Glioma remains the most common malignant tumors in the central nervous system and often has poor prognosis. In recent years, it has been gradually revealed that non-coding RNA effects glioma progression. In this study, we aimed to investigate the significance of circular RNA TLK1 (Circ-TLK1) in predicting the survival of glioma patients as well as its role in glioma development via both in-vitro and in-vivo experiments. We found that Circ-TLK1 was conspicuously up-regulated in glioma tissues compared with adjacent normal tissues, and the up-regulated Circ-TLK1 was significantly correlated with glioma patients’ larger tumor volume and higher grades. Functionally, Circ-TLK1 over-expression facilitated glioma growth, migration and invasion, inhibited cell apoptosis, and accelerated PANX1/MAPK/ERK expression, while Circ-TLK1 low expression had the opposite effects. In addition, bioinformatics analysis showed that miR-17-5p was a potential target of Circ-TLK1 and targeted at PANX1. Furthermore, through dual luciferase viability assay, Circ-TLK1 acted as a competing endogenous RNA by sponging miR-17-5p, which targeted and inhibited PANX1/MAPK/ERK expression. MiR-17-5p overexpression mitigated glioma progression, which was significantly inhibited with Circ-TLK1 upregulation. In conclusion, this study confirmed a novel axis of Circ-TLK1-miR-17-5p-PANX1 in modulating glioma development, providing more references for glioma diagnosis and targeted therapy.

胶质瘤仍然是中枢神经系统中最常见的恶性肿瘤，预后往往很差。近年来，逐渐揭示非编码RNA影响胶质瘤进展。在这项研究中，我们旨在通过体外和体内实验研究环状 RNA TLK1 (Circ-TLK1) 在预测神经胶质瘤患者存活率及其在神经胶质瘤发展中的作用的意义。我们发现与邻近的正常组织相比，Circ-TLK1 在胶质瘤组织中显着上调，并且上调的 Circ-TLK1 与胶质瘤患者更大的肿瘤体积和更高的等级显着相关。在功能上，Circ-TLK1 过表达促进胶质瘤生长、迁移和侵袭，抑制细胞凋亡，加速 PANX1/MAPK/ERK 表达，而 Circ-TLK1 低表达有相反的效果。此外，生物信息学分析表明，miR-17-5p是Circ-TLK1的潜在靶点，靶向PANX1。此外，通过双荧光素酶活力测定，Circ-TLK1 通过海绵化 miR-17-5p 充当竞争性内源性 RNA，靶向并抑制 PANX1/MAPK/ERK 表达。MiR-17-5p 过表达减缓了胶质瘤进展，而 Circ-TLK1 上调显着抑制了这一进展。总之，本研究证实了Circ-TLK1-miR-17-5p-PANX1在调节胶质瘤发展中的新轴，为胶质瘤的诊断和靶向治疗提供更多参考。Circ-TLK1 通过海绵化 miR-17-5p 充当竞争性内源性 RNA，靶向并抑制 PANX1/MAPK/ERK 表达。MiR-17-5p 过表达减缓了胶质瘤进展，而 Circ-TLK1 上调显着抑制了这一进展。综上所述，本研究证实了Circ-TLK1-miR-17-5p-PANX1在调节胶质瘤发展中的新轴，为胶质瘤的诊断和靶向治疗提供更多参考。Circ-TLK1 通过海绵化 miR-17-5p 充当竞争性内源性 RNA，靶向并抑制 PANX1/MAPK/ERK 表达。MiR-17-5p 过表达减缓了胶质瘤进展，而 Circ-TLK1 上调显着抑制了这一进展。综上所述，本研究证实了Circ-TLK1-miR-17-5p-PANX1在调节胶质瘤发展中的新轴，为胶质瘤的诊断和靶向治疗提供更多参考。