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长链非编码 RNA LINC01554 通过与 microRNA-3681-3p 结合促进神经生长因子受体表达并抑制肝癌细胞增殖、迁移和侵袭。

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.

机构信息

Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Nantong University; the First People's Hospital of Nantong City, Nantong, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12667-12674. doi: 10.26355/eurrev_202012_24164.

DOI:10.26355/eurrev_202012_24164
PMID:33378013
Abstract

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.

摘要

目的

本研究旨在分析 LINC01554 在肝细胞癌(HCC)发病机制中的作用,并通过研究 LINC01554 影响 HCC 细胞迁移和增殖的潜在机制来探讨其作用机制。

患者和方法

通过癌症基因组图谱(TCGA)数据库分析 HCC 组织中 LINC01554 的表达及其与患者预后的关系。采用实时定量聚合酶链反应(qRT-PCR)检测 60 例 HCC 临床组织和 HCC 细胞系中 LINC01554 的水平。然后,通过慢病毒构建 HCC 细胞系中的 LINC01554 过表达模型。通过细胞计数试剂盒(CCK-8)和 Transwell 实验分别评估 HCC 增殖和侵袭能力。此外,通过生物信息学分析和体外细胞实验探讨 LINC01554 的潜在作用机制。

结果

TCGA 数据库分析显示,LINC01554 在 HCC 组织中明显低表达。LINC01554 表达下调预示着患者预后不良。此外,LINC01554 过表达显著抑制 HCC 细胞的增殖和迁移能力。LINC01554 与 NGFR 竞争结合 microRNA-3681-3p,从而为 LINC01554 参与 HCC 进展提供了可能的机制。

结论

本研究首次表明,LINC01554 通过与 microRNA-3681-3p 结合来调节 NGFR 的表达,从而参与 HCC 的进展。

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