Activation of LINC01515 transcription by MEOX2 contributes to the malignant progression of glioblastoma

Glioblastoma (GBM) is the most common malignant brain tumor with a low 5-year survival rate. The search for therapeutic agents for GBM from the perspective of lncRNA has attracted widespread attention. Bioinformatics analysis was used to explore GBM-related lncRNA and target genes. GBM patient clinical samples and cells (U87MG, LN-229, T98G, U373, and U251) were used for validation. Knockdown of LINC01515 was used to evaluate its effects on GBM cells. Moreover, protein expression levels of caspase-3, cleaved-caspase-3, p21, p53, Snail, N-cadherin, and E-cadherin were analyzed. Balb/c nude mouse subcutaneous tumor formation assay and HE staining were used to observe the effect of LINC01515 on GBM. ChIP-PCR was used to explore the relationship between MEOX2 and LINC01515. Here, the potential association of LINC01515 and MEOX2 with GBM was confirmed by clinical samples and GBM cells. MEOX2 is involved in the transcriptional activation of LINC01515. In vitro cellular experiments have shown that down-regulation of LINC01515 resulted in increased apoptosis and decreased activity, invasion, and migration capacity in GBM cells LN-229 and U251. Furthermore, GBM cells showed G1-phase cell cycle arrest accompanied by high protein expression of p53 and p21 due to LINC01515 downregulation. In vivo experiments in mice demonstrated that down-regulation of LINC01515 reduced the weight and volume of tumors and was accompanied by an increase in apoptosis and a decrease in inflammatory infiltration of GBM cells. MEOX2 activates LINC01515 transcription. Down-regulation of LINC01515 promotes GBM cell apoptosis and inhibits GBM cell function and activity, improves inflammatory infiltration, and plays a therapeutic role in GBM.