LINC00467 通过与 miRNA-485-5p 相互作用促进脑胶质瘤的增殖和侵袭。
LINC00467 promotes proliferation and invasion in glioma via interacting with miRNA-485-5p.
机构信息
Department of Neurosurgery, Sichuan Academy of Medical Sciences, Sichuan Provincial People's Hospital, Chengdu, Sichuan Province, China.
出版信息
Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):766-772. doi: 10.26355/eurrev_202001_20057.
OBJECTIVE
Long non-coding RNA (lncRNA) LINC00467 was found to be upregulated in glioma tissues by analyzing The Cancer Genome Atlas (TCGA) database. This study aims to uncover the biological role of LINC00467 in influencing the progression of glioma and to provide novel directions for clinical treatment of glioma.
PATIENTS AND METHODS
The expression levels of LINC00467 in glioma tissues were analyzed in the downloaded Gene Expression Profiling Interactive Analysis (GEPIA) dataset. Meanwhile, LINC00467 levels in glioma tissues collected in our hospital and glioma cell lines were determined as well. Proliferative, apoptotic, and invasive changes in U87 and U251 cells transfected with si-LINC00457 or si-NC were assessed. The binding between LINC00467 and microRNA-385-5p (miR-385-5p) was predicted through online bioinformatics and verified by the Dual-Luciferase reporter gene assay. The interaction between LINC00467 and miR-385-5p involved in the progression of glioma was finally verified through rescue experiments.
RESULTS
LINC00467 was upregulated in glioma. The knockdown of LINC00467 attenuated proliferative and invasive abilities, and induced apoptosis in U87 and U251 cells. LINC00467 could bind miRNA-485-5p and negatively regulate its level. Moreover, miRNA-485-5p was responsible for the development of glioma influenced by LINC00467.
CONCLUSIONS
LINC00467 aggravates the progression of glioma by negatively regulating miRNA-485-5p, which may be a potential therapeutic target for glioma.
目的
通过分析癌症基因组图谱（TCGA）数据库，发现长链非编码 RNA（lncRNA）LINC00467 在胶质瘤组织中上调。本研究旨在揭示 LINC00467 影响胶质瘤进展的生物学作用，并为胶质瘤的临床治疗提供新的方向。
患者和方法
在下载的基因表达谱交互式分析（GEPIA）数据集分析 LINC00467 在胶质瘤组织中的表达水平。同时，还测定了我院收集的胶质瘤组织和胶质瘤细胞系中的 LINC00467 水平。评估转染 si-LINC00457 或 si-NC 的 U87 和 U251 细胞的增殖、凋亡和侵袭变化。通过在线生物信息学预测 LINC00467 与 microRNA-385-5p（miR-385-5p）之间的结合，并通过双荧光素酶报告基因检测验证。最后通过挽救实验验证 LINC00467 与 miR-385-5p 之间参与胶质瘤进展的相互作用。
结果
LINC00467 在胶质瘤中上调。LINC00467 的敲低减弱了 U87 和 U251 细胞的增殖和侵袭能力，并诱导了细胞凋亡。LINC00467 可以与 miR-385-5p 结合并负调控其水平。此外，miR-385-5p 负责受 LINC00467 影响的胶质瘤的发展。
结论
LINC00467 通过负调控 miR-385-5p 加重胶质瘤的进展，可能是治疗胶质瘤的潜在靶点。
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