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长链非编码RNA OIP5-AS1通过抑制miR-143-3p促进胆囊癌细胞的侵袭和迁移。

Long Non-Coding RNA OIP5-AS1 Contributes to Gallbladder Cancer Cell Invasion and Migration by miR-143-3p Suppression.

作者信息

Li Jing, Zhang Hui, Luo Hongwu

机构信息

Department of Hepatopancreatobiliary Surgery, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Dec 17;12:12983-12992. doi: 10.2147/CMAR.S278719. eCollection 2020.

DOI:10.2147/CMAR.S278719
PMID:33364844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7751711/
Abstract

OBJECTIVE

This study was designed to investigate the effect of long non-coding RNA (lncRNA) OIP5-AS1 on cell migration and invasion of gallbladder cancer (GBC) and its specific mechanism.

METHODS

The expressions of lncRNA OIP5-AS1 and in GBC cell lines (GBC-SD, SGC996 and NOZ) and gallbladder epithelial cells (HGBE cells) were measured by qRT-PCR. After loss- and gain-of-function experiments for OIP5-AS1 and in GBC-SD cells, CCK-8 was applied to examine cell viability, cell scratch assay to measure cell migration, and transwell chamber to inspect cell invasion capacity. The interaction between OIP5-AS1 and was predicted by StarBase. Then, luciferase reporter gene assay and RNA pull-down were used to verify the targeting relationship between and OIP5-AS1.

RESULTS

OIP5-AS1 was highly expressed and was downregulated in GBC cell lines, when compared with HGBE cells. Overexpression of OIP5-AS1 or downregulation of facilitated GBC-SD cell invasion, proliferation and migration, while different expression patterns were found in GBC-SD cells in response to OIP5-AS1 suppression or overexpression. OIP5-AS1 negatively mediated . upregulation partially reversed the inhibitory effect of OIP5-AS1 knockdown on GBC-SD cell activities.

CONCLUSION

LncRNA OIP5-AS1 accelerates the progression of GBC by suppressing miR-143-3p.

摘要

目的

本研究旨在探讨长链非编码RNA（lncRNA）OIP5-AS1对胆囊癌（GBC）细胞迁移和侵袭的影响及其具体机制。

方法

采用qRT-PCR检测lncRNA OIP5-AS1和[此处原文缺失某个基因名称]在GBC细胞系（GBC-SD、SGC996和NOZ）及胆囊上皮细胞（HGBE细胞）中的表达。在GBC-SD细胞中对OIP5-AS1和[此处原文缺失某个基因名称]进行功能缺失和功能获得实验后，应用CCK-8检测细胞活力，采用细胞划痕实验检测细胞迁移，利用Transwell小室检测细胞侵袭能力。通过StarBase预测OIP5-AS1与[此处原文缺失某个基因名称]之间的相互作用。然后运用荧光素酶报告基因实验和RNA下拉实验验证[此处原文缺失某个基因名称]与OIP5-AS1之间的靶向关系。

结果

与HGBE细胞相比，lncRNA OIP5-AS1在GBC细胞系中高表达，而[此处原文缺失某个基因名称]表达下调。OIP5-AS1的过表达或[此处原文缺失某个基因名称]的下调促进了GBC-SD细胞的侵袭、增殖和迁移，而在GBC-SD细胞中，针对OIP5-AS1抑制或[此处原文缺失某个基因名称]过表达则出现了不同的表达模式。OIP5-AS1负向介导[此处原文缺失某个基因名称]。[此处原文缺失某个基因名称]的上调部分逆转了OIP5-AS1敲低对GBC-SD细胞活性的抑制作用。

结论

lncRNA OIP5-AS1通过抑制miR-143-3p促进GBC进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/7a726105c97a/CMAR-12-12983-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/67568a514925/CMAR-12-12983-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/7bb083851712/CMAR-12-12983-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/a68b0e414767/CMAR-12-12983-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/0e8c145954ed/CMAR-12-12983-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/7a726105c97a/CMAR-12-12983-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/67568a514925/CMAR-12-12983-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/7bb083851712/CMAR-12-12983-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/a68b0e414767/CMAR-12-12983-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/0e8c145954ed/CMAR-12-12983-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec8c/7751711/7a726105c97a/CMAR-12-12983-g0005.jpg

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