Department of Neurosurgery, The First Affiliated Hospital of Hebei North, Hebei, Zhangjiakou 075000, PR China.
Department of Neurosurgery, The First Affiliated Hospital of Hebei North, Hebei, Zhangjiakou 075000, PR China.
Life Sci. 2020 Mar 15;245:117363. doi: 10.1016/j.lfs.2020.117363. Epub 2020 Jan 27.
CircRNAs are emerging as a novel class of non-coding RNAs that play crucial roles in malignant cancer. However, the expression profile and potential mechanism of circRNAs in gliomas remain uncharacterized. In this study, we aim to investigate abnormally expressed circRNAs during glioma pathogenesis and find out potential therapeutic targets for treatment.
The glioma cell lines (U251 and SHG-44), 32 pairs of glioma tissue samples and adjacent control samples were used in this study. Microarray and bioinformatics tools were performed to identify circRNAs expression in glioma. QRT-PCR experiment was used to confirm gene expression. CCK-8 and transwell assay were conducted to measure cell viability and invasion. Dual-luciferase reporter experiment was performed to identify target bindings between RNAs.
The circRNA circ_0037655 was highly expressed in both glioma tissues and cell lines (U251 and SHG-44) compared to control. Inhibition of circ_0037655 could suppress the viability and invasion of glioma cells. Circ_0037655 acts as a sponge of miR-214 and inhibition of miR-214 could reverse cell viability and invasion ability induced by si-circ_0037655. Over-expression of miR-214 could reduce the expression of p-Akt (PI3K pathway indicator).
This study identified circRNAs expression profile in gliomas and revealed that circ_0037655 could promote glioma progression by regulating miR-214/PI3K signaling, which may provide new therapeutic approach for gliomas.
CircRNAs 作为一类新的非编码 RNA,在恶性肿瘤中发挥着关键作用。然而,circRNAs 在神经胶质瘤中的表达谱和潜在机制仍不清楚。本研究旨在探讨神经胶质瘤发病过程中异常表达的 circRNAs,并寻找潜在的治疗靶点。
本研究使用了神经胶质瘤细胞系(U251 和 SHG-44)、32 对神经胶质瘤组织样本和相邻对照样本。使用微阵列和生物信息学工具来鉴定神经胶质瘤中 circRNAs 的表达。实时定量 PCR 实验用于验证基因表达。CCK-8 和 Transwell 实验用于测量细胞活力和侵袭。双荧光素酶报告实验用于鉴定 RNA 之间的靶结合。
与对照相比,circ_0037655 在神经胶质瘤组织和细胞系(U251 和 SHG-44)中均高度表达。抑制 circ_0037655 可抑制神经胶质瘤细胞的活力和侵袭。circ_0037655 作为 miR-214 的海绵,抑制 miR-214 可逆转 si-circ_0037655 诱导的细胞活力和侵袭能力。miR-214 的过表达可降低 p-Akt(PI3K 通路标志物)的表达。
本研究鉴定了神经胶质瘤中 circRNAs 的表达谱,并揭示 circ_0037655 可能通过调节 miR-214/PI3K 信号通路促进神经胶质瘤的进展,这可能为神经胶质瘤提供新的治疗方法。