAT1 exhibited the opposite effect. In addition, it was confirmed that NEAT1 could modulate the expression of microRNA (miR)-129-5p in HepG2 cells, and that NEAT1 may exert its effect on the metastatic behaviors and epithelial-mesenchymal transition of HepG2 cells by inhibiting miR-129-5p. In conclusion, the present study indicated that NEAT1 expression was aberrantly increased in HB and that it may promote the metastasis of HB cells by inhibiting miR-129-5p. Targeting NEAT1 may potentially be a novel therapeutic option for treating patients with HB.
机译:核副斑点装配转录本1(NEAT1)的异常表达可能对各种类型的人类肿瘤的发生和发展起关键作用。但是,NEAT1在肝母细胞瘤(HB)中的表达和生物学功能以及NEAT1在HB中的潜在机制尚不十分清楚。在本研究中,逆转录-定量聚合酶链反应的结果表明,NEAT1的表达在HB组织中显着升高。与没有转移的组织相比,具有转移的HB组织也显示出明显增加的NEAT1水平。然后使用功能获得/丧失研究评估NEAT1的生物学功能。体外测定的结果表明,抑制NEAT1的表达减少了HepG2细胞的迁移和侵袭。相反,诱导的NEAT1表达表现出相反的作用。本研究还表明,抑制NEAT1的表达可阻止HepG2细胞的上皮-间充质转化,而强制表达的NEAT1则具有相反的作用。此外,已证实NEAT1可以调节HepG2细胞中microRNA(miR)-129-5p的表达,并且NEAT1可以通过抑制miR-129-N对HepG2细胞的转移行为和上皮间质转化发挥作用。 5便士总之,本研究表明NEAT1在HB中的表达异常增加,并且可能通过抑制miR-129-5p促进HB细胞的转移。靶向NEAT1可能是治疗HB患者的新型治疗选择。

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