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.

中文翻译：

---

LncRNA FEZF1-AS1 加重胶质母细胞瘤的细胞增殖和迁移

目标

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 RNA 1 (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 中的功能尚未大量报道。我们旨在确定 FEZF1-AS1 在 GBM 中的调节机制。

材料与方法

使用 RT-qPCR 首次在 GBM 细胞中发现了 FEZF1-AS1 的表达模式。然后，进行功能测定以检查 FEZF1-AS1 对 GBM 细胞生物学特性的影响。预测了 FEZF1-AS1 的下游靶点，并通过机制分析确定了潜在的调控机制。

结果

FEZF1-AS1 在 GBM 细胞中具有高表达。FEZF1-AS1的下调抑制GBM细胞增殖、迁移和侵袭，同时诱导细胞凋亡。在生物信息学预测和机制分析的帮助下，发现FEZF1-AS1与miR-363-3p结合，NOB1被确定为下游基因。最后，救援试验的结果证实，通过 miR-363-3p 消耗或 NOB1 过表达，FEZF1-AS1 抑制 GBM 发育的抑制功能得以恢复。

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。