Studies have found that LINC00467 is an important regulator of cancer. However, the function of LINC00467 in glioma cell is unclear. Therefore, this experimental design based on LINC00467 to explore its mechanism of action in glioma cell. RT-qPCR was used to detect the expression of LINC0046 and miR-200a in glioma cell lines. MTT assay, Edru assay and Transwell assay and flow cytometry were used to detect the effects of LINC0046 and miR-200a on PC cell proliferation, migration and apoptosis. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for LINC0046 and miR-200a. Western blotting was used to detect the protein expression of E2F3. The tumor changes in mice were detected by in vivo experiments in nude mice. LINC00467 was up-regulated in glioma cells. Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. In glioma cells, miR-200a was significantly reduced, while E2F3 was significantly rised. LINC00467 negatively regulated the expression of miR-200a in gliomas, while miR-200a negatively regulated the expression of E2F3 in gliomas. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression. LINC00467 may be a potential therapeutic target for gliomas.

研究发现LINC00467是癌症的重要调节因子。然而，LINC00467在神经胶质瘤细胞中的功能尚不清楚。因此，本实验设计基于LINC00467来探讨其在胶质瘤细胞中的作用机制。RT-qPCR检测胶质瘤细胞系中LINC0046和miR-200a的表达。采用MTT法、Edru法、Transwell法和流式细胞术检测LINC0046和miR-200a对PC细胞增殖、迁移和凋亡的影响。靶基因预测和筛选、荧光素酶报告基因测定用于验证 LINC0046 和 miR-200a 的下游靶基因。Western blotting检测E2F3蛋白表达。通过裸鼠体内实验检测小鼠肿瘤的变化。LINC00467 在神经胶质瘤细胞中上调。LINC00467 的敲低抑制了神经胶质瘤细胞的活力、迁移和侵袭。在神经胶质瘤细胞中，miR-200a显着降低，而E2F3显着升高。LINC00467负向调节神经胶质瘤中miR-200a的表达，而miR-200a负向调节神经胶质瘤中E2F3的表达。INC00467通过抑制miR-200a和促进E2F3表达来促进神经胶质瘤的发展。LINC00467可能是神经胶质瘤的潜在治疗靶点。