长非编码 RNA DLGAP1 反义 RNA 1 通过 microRNA-628-5p/DEAD -box 解旋酶 59 通路促进神经胶质瘤进展。
Long non-coding RNA DLGAP1 antisense RNA 1 accelerates glioma progression via the microRNA-628-5p/DEAD-box helicase 59 pathway.
机构信息
Department of Neurosurgery, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, China.
Department of Neurosurgery, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, China.
出版信息
Clinics (Sao Paulo). 2022 Jan 31;77:100002. doi: 10.1016/j.clinsp.2021.100002. eCollection 2022.
OBJECTIVES
Abnormal expression of long non-coding RNAs (lncRNAs) plays a prominent role in glioma progression. However, the biological function and mechanism of lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) in gliomas are still unknown.
METHODS
The authors assessed DLGAP1-AS1 and miR-628-5p expression in glioma tissues and cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and evaluated their effects on glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) using the cell counting kit-8 (CCK-8) assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay, Transwell assay, and western blot, respectively. The expression of DEAD-box helicase 59 (DDX59) was quantified using western blotting, and a dual-luciferase reporter gene assay was performed to detect the interaction between DLGAP1-AS1 and miR-628-5p.
RESULTS
The authors observed increased DLGAP1-AS1 expression in glioma tissues and cell lines with higher WHO grades and shorter survival time. DLGAP1-AS1 promoted the proliferation, migration, invasion, and EMT of glioma cells, while miR-628-5p counteracted these effects. The authors identified DLGAP1-AS1 as a molecular sponge of miR-628-5p in glioma cells as the biological functions of DLGAP1-AS1 are partially mediated via miR-628-5p. In addition, DLGAP1-AS1 upregulated DDX59 expression by inhibiting miR-628-5p expression.
CONCLUSION
The DLGAP1-AS1/miR-628-5p/DDX59 axis regulates glioma progression.
目的
长链非编码 RNA（lncRNA）的异常表达在神经胶质瘤的进展中起着重要作用。然而，lncRNA DLGAP1 反义 RNA 1（DLGAP1-AS1）在神经胶质瘤中的生物学功能和机制尚不清楚。
方法
作者使用实时定量聚合酶链反应（qRT-PCR）评估了神经胶质瘤组织和细胞系中 DLGAP1-AS1 和 miR-628-5p 的表达，并使用细胞计数试剂盒-8（CCK-8）检测、5-乙炔基-2'-脱氧尿苷（EdU）检测、Transwell 检测和 Western blot 分别评估它们对神经胶质瘤细胞增殖、迁移、侵袭和上皮-间充质转化（EMT）的影响。使用 Western blot 定量检测 DEAD 框解旋酶 59（DDX59）的表达，并进行双荧光素酶报告基因检测以检测 DLGAP1-AS1 与 miR-628-5p 之间的相互作用。
结果
作者观察到，随着 WHO 分级的升高和生存时间的缩短，神经胶质瘤组织和细胞系中 DLGAP1-AS1 的表达增加。DLGAP1-AS1 促进神经胶质瘤细胞的增殖、迁移、侵袭和 EMT，而 miR-628-5p 则拮抗这些作用。作者发现 DLGAP1-AS1 是神经胶质瘤细胞中 miR-628-5p 的分子海绵，因为 DLGAP1-AS1 的部分生物学功能是通过 miR-628-5p 介导的。此外，DLGAP1-AS1 通过抑制 miR-628-5p 的表达而上调 DDX59 的表达。
结论
DLGAP1-AS1/miR-628-5p/DDX59 轴调节神经胶质瘤的进展。
Zotero 插件