Several studies have shown the ability of transcription factor 12 (TCF12) to promote tumor malignant progression, but its function in glioma cells has not been fully elucidated. In this study, we analyzed the data from TCGA by bioinformatics and found that in glioma tissue, TCF12 was conspicuously highly expressed while miR-218-5p was significantly low-expressed. The downregulation of miR-218-5p was correlated with adverse prognosis in patients with glioma. miR-218-5p was found to be negatively associated with TCF12 by Pearson correlation analysis, and dual luciferase assay was employed to verify that miR-218-5p and TCF12 had a targeting relationship. qRT-PCR and Western blot assays were used to verify that the expression of TCF12 was regulated by its upstream regulator miR-218-5p. Moreover, cell experiments validated that overexpressed TCF12 could promote the proliferation, migration, and invasion of glioma cells and inhibit their apoptosis, whereas overexpressing miR-218-5p at the same time could reverse this phenomenon. Our study demonstrates the regulatory mechanism of the miR-218-5p/TCF12 axis in gliomas, which lays a foundation for searching for new therapeutic approaches for glioma.

多项研究表明转录因子 12 (TCF12) 具有促进肿瘤恶性进展的能力，但其在胶质瘤细胞中的功能尚未完全阐明。在这项研究中，我们通过生物信息学分析了来自 TCGA 的数据，发现在胶质瘤组织中，TCF12 显着高表达，而 miR-218-5p 显着低表达。miR-218-5p的下调与胶质瘤患者的不良预后相关。Pearson相关分析发现miR-218-5p与TCF12呈负相关，采用双荧光素酶检测验证miR-218-5p与TCF12具有靶向关系。qRT-PCR 和蛋白质印迹分析用于验证 TCF12 的表达受其上游调节因子 miR-218-5p 的调节。而且，细胞实验证实，过表达TCF12可以促进胶质瘤细胞的增殖、迁移和侵袭，抑制其凋亡，而同时过表达miR-218-5p可以逆转这种现象。我们的研究证实了 miR-218-5p/TCF12 轴在胶质瘤中的调控机制，为寻找新的胶质瘤治疗方法奠定了基础。