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长链非编码 RNA-MEG3 通过调控 miR-6088/SMARCB1 轴抑制胶质瘤细胞中的肿瘤抑制功能。

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis.

机构信息

Department of Neurosurgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan 410005, China.

出版信息

Biomed Res Int. 2020 Jan 11;2020:4309161. doi: 10.1155/2020/4309161. eCollection 2020.

DOI:10.1155/2020/4309161
PMID:32420340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7201742/
Abstract

OBJECTIVE

Mounting evidence has elaborated the implication of long noncoding RNAs (lncRNAs) in tumorigenesis of several cancers, including glioma. However, little was known about the mechanism of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of glioma. This work is designed to explore the effect of MEG3 on glioma progression and its possible mechanism.

METHODS

Expressions of lncRNA-MEG3 and SMARCB1 were detected in human glioblastoma U87 and U251 cell lines. Gain and loss of function of MEG3 or/and miR-6088 was performed in U87 and U251 cells to observe its effect on cell proliferation and migration as well as on epithelial-mesenchymal transition (EMT) related markers. Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1.

RESULTS

MEG3 and SMARCB1 expressions were downregulated in glioma cells. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088. Transfection of miR-6088 mimic or si-SMARCB1 could obviously reverse the favorable effect of pcDNA3.1-MEG3 on glioma progression.

CONCLUSION

Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis.

摘要

目的

越来越多的证据阐述了长链非编码 RNA（lncRNA）在几种癌症包括神经胶质瘤的发生中的作用。然而，lncRNA 母系表达基因 3（MEG3）在神经胶质瘤发生和发展中的作用机制知之甚少。本研究旨在探讨 MEG3 对神经胶质瘤进展的影响及其可能的机制。

方法

检测人神经胶质瘤 U87 和 U251 细胞系中 lncRNA-MEG3 和 SMARCB1 的表达。在 U87 和 U251 细胞中进行 MEG3 或/和 miR-6088 的功能获得和功能丧失实验，观察其对细胞增殖和迁移以及上皮-间充质转化（EMT）相关标志物的影响。采用荧光素酶报告基因检测方法检测 MEG3、miR-6088 和 SMARCB1 之间的相互作用。

结果

在神经胶质瘤细胞中，MEG3 和 SMARCB1 的表达下调。pcDNA3.1-MEG3 或 pcDNA3.1-SMARCB1 质粒的转染可明显阻断细胞增殖、迁移和 EMT 进展。MEG3 作为 miR-6088 的海绵，而 SMARCB1 是 miR-6088 的下游蛋白。miR-6088 模拟物或 si-SMARCB1 的转染可明显逆转 pcDNA3.1-MEG3 对神经胶质瘤进展的有利影响。

结论

综上所述，本研究结果表明，MEG3 在神经胶质瘤细胞中下调，并通过调节 miR-6088/SMARCB1 轴抑制神经胶质瘤细胞的增殖和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/d60027bf5ba8/BMRI2020-4309161.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/dd6ba8e5cb32/BMRI2020-4309161.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/ebfb9343237c/BMRI2020-4309161.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/eae4adb34a4b/BMRI2020-4309161.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/05d49323c979/BMRI2020-4309161.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/d60027bf5ba8/BMRI2020-4309161.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/dd6ba8e5cb32/BMRI2020-4309161.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/ebfb9343237c/BMRI2020-4309161.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/eae4adb34a4b/BMRI2020-4309161.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/05d49323c979/BMRI2020-4309161.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da0/7201742/d60027bf5ba8/BMRI2020-4309161.005.jpg

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