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长链非编码RNA DDX11-AS1通过调控miR-499b-5p/RWDD4轴在胶质瘤中发挥致癌作用。

LncRNA DDX11-AS1 Exerts Oncogenic Roles in Glioma Through Regulating miR-499b-5p/RWDD4 Axis.

作者信息

Zheng Yanyan, Xie Jing, Xu Xiaomin, Yang Xiaoguo, Zhou Yi, Yao Qiong, Xiong Ye

机构信息

Department of Neurology, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou 325000, People's Republic of China.

Department of Dermatology, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou 325000, People's Republic of China.

出版信息

Onco Targets Ther. 2021 Jan 8;14:157-164. doi: 10.2147/OTT.S278986. eCollection 2021.

DOI:10.2147/OTT.S278986
PMID:33447057
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7802781/
Abstract

BACKGROUND

Long noncoding RNAs (lncRNA) exert essential functions during tumorigenesis. However, how lncRNAs participate in glioma development remains poorly researched. This study aimed to determine how DDX11-AS1 affects glioma progression.

METHODS

Gene expression was analyzed by qRT-PCR. Survival rate curve was plotted in 56 glioma patients. Loss-of-function assays were performed to analyze proliferation, migration, and invasion through CCK8, colony formation, and transwell assays. Luciferase assay and RNA pulldown assays were conducted to illustrate the underlying molecular mechanism.

RESULTS

DDX11-AS1 expression was upregulated in glioma tissues and cells. DDX11-AS1 overexpression was linked with poor prognostic value. DDX11-AS1 knockdown suppressed proliferation, migration, and invasion while inducing apoptosis. DDX11-AS1 interacted with miR-499b-5p to eliminate it, leading to upregulation of RWDD4 expression. RWDD4 was upregulated in glioma while miR-499b-5p was downregulated.

CONCLUSION

DDX11-AS1 upregulation promotes glioma progression through acting as a competing endogenous RNA for miR-499b-5p to upregulate RWDD4.

摘要

背景

长链非编码RNA（lncRNA）在肿瘤发生过程中发挥重要作用。然而，lncRNA如何参与胶质瘤的发展仍研究不足。本研究旨在确定DDX11-AS1如何影响胶质瘤进展。

方法

采用qRT-PCR分析基因表达。绘制56例胶质瘤患者的生存率曲线。通过CCK8、集落形成和transwell实验进行功能缺失实验，以分析增殖、迁移和侵袭情况。进行荧光素酶实验和RNA下拉实验以阐明潜在的分子机制。

结果

DDX11-AS1在胶质瘤组织和细胞中表达上调。DDX11-AS1过表达与不良预后相关。DDX11-AS1敲低抑制增殖、迁移和侵袭，同时诱导凋亡。DDX11-AS1与miR-499b-5p相互作用以消除它，导致RWDD4表达上调。RWDD4在胶质瘤中上调，而miR-499b-5p下调。

结论

DDX11-AS1上调通过作为miR-499b-5p的竞争性内源性RNA上调RWDD4促进胶质瘤进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/ab3695885be9/OTT-14-157-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/ad4a6389ca18/OTT-14-157-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/c4dddaa949d6/OTT-14-157-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/1b8734a7037f/OTT-14-157-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/f6e39c1ac3cf/OTT-14-157-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/ab3695885be9/OTT-14-157-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/ad4a6389ca18/OTT-14-157-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/c4dddaa949d6/OTT-14-157-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/1b8734a7037f/OTT-14-157-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/f6e39c1ac3cf/OTT-14-157-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/140a/7802781/ab3695885be9/OTT-14-157-g0005.jpg

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