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长链非编码RNA VPS9D1-AS1通过靶向miRNA-30a-5p/KIF11轴促进肺腺癌的恶性进展。

LncRNA VPS9D1-AS1 Promotes Malignant Progression of Lung Adenocarcinoma by Targeting miRNA-30a-5p/KIF11 Axis.

作者信息

Liu Jiefeng, Feng Yuhua, Zeng Xinyu, He Miao, Gong Yujing, Liu Yiping

机构信息

Department of General Surgery, Changsha Hospital Affiliated to Hunan Normal University/the Fourth Hospital of Changsha, Changsha, China.

Department of Oncology, the Second Xiangya Hospital Central South University, Changsha, China.

出版信息

Front Genet. 2022 Jan 24;12:807628. doi: 10.3389/fgene.2021.807628. eCollection 2021.

DOI:10.3389/fgene.2021.807628
PMID:35140744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8819668/
Abstract

This research probed into the molecular mechanisms of long non-coding RNA (lncRNA) VPS9D1 Antisense RNA 1 (VPS9D1-AS1) in lung adenocarcinoma (LUAD). lncRNA expression level was evaluated bioinformatically, and its downstream miRNA/mRNA regulatory axis was predicted by bioinformatics methods as well. qRT-PCR was used to measure VPS9D1-AS1, miRNA-30a-5p, and kinesin family member 11 (KIF11) expression. Western blot was performed to measure KIF11 protein expression. Proliferation, migration, and invasion of LUAD cells were all observed by cell biological function experiments. Dual-luciferase assay detected binding between miRNA-30a-5p and VPS9D1-AS1 or KIF11, respectively. RIP experiment detected interaction between VPS9D1-AS1 and miRNA-30a-5p. VPS9D1-AS1 and KIF11 were increased in LUAD, whereas miRNA-30a-5p was decreased. VPS9D1-AS1 promoted the malignant progression of LUAD cells and could sponge miRNA-30a-5p. MiRNA-30a-5p could restore the impact of VPS9D1-AS1 on LUAD cells. KIF11 was a target downstream of miRNA-30a-5p. VPS9D1-AS1 could upregulate KIF11 expression through competitively sponging miRNA-30a-5p, and KIF11 could restore the impact of miRNA-30a-5p on LUAD cells. VPS9D1-AS1 could foster malignant progression of LUAD regulating miRNA-30a-5p/KIF11 axis, suggesting that VPS9D1-AS1 is key to regulating the malignant progression of LUAD.

摘要

本研究探讨了长链非编码RNA（lncRNA）VPS9D1反义RNA 1（VPS9D1-AS1）在肺腺癌（LUAD）中的分子机制。通过生物信息学方法评估lncRNA表达水平，并预测其下游miRNA/mRNA调控轴。采用qRT-PCR检测VPS9D1-AS1、miRNA-30a-5p和驱动蛋白家族成员11（KIF11）的表达。进行蛋白质免疫印迹法检测KIF11蛋白表达。通过细胞生物学功能实验观察LUAD细胞的增殖、迁移和侵袭情况。双荧光素酶报告基因检测分别检测miRNA-30a-5p与VPS9D1-AS1或KIF11之间的结合。RNA免疫沉淀实验检测VPS9D1-AS1与miRNA-30a-5p之间的相互作用。VPS9D1-AS1和KIF11在LUAD中表达升高，而miRNA-30a-5p表达降低。VPS9D1-AS1促进LUAD细胞的恶性进展，并可吸附miRNA-30a-5p。miRNA-30a-5p可恢复VPS9D1-AS1对LUAD细胞的影响。KIF11是miRNA-30a-5p的下游靶点。VPS9D1-AS1可通过竞争性吸附miRNA-30a-5p上调KIF11表达，且KIF11可恢复miRNA-30a-5p对LUAD细胞的影响。VPS9D1-AS1可通过调控miRNA-30a-5p/KIF11轴促进LUAD的恶性进展，提示VPS9D1-AS1是调控LUAD恶性进展的关键因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/8aac6f165f59/fgene-12-807628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/86277bfa78a9/fgene-12-807628-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/43d6170f292b/fgene-12-807628-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/6386f8d73d21/fgene-12-807628-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/da4c81ab8d6b/fgene-12-807628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/ea01d77a06e1/fgene-12-807628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/8aac6f165f59/fgene-12-807628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/86277bfa78a9/fgene-12-807628-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/43d6170f292b/fgene-12-807628-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/6386f8d73d21/fgene-12-807628-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/da4c81ab8d6b/fgene-12-807628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/ea01d77a06e1/fgene-12-807628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1a/8819668/8aac6f165f59/fgene-12-807628-g006.jpg

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