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MAFG-AS1 通过吸附 miR-3196 以增强 NFIX 来促进胰腺癌的进展。

MAFG-AS1 aggravates the progression of pancreatic cancer by sponging miR-3196 to boost NFIX.

作者信息

Ye Liqing, Feng Weijian, Weng Hanqin, Yuan Chongde, Liu Jia, Wang Zaiguo

机构信息

Department of Hepato-Billiary Surgery, Dongguan People's Hospital, Southern Medical University, Guangming Road, Dongcheng District, Dongguan, 523059, Guangdong, China.

出版信息

Cancer Cell Int. 2020 Dec 9;20(1):591. doi: 10.1186/s12935-020-01669-y.

DOI:10.1186/s12935-020-01669-y
PMID:33298078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7724861/
Abstract

BACKGROUND

A host of researches have demonstrated the regulation of long non-coding RNAs (lncRNAs) in the progression of pancreatic cancers (PC). In this study, our main task was to analyze the function of MAF bZIP transcription factor G antisense RNA 1 (MAFG-AS1) in PC.

METHODS

RT-qPCR measured gene expression. Functional experiments, including EdU assay, flow cytometry analysis, TUNEL assay and transwell assay, assessed the biological changes of PC cells. RNA pull down assay, luciferase reporter assay and RIP assay verified the interaction between RNAs.

RESULTS

MAFG-AS1 was lowly expressed in normal pancreatic samples but up-regulated in PC tissues and cell lines. Besides, MAFG-AS1 silence suppressed cell proliferation and migration whereas promoted cell apoptosis in PC. Mechanism assays verified that miR-3196 could bind with MAFG-AS1. Moreover, miR-3196 was discovered to be lowly expressed in PC cell lines, and its overexpression inhibited PC cell growth and migration. Importantly, nuclear factor I X (NFIX), overexpressed in PC cell lines, was validated to be positively modulated by MAFG-AS1 through absorbing miR-3196. Moreover, overexpression of NFIX could countervail the restraining effects of MAFG-AS1 knockdown on the growth and migration of PC cells.

CONCLUSION

MAFG-AS1 had an oncogenic function in the progression of PC via regulating miR-3196/NFIX pathway, and decreasing MAFG-AS1 expression could attenuate PC progression.

摘要

背景

大量研究已证实长链非编码RNA（lncRNA）在胰腺癌（PC）进展中的调控作用。在本研究中，我们的主要任务是分析MAF bZIP转录因子G反义RNA 1（MAFG-AS1）在PC中的功能。

方法

RT-qPCR检测基因表达。包括EdU检测、流式细胞术分析、TUNEL检测和Transwell检测在内的功能实验评估了PC细胞的生物学变化。RNA下拉检测、荧光素酶报告基因检测和RIP检测验证了RNA之间的相互作用。

结果

MAFG-AS1在正常胰腺样本中低表达，但在PC组织和细胞系中上调。此外，MAFG-AS1沉默抑制了PC细胞的增殖和迁移，同时促进了细胞凋亡。机制分析证实miR-3196可以与MAFG-AS1结合。此外，发现miR-3196在PC细胞系中低表达，其过表达抑制了PC细胞的生长和迁移。重要的是，在PC细胞系中过表达的核因子I X（NFIX）被证实可通过吸收miR-3来被MAFG-AS1正向调控。此外，NFIX的过表达可以抵消MAFG-AS1敲低对PC细胞生长和迁移的抑制作用。

结论

MAFG-AS1通过调节miR-3196/NFIX通路在PC进展中具有致癌功能，降低MAFG-AS1表达可减弱PC进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/905f533efc03/12935_2020_1669_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/46a70ee2dd9c/12935_2020_1669_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/8f5aeb370885/12935_2020_1669_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/23e1b15defdb/12935_2020_1669_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/7cd6b0417e34/12935_2020_1669_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/905f533efc03/12935_2020_1669_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/46a70ee2dd9c/12935_2020_1669_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/8f5aeb370885/12935_2020_1669_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/23e1b15defdb/12935_2020_1669_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/7cd6b0417e34/12935_2020_1669_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a664/7724861/905f533efc03/12935_2020_1669_Fig5_HTML.jpg

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