首页> 外文期刊>European review for medical and pharmacological sciences. >Long-chain non-coding RNA LINC01554 promotes NGFR expression and inhibits cell proliferation, migration, and invasion in hepatocellular carcinoma by binding to microRNA-3681-3p
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Long-chain non-coding RNA LINC01554 promotes NGFR expression and inhibits cell proliferation, migration, and invasion in hepatocellular carcinoma by binding to microRNA-3681-3p

机译:长链非编码RNA LINC01554促进NGFR表达,并通过与MicroRNA-3681-3P结合,抑制肝细胞癌中的细胞增殖,迁移和侵袭

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OBJECTIVE: The aim of this study was to analyze the role of LINC01554 in the pathogenesis of hepatocellular carcinoma (HCC) and explore the potential mechanism through which LINC01554 affects the migration and proliferation of HCC cells. PATIENTS AND METHODS: LINC01554 expression in HCC tissues and its link to the prognosis of patients were analyzed by The Cancer Genome Atlas (TCGA) database. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to examine LINC01554 levels in 60 cases of HCC clinical tissues and HCC cell lines. Then, LINC01554 overexpression model was constructed using lentivirus in HCC cell lines. HCC proliferation and invasive ability were evaluated through Cell Counting Kit (CCK-8) and transwell tests, respectively. Furthermore, the potential action mechanism of LINC01554 was explored using bioinformatics analysis and in vitro cell experiments. RESULTS: Analysis of the TCGA database revealed that LINC01554 was remarkably under-expressed in HCC tissues. Decreased expression of LINC01554 predicted a poor prognosis for patients. Besides, LINC01554 overexpression markedly blunted the proliferation and migratory capacities of HCC cells. LINC01554 competed with NGFR to bind to microRNA-3681-3p, thereby providing possible mechanisms by which LINC01554 could participate in the progression of HCC. CONCLUSIONS: This study shows for the first time that LINC01554 modulates NGFR expression by binding to microRNA-3681-3p, thereby participating in the progression of HCC.
机译:目的:本研究的目的是分析LINC01554在肝细胞癌(HCC)的发病机制中的作用,并探索通过该LINC01554影响HCC细胞的迁移和增殖的潜在机制。患者和方法:在肝癌组织和其连结的患者的预后LINC01554表达水平的癌症基因组图谱(TCGA)数据库进行分析。实时定量聚合酶链反应(定量RT-PCR)进行了检查60例临床肝癌组织和肝癌细胞株的LINC01554水平。然后,过表达LINC01554模型在HCC细胞系中使用的慢病毒构建。 HCC细胞增殖和侵袭能力是通过细胞计数试剂盒(CCK-8)和转孔试验分别进行评价。此外,LINC01554的潜在作用机制使用体外细胞实验生物信息学分析和进行了探讨。结果:TCGA数据库的分析表明,LINC01554是明显的肝癌组织中表达不足。 LINC01554的减少的表达预测患者的预后较差。此外,LINC01554表达显着减弱的增殖和肝癌细胞迁移的能力。 LINC01554竞争与NGFR结合于微小RNA-3681-3p,从而提供由LINC01554可以参与HCC的进展可能机制。结论:本研究示出了用于第一次LINC01554通过结合微小RNA-3681-3p,从而参与HCC的进展调制NGFR表达。

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