Long noncoding RNAs (lncRNAs) play crucial roles in tumor progression and are dysregulated in glioma. However, the functional roles of lncRNAs in glioma remain largely unknown. In this study, we utilized the TCGA (the Cancer Genome Atlas database) and GEPIA2 (Gene Expression Profiling Interactive Analysis 2) databases and observed the overexpression of lncRNA CHASERR in glioma tissues. We subsequently investigated this phenomenon in glioma cell lines. The effects of lncRNA CHASERR on glioma proliferation, migration, and invasion were analyzed using in vitro and in vivo experiments. Additionally, the regulatory mechanisms among PTEN/p-Akt/mTOR and Wnt/β-catenin, lncRNA CHASERR, Micro-RNA-6893-3p(miR-6893-3p), and tripartite motif containing14 (TRIM14) were investigated via bioinformatics analyses, quantitative real-time PCR (qRT-PCR), western blot (WB), RNA immunoprecipitation (RIP), dual luciferase reporter assay, fluorescence in situ hybridization (FISH), and RNA sequencing assays. RIP and RT-qRCR were used to analyze the regulatory effect of N⁶-methyladenosine(m⁶A) on the aberrantly expressed lncRNA CHASERR. High lncRNA CHASERR expression was observed in glioma tissues and was associated with unfavorable prognosis in glioma patients. Further functional assays showed that lncRNA CHASERR regulates glioma growth and metastasis in vitro and in vivo. Mechanistically, lncRNA CHASERR sponged miR-6893-3p to upregulate TRIM14 expression, thereby facilitating glioma progression. Additionally, the activation of PTEN/p-Akt/mTOR and Wnt/β-catenin pathways by lncRNA CHASERR, miR-6893-3p, and TRIM14 was found to regulate glioma progression. Moreover, the upregulation of lncRNA CHASERR was observed in response to N6-methyladenosine modification, which was facilitated by METTL3/YTHDF1-mediated RNA transcripts. This study elucidates the m6A/lncRNACHASERR/miR-6893-3p/TRIM14 pathway that contributes to glioma progression and underscores the potential of lncRNA CHASERR as a novel prognostic indicator and therapeutic target for glioma.

长非编码 RNA (lncRNA) 在肿瘤进展中发挥着至关重要的作用，并且在神经胶质瘤中失调。然而，lncRNA 在神经胶质瘤中的功能作用仍然很大程度上未知。在本研究中，我们利用TCGA（癌症基因组图谱数据库）和GEPIA2（基因表达谱交互分析2）数据库，观察了胶质瘤组织中lncRNA CHASERR的过度表达。我们随后在神经胶质瘤细胞系中研究了这种现象。使用体外和体内实验分析lncRNA CHASERR对神经胶质瘤增殖、迁移和侵袭的影响。此外，通过生物信息学分析研究了PTEN/p-Akt/mTOR和Wnt/β-catenin、lncRNA CHASERR、Micro-RNA-6893-3p(miR-6893-3p)和含有14的三联基序(TRIM14)之间的调控机制。 、定量实时 PCR (qRT-PCR)、蛋白质印迹 (WB)、RNA 免疫沉淀 (RIP)、双荧光素酶报告基因测定、荧光原位杂交 (FISH) 和 RNA 测序测定。采用RIP和RT-qRCR分析N ⁶ -甲基腺苷(m ⁶ A)对异常表达的lncRNA CHASERR的调控作用。在神经胶质瘤组织中观察到高 lncRNA CHASERR 表达，并且与神经胶质瘤患者的不良预后相关。进一步的功能测定表明，lncRNA CHASERR 在体外和体内调节神经胶质瘤的生长和转移。从机制上讲，lncRNA CHASERR 海绵 miR-6893-3p 上调 TRIM14 表达，从而促进神经胶质瘤进展。此外，lncRNA CHASERR、miR-6893-3p 和 TRIM14 激活 PTEN/p-Akt/mTOR 和 Wnt/β-catenin 通路可调节神经胶质瘤进展。 此外，观察到 lncRNA CHASERR 上调是对 N6-甲基腺苷修饰的反应，这是由 METTL3/YTHDF1 介导的 RNA 转录本促进的。这项研究阐明了 m6A/lncRNACHASERR/miR-6893-3p/TRIM14 通路有助于神经胶质瘤的进展，并强调了 lncRNA CHASERR 作为神经胶质瘤新型预后指标和治疗靶点的潜力。