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长链非编码RNA FEZF1-AS1加剧胶质母细胞瘤中的细胞增殖和迁移。

LncRNA FEZF1-AS1 aggravates cell proliferation and migration in glioblastoma.

作者信息

Zhou Chaoyang, Jiang Xingxing, Liang Aijun, Zhu Ronglan, Yang Yu, Zhong Liangchen, Wan Dengfeng

机构信息

Department of Neurosurgery, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang 330038, Jiangxi, China.

Department of Neurosurgery, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang 330038, Jiangxi, China.

出版信息

Neurosci Lett. 2021 Nov 1;764:136245. doi: 10.1016/j.neulet.2021.136245. Epub 2021 Sep 14.

Abstract

OBJECTIVES

Glioblastoma (GBM) represents the commonest malignant glioma. Long non-coding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) has been validated to play an oncogenic role in multiple human malignancies, while its function in GBM has not been largely reported. We aim to identify the regulatory mechanism of FEZF1-AS1 in GBM.

MATERIALS & METHODS: The expression pattern of FEZF1-AS1 was firstly figured out in GBM cells using RT-qPCR. Then, functional assays were conducted to examine the influence FEZF1-AS1 had on the biological properties of GBM cells. The downstream targets of FEZF1-AS1 were predicted and the underlying regulatory mechanism was determined by mechanism assays.

RESULTS

FEZF1-AS1 possessed high expression in GBM cells. Down-regulation of FEZF1-AS1 suppressed GBM cell proliferation, migration and invasion while inducing cell apoptosis. With the help of bioinformatics prediction and mechanism assays, FEZF1-AS1 was found to bind to miR-363-3p and NOB1 was determined to be the downstream gene. Finally, results of rescue assays verified that the suppressive function of FEZF1-AS1 inhibition on GBM development were restored by miR-363-3p depletion or overexpression of NOB1.

CONCLUSION

FEZF1-AS1 had oncogenic function in the advancement of GBM by targeting miR-363-3p/NOB1, which made FEZF1-AS1 a potential biomarker for GBM treatment.

摘要

目的

胶质母细胞瘤(GBM)是最常见的恶性胶质瘤。长链非编码RNA(lncRNA)FEZ家族锌指1反义RNA1(FEZF1-AS1)已被证实在多种人类恶性肿瘤中发挥致癌作用,而其在GBM中的功能尚未见大量报道。我们旨在确定FEZF1-AS1在GBM中的调控机制。

材料与方法

首先用RT-qPCR检测GBM细胞中FEZF1-AS1的表达模式。然后,进行功能试验以检测FEZF1-AS1对GBM细胞生物学特性的影响。预测FEZF1-AS1的下游靶点,并通过机制试验确定潜在的调控机制。

结果

FEZF1-AS1在GBM细胞中高表达。下调FEZF1-AS1可抑制GBM细胞增殖、迁移和侵袭,同时诱导细胞凋亡。借助生物信息学预测和机制试验,发现FEZF1-AS1与miR-363-3p结合,且确定NOB1为下游基因。最后,挽救试验结果证实,通过miR-363-3p缺失或NOB1过表达可恢复FEZF1-AS1抑制对GBM发展的抑制作用。

结论

FEZF1-AS1通过靶向miR-363-3p/NOB1在GBM进展中具有致癌功能,这使得FEZF1-AS1成为GBM治疗的潜在生物标志物。

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