Department of Neurosurgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Department of Neurosurgery, PLA 904 Hospital, Wuxi, 214000, China.
Biochem Biophys Res Commun. 2019 Mar 19;510(4):614-620. doi: 10.1016/j.bbrc.2019.02.019. Epub 2019 Feb 8.
RNA back splicing produces circRNA, a new type of non-coding RNA. Studies have indicated that circRNAs play important roles in malignant tumors of the central nervous system. Here, we aimed to evaluate the expression of the circRNA, hsa-circ-0014359 (circ-0014359) in human glioma cell lines to assess its function in glioma progression and prognosis. The expression of circ-0014359 was increased in T98G and SHG44 cancer cell lines and glioma tissues from patients, when compared with control cells and tissue. SiRNA-mediated silencing of circ-0014359 potently inhibited cell viability, migration, invasion, and apoptosis of glioma cells. Further, our observations indicated that circ-0014359 acted as a miRNA-153 (miR-153) sponge in glioma cells. Transfection of miR-153 inhibitor significantly suppressed si-circ-0014359-induced inhibition of cell viability, cell migration, and invasion. The increased expression of circ-0014359 levels in glioma cells was correlated with downregulated expression of miR-153. Overexpression of miR-153 reduced p-AKT (a PI3K pathway indicator) and the rescue experiment showed enhanced p-AKT expression. Together, our study suggests that circ-0014359 promotes glioma progression via targeting miR-153/PI3K signaling pathway. Thus, our study provides insights into glioma progression and reveals potential new targets for treatment of glioma.
RNA 反向剪接产生 circRNA，这是一种新型的非编码 RNA。研究表明 circRNA 在中枢神经系统恶性肿瘤中发挥重要作用。在这里，我们旨在评估人神经胶质瘤细胞系中 circRNA hsa-circ-0014359（circ-0014359）的表达，以评估其在神经胶质瘤进展和预后中的功能。与对照细胞和组织相比，circ-0014359 在 T98G 和 SHG44 癌细胞系和患者的胶质瘤组织中表达增加。siRNA 介导的 circ-0014359 沉默强烈抑制神经胶质瘤细胞的活力、迁移、侵袭和凋亡。此外，我们的观察表明 circ-0014359 在神经胶质瘤细胞中作为 miRNA-153（miR-153）海绵起作用。转染 miR-153 抑制剂可显著抑制 si-circ-0014359 诱导的细胞活力、细胞迁移和侵袭抑制。神经胶质瘤细胞中 circ-0014359 水平的增加与 miR-153 表达的下调相关。miR-153 的过表达降低了 p-AKT（PI3K 通路标志物），并且挽救实验显示增强的 p-AKT 表达。总之，我们的研究表明 circ-0014359 通过靶向 miR-153/PI3K 信号通路促进神经胶质瘤的进展。因此，我们的研究提供了对神经胶质瘤进展的深入了解，并揭示了治疗神经胶质瘤的潜在新靶点。
