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长链非编码 RNA SNHG20 通过海绵吸附 miR-342 和上调 DDX49 促进肺腺癌的增殖、侵袭,抑制细胞凋亡。

LncRNA SNHG20 promoted proliferation, invasion and inhibited cell apoptosis of lung adenocarcinoma via sponging miR-342 and upregulating DDX49.

机构信息

Pulmonary Medicine Department, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.

出版信息

Thorac Cancer. 2020 Dec;11(12):3510-3520. doi: 10.1111/1759-7714.13693. Epub 2020 Oct 22.

Abstract

BACKGROUND

There is increasing evidence that long non-coding RNA (lncRNA) small nucleolar RNA host gene 20 (SNHG20) plays an important role in cancer. However, the function of SNHG20 in lung adenocarcinoma is unclear. The aim of our study was to investigate the roles of SNHG20 in lung adenocarcinoma.

METHODS

Real-time quantitative polymerasechain reaction (RT-qPCR) was used to calculate the expression of SNHG20, miR-342 and DEAD-box helicase 49 (DDX49). Dual luciferase reporter gene assay was applied to verify whether miR-342 binding to SNHG20 and DDX49. The expression correlation between miR-342 and SNHG20 or DDX49 was assessed using Pearson's correlation analysis.

RESULTS

SNHG20 and DDX49 were overexpressed, while miR-342 was lowly expressed in lung adenocarcinoma tissues and cell lines. Knockdown of SNHG20 suppressed cell proliferation, invasion and enhanced cell apoptosis. SNHG20 was found to directly bind to miR-342 and regulate the expression of miR-342. MiR-342 directly targeted DDX49 and the expression of miR-342 had negative connection with DDX49 in lung adenocarcinoma tissues. Knockdown of DDX49 inhibited the progression of lung adenocarcinoma. DDX49 partially restored the functions of SNHG20 in A549 cells.

CONCLUSIONS

SNHG20 regulated lung adenocarcinoma cell proliferation, invasion and promoted cell apoptosis via miR-342/DDX49 axis. Our findings demonstrate that SNHG20/miR-342/DDX49 axis plays an important role in lung adenocarcinoma, providing a novel insight into the treatment of lung adenocarcinoma.

摘要

背景

越来越多的证据表明,长链非编码 RNA(lncRNA)小核仁 RNA 宿主基因 20(SNHG20)在癌症中发挥重要作用。然而,SNHG20 在肺腺癌中的功能尚不清楚。本研究旨在探讨 SNHG20 在肺腺癌中的作用。

方法

实时定量聚合酶链反应(RT-qPCR)用于计算 SNHG20、miR-342 和 DEAD 框解旋酶 49(DDX49)的表达。双荧光素酶报告基因检测用于验证 miR-342 是否与 SNHG20 和 DDX49 结合。采用 Pearson 相关分析评估 miR-342 与 SNHG20 或 DDX49 的表达相关性。

结果

SNHG20 和 DDX49 在肺腺癌组织和细胞系中表达上调,而 miR-342 表达下调。敲低 SNHG20 抑制细胞增殖、侵袭,增强细胞凋亡。发现 SNHG20 可直接与 miR-342 结合,调节 miR-342 的表达。miR-342 直接靶向 DDX49,miR-342 在肺腺癌组织中的表达与 DDX49 呈负相关。敲低 DDX49 抑制肺腺癌的进展。DDX49 部分恢复 SNHG20 在 A549 细胞中的功能。

结论

SNHG20 通过 miR-342/DDX49 轴调控肺腺癌细胞增殖、侵袭,促进细胞凋亡。我们的研究结果表明,SNHG20/miR-342/DDX49 轴在肺腺癌中发挥重要作用,为肺腺癌的治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc9c/7705913/c8aa44d96f13/TCA-11-3510-g001.jpg

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