LncRNA LINC00689 Promotes the Tumorigenesis of Glioma via Mediation of miR-526b-3p/IGF2BP1 Axis.

Abstract

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 andinduced 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.