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LINC01094下调miR-330-3p并增强MSI1的表达以促进胶质瘤进展。

LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma.

作者信息

Zhu Bin, Liu Wei, Liu Hongliang, Xu Qiang, Xu Wei

机构信息

Department of Neurosurgery, Huashan North Hospital, Baoshan Branch, Fudan University, Shanghai 200431, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Jul 28;12:6511-6521. doi: 10.2147/CMAR.S254630. eCollection 2020.

DOI:10.2147/CMAR.S254630
PMID:32801889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7395698/
Abstract

BACKGROUND

This study aims at probing into the expression, function, and mechanism of LINC01094 and miR-330-3p in glioma.

MATERIALS AND METHODS

qRT-PCR was employed to examine LINC01094 and miR-330-3p expressions in gliomas. After gain-of-function and loss-of-function models were constructed, CCK-8 and Transwell assays were used to detect the proliferation, migration and invasion of LN229 and U251 cells, respectively. Additionally, dual luciferase reporter gene assay was utilized to verify the binding site between m4iR-330-3p and LINC01094, miR-330-3p, and the 3'UTR of musashi RNA binding protein 1 (MSI1). Then, RNA pull-down, RIP, qRT-PCR and Western blot were employed to detect the regulatory relationships among LINC01094, miR-330-3p, and MSI1.

RESULTS

The expression of LINC01094 was elevated in glioma tissues and cell lines, and the high expression of LINC01094 was associated with high grade of glioma. In contrast, miR-330-3p was lowly expressed in glioma tissue. Overexpression of LINC01094 or down-regulation of miR-330-3p promoted the proliferation, migration, and invasion of glioma cells, while LINC01094 knockdown or miR-330-3p up-regulation impeded these processes. miR-330-3p was identified as a target miRNA of LINC01094, and it could be negatively regulated by LINC01094. In addition, miR-330-3p antagonized the function of LINC01094 by negatively regulating MSI1.

CONCLUSION

LINC01094 promotes the proliferation, migration, and invasion of glioma cells by adsorbing miR-330-3p and up-regulating the expression of MSI1.

摘要

背景

本研究旨在探究LINC01094和miR - 330 - 3p在胶质瘤中的表达、功能及机制。

材料与方法

采用qRT - PCR检测胶质瘤中LINC01094和miR - 330 - 3p的表达。构建功能获得和功能缺失模型后，分别用CCK - 8和Transwell实验检测LN229和U251细胞的增殖、迁移和侵袭能力。此外，利用双荧光素酶报告基因实验验证miR - 330 - 3p与LINC01094、miR - 330 - 3p与musashi RNA结合蛋白1（MSI1）的3'UTR之间的结合位点。然后，采用RNA下拉、RIP、qRT - PCR和蛋白质免疫印迹法检测LINC01094、miR - 330 - 3p和MSI1之间的调控关系。

结果

LINC01094在胶质瘤组织和细胞系中表达升高，且LINC01094的高表达与高级别胶质瘤相关。相反，miR - 330 - 3p在胶质瘤组织中低表达。LINC01094的过表达或miR - 330 - 3p的下调促进了胶质瘤细胞的增殖、迁移和侵袭，而LINC01094的敲低或miR - 330 - 3p的上调则抑制了这些过程。miR - 330 - 3p被鉴定为LINC01094的靶标miRNA，且可被LINC01094负调控。此外，miR - 330 - 3p通过负调控MSI1拮抗LINC01094的功能。

结论

LINC01094通过吸附miR - 330 - 3p并上调MSI1的表达促进胶质瘤细胞的增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/0ce9d735946a/CMAR-12-6511-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/8deb139005ad/CMAR-12-6511-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/0cee4f33e8a2/CMAR-12-6511-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/7431ee15b91c/CMAR-12-6511-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/d0e91fe47d25/CMAR-12-6511-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/b63e0e0f9e3f/CMAR-12-6511-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/0ce9d735946a/CMAR-12-6511-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/8deb139005ad/CMAR-12-6511-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/0cee4f33e8a2/CMAR-12-6511-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/7431ee15b91c/CMAR-12-6511-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/d0e91fe47d25/CMAR-12-6511-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/b63e0e0f9e3f/CMAR-12-6511-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a44d/7395698/0ce9d735946a/CMAR-12-6511-g0006.jpg

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