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Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma.
Bioscience Reports ( IF 4 ) Pub Date : 2020-09-07 , DOI: 10.1042/bsr20191571
Li-Li Zhou 1 , Meng Zhang 2 , Yan-Zhen Zhang 1 , Mei-Fen Sun 1
Affiliation  

Glioma is the most prevalent solid tumor in the central nervous system. Recently, it has been indicated that lncRNAs substantially adjust the development of a variety of human cancers. In this study, it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines. Then CCK-8, EdU staining, plate clone assay, Transwell assay, Western blotting and nude mouse model were adopted to verify PSMA3-AS1's effects on glioma. Knockdown of PSMA3-AS1 inhibited the migration, proliferation and invasion of glioma cells in vivo and in vitro. Besides, PSMA3-AS1 bound to miR-302a-3p directly and reduced the expression of miR-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis. PSMA3-AS1 knockdown remarkably enhanced the role of miR-302a-3p overexpression in cell behaviors in glioma. Moreover, these assays also confirmed that RAB22A was a target of miR-302a-3p. In this research, therefore, the PSMA3-AS1/miR-302a-3p/RAB22A pathway regulatory axis may be revealed in the pathogenesis of glioma, and PSMA3-AS1 can be used as an underlying target for the treatment and prognosis of glioma.

中文翻译:

长链非编码 RNA PSMA3-AS1 通过调节胶质瘤中的 miR-302a-3p/RAB22A 增强细胞增殖、迁移和侵袭。

神经胶质瘤是中枢神经系统中最普遍的实体瘤。最近,已表明 lncRNA 可显着调节多种人类癌症的发展。在本研究中,通过微阵列分析发现并验证了 lncRNA PSMA3-AS1 在神经胶质瘤组织和细胞系中表现出高表达。然后采用CCK-8、EdU染色、平板克隆试验、Transwell试验、Western blotting和裸鼠模型验证PSMA3-AS1对胶质瘤的作用。PSMA3-AS1 的敲低抑制胶质瘤细胞在体内和体外的迁移、增殖和侵袭。此外,PSMA3-AS1 直接与 miR-302a-3p 结合并降低 miR-302a-3p 的表达,从而通过荧光素酶报告基因测定和生物信息学分析证实其作为内源性海绵发挥作用。PSMA3-AS1 敲低显着增强了 miR-302a-3p 过表达在神经胶质瘤细胞行为中的作用。此外,这些测定还证实 RAB22A 是 miR-302a-3p 的靶标。因此,本研究有望揭示PSMA3-AS1/miR-302a-3p/RAB22A通路调控轴在胶质瘤发病机制中的作用,PSMA3-AS1可作为胶质瘤治疗和预后的潜在靶点。
更新日期:2020-09-09
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