AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-B Pathway.

Objective: Our study was aimed at investigating the mechanistic consequences of the upregulation of () in glioblastoma (GBM).

Methods: The expression of in GBM was assessed by bioinformatics analysis and qRT-PCR; the effects of on GBM cell proliferation, migration, invasion, and tumor growth in vitro and in vivo were detected by a CCK-8 assay, colony formation assay, scratch assay, Transwell assay, and subcutaneous tumor formation, respectively. The activation of related signaling pathways was monitored using western blot.

Results: Tumor-related databases and bioinformatics analysis revealed that was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. The results of in vitro experiments showed that could significantly promote GBM cell proliferation, migration, and invasion; in vivo experiments suggested that could contribute to the growth of GBM tumors. could upregulate the level of phosphorylation, decrease expression, activate the NF-B signaling pathway, and promote the expression of downstream oncogenes.

Conclusion: Upregulated in GBM promotes GBM cell proliferation, migration, and invasion and facilitates tumor growth in vivo by activating the classical NF-B pathway.