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首页> 外文期刊>Journal of Cellular Physiology >The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR‐485 and enhancing the expression of the STAT3
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The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR‐485 and enhancing the expression of the STAT3

机译：长非编码RNA NEAT1导致肝细胞癌发展骗取米尔485和加强STAT3的表达

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摘要

Accumulating evidence has supported the significance of lncRNAs in tumorigenesis. Recently, some studies indicate the oncogenic role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in hepatocellular carcinoma (HCC). In our present study, we focused on the biological mechanisms through which NEAT1 can regulate HCC development. We found that NEAT1 was greatly upregulated in human HCC cell lines including Huh7, Hep3B, HepG2, Bel‐7404, and SK‐Hep1 cells compared to the normal human liver cell line LO2. In addition, we observed that miR‐485 was significantly downregulated in HCC cells. It was implied that miR‐485 was increased by sh‐NEAT1 and miR‐485 can modulate NEAT1 expression negatively. Meanwhile, NEAT1inhibiton can repress HCC growth, migration, and invasion capacity in HepG2 and Hep3B cells. Through performing bioinformatic analysis, dual‐luciferase reporter test, RNA‐binding protein immunoprecipitation, and RNA pull‐down assay, miR‐485 was confirmed as a interacting target of NEAT1. Additionally, STAT3 was recognized as a direct target of miR‐485 and miR‐485 mimics can inhibit STAT3 expression. It was demonstrated that NEAT1 can increase STAT3 levels while miR‐485 mimics can repress STAT3. Moreover, we found that sh‐STAT3 was able to restrain HCC cell migration and invasion process. NEAT1 can act as a competing endogenous lncRNA (ceRNA) to regulated STAT3 by sponging miR‐485 in HCC. Taken these together, NEAT1 can be used as an important biomarker in HCC diagnosis and treatment.
机译：越来越多的证据支持lncRNAs在肿瘤发生的重要性。最近,一些研究表明致癌lncRNA核充实丰富的角色记录1 (NEAT1)在肝细胞癌(HCC)。通过NEAT1可以生物机制调节肝细胞癌的发展。在很大程度上调节人类肝癌细胞株包括Huh7、Hep3B HepG2,贝尔还是7404年SK Hep1应承担的细胞比正常人类的肝脏LO2细胞线。米尔485年肝癌显著下调细胞。通过sh NEAT1和miR量485可以调节NEAT1表达负面。可以抑制肝癌生长、迁移和入侵HepG2和Hep3B细胞的能力。进行生物信息学分析,双荧光素酶报告应承担的测试中,RNA的绑定蛋白质免疫沉淀反应和RNA拉下来化验,米尔485确认交互NEAT1的目标。公认的米尔485和应承担的直接目标米尔485模仿可以抑制STAT3的表达。是证明NEAT1可以增加STAT3虽然miR量485模仿可以抑制STAT3的水平。此外,我们发现sh STAT3能够抑制肝癌细胞迁移和入侵过程。内生lncRNA NEAT1可以作为竞争(龙头)监管STAT3,骗取米尔的485年肝细胞癌。一个重要的在肝癌诊断和生物标志物治疗。

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