基因敲除
胶质瘤
长非编码RNA
细胞生长
癌症研究
转染
竞争性内源性RNA
干细胞
小RNA
生物
细胞
核糖核酸
细胞生物学
分子生物学
细胞培养
基因
遗传学
作者
Chao‐Jie Wang,Chu‐Rui Chao,Wei‐Feng Zhao,Huimin Liu,Jiang‐Shan Feng,Yongxia Cui
摘要
Abstract Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment.
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