CircBUB1 activates the PI3K/AKT signaling pathway to promote the migration and invasion of glioblastoma cells

Background

Glioblastoma (GBM) is the most aggressive primary brain tumor, characterized by rapid growth and resistance to treatment, leading to poor survival rates. The molecular mechanisms underlying GBM progression remain unclear, necessitating further research. This study focuses on the role of circBUB1, a circular RNA, in GBM cell migration and invasion, and the associated molecular mechanisms.

Methods

RNA/protein expression was detected using RT-qPCR/western blot assay. Transwell and wound healing assays were conducted to assess GBM cell migration and invasion. Detailed mechanistic analyses were carried out to understand the role of circBUB1 in GBM cells.

Results

CircBUB1 was found to be highly expressed and functioned as an oncogene in GBM cells. Functional assays revealed that knockdown of circBUB1 suppressed the migration and invasion of GBM cells. Mechanistic analyses showed that circBUB1 sequestered miR-1296-5p, thereby elevating TRIM14 expression. TRIM14 was also found to promote PTEN ubiquitination, ultimately leading to the down-regulation of PTEN protein and activation of the PI3K/AKT signaling pathway. Through rescue assays, this study confirmed that circBUB1 promoted GBM cell migration and invasion by reducing PTEN protein levels.

Conclusion

Our findings indicate that circBUB1 activates the PI3K/AKT signaling pathway, promoting the migration and invasion of GBM cells via the miR-1296-5p/TRIM14 axis. This provides new insights into the molecular mechanisms of GBM progression and potential therapeutic targets.