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Long noncoding RNA NEAT1 promotes cell proliferation migration and invasion in hepatocellular carcinoma through interacting with miR‐384

机译:长非编码RNA NEAT1通过与miR-384相互作用促进肝细胞癌的细胞增殖迁移和侵袭

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摘要

It was reported that long non‐coding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is involved in hepatocellular carcinoma (HCC). However, the underlying mechanism of tumorigenesis is still largely unclear. Here, we found that NEAT1 is remarkably upregulated in HCC tissues and cell lines. Overexpression of NEAT1 notably accelerated HCC cell proliferation, migration, and invasion. Knockdown of NEAT1 significantly inhibited HCC cell proliferation, migration and invasion. MiR‐384 expression was lower in HCC tissues and cell lines than adjacent nontumor tissues and L02 cell. MiR‐384 exhibited the functions of tumor‐suppressive. The expression of miR‐384 was negatively correlated with the expression of NEAT1. Overexpression of NEAT1 reduced miR‐384 expression, whereas inhibition of miR‐384 led to a distinct upregulation of NEAT1 expression. In addition, we provided evidence that miR‐384 was directly bound to the sequence of NEAT1 by luciferase reporter and RNA‐binding protein immunoprecipitation assays. Overexpression of miR‐384 inhibited NEAT1 function. Thus, we demonstrated that NEAT1 promotes the malignant biological properties of hepatocellular carcinoma by negatively regulating miR‐384.
机译:据报道,肝细胞癌(HCC)涉及长的非编码RNA核富集丰富转录本1(NEAT1)。但是,肿瘤发生的潜在机制仍不清楚。在这里,我们发现NEAT1在HCC组织和细胞系中显着上调。 NEAT1的过表达明显加速了HCC细胞的增殖,迁移和侵袭。击倒NEAT1可以显着抑制HCC细胞的增殖,迁移和侵袭。在肝癌组织和细胞系中,MiR-384表达低于相邻的非肿瘤组织和L02细胞。 MiR-384具有抑制肿瘤的功能。 miR‐384的表达与NEAT1的表达负相关。 NEAT1的过表达降低了miR-384的表达,而miR-384的抑制导致NEAT1的表达明显上调。此外,我们提供的证据表明,通过荧光素酶报道分子和RNA结合蛋白免疫沉淀测定法,miR-384直接与NEAT1序列结合。 miR‐384的过表达抑制了NEAT1的功能。因此,我们证明了NEAT1通过负调控miR-384促进肝细胞癌的恶性生物学特性。

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