Glioma ranks first among the aggressive brain tumors all over the world. LncRNA LINC00689 has been confirmed to play key roles in the progression of cancers, and LINC00689 was upregulated in glioma. However, the biological function of LINC00689 in glioma is unclear. qRT-PCR was applied to detect the expressions of LINC00689 and miR-526b-3p in glioma cells. Dual-luciferase report was performed to examine the relation among LINC00689, miR-526b-3p, and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1). Then, the growth, migration, and invasion of glioma cells were detected by colony formation, flow cytometry, and transwell assay, respectively. The expressions of p21, cleaved caspase 3, and MAPK signaling-related proteins in glioma cells were tested by western blotting. Finally, xenograft mice model was established to detect the effect of LINC00689 on tumor growth of glioma in vivo. LINC00689 was upregulated in glioma cells, while miR-526b-3p was downregulated. In addition, LINC00689 bound to miR-526b-3p, and IGFBP1 was targeted by miR-526b-3p. Moreover, LINC00689 knockdown or upregulation of miR-526b-3p inhibited the proliferation of glioma cells and induced the apoptosis. Consistently, the migration and invasion of glioma cells were notably reduced by LINC00689 shRNA/miR-526-3p mimics. miR-526b-3p inhibitor or IGF2BP1 upregulation could reverse the effect of LINC00689 knockdown or miR-526b-3p mimics. Finally, knockdown of LINC00689 inhibited the tumor growth of glioma in vivo through regulating miR-526b-3p/IGF2BP1/MAPK axis. In conclusion, silencing of LINC00689 could inhibit the tumorigenesis of glioma via mediation of miR-526b-3p/IGF2BP1 axis. LINC00689 may serve as a new target for the treatment of glioma.

胶质瘤在全球侵袭性脑肿瘤中排名第一。LncRNA LINC00689 已被证实在癌症进展中发挥关键作用，并且 LINC00689 在胶质瘤中上调。然而，LINC00689 在胶质瘤中的生物学功能尚不清楚。应用qRT-PCR检测胶质瘤细胞中LINC00689和miR-526b-3p的表达。进行双荧光素酶报告以检查 LINC00689、miR-526b-3p 和胰岛素样生长因子 2 mRNA 结合蛋白 1 (IGF2BP1) 之间的关系。然后，分别通过集落形成、流式细胞术和transwell检测检测胶质瘤细胞的生长、迁移和侵袭。采用蛋白质印迹法检测胶质瘤细胞中 p21、cleaved caspase 3 和 MAPK 信号相关蛋白的表达。最后，建立异种移植小鼠模型，检测LINC00689对体内胶质瘤肿瘤生长的影响。LINC00689 在胶质瘤细胞中上调，而 miR-526b-3p 下调。此外，LINC00689 与 miR-526b-3p 结合，IGFBP1 被 miR-526b-3p 靶向。此外，LINC00689 敲低或上调 miR-526b-3p 可抑制胶质瘤细胞的增殖并诱导细胞凋亡。一致地，LINC00689 shRNA/miR-526-3p 模拟物显着降低了胶质瘤细胞的迁移和侵袭。miR-526b-3p 抑制剂或 IGF2BP1 上调可以逆转 LINC00689 敲低或 miR-526b-3p 模拟物的作用。最后，敲低 LINC00689 通过调节 miR-526b-3p/IGF2BP1/MAPK 轴抑制体内胶质瘤的肿瘤生长。综上所述，LINC00689 的沉默可以通过 miR-526b-3p/IGF2BP1 轴的介导抑制胶质瘤的肿瘤发生。LINC00689可能作为治疗胶质瘤的新靶点。