ZBED6 inhibits the migration of glioblastoma cells by regulating the Wnt/β-catenin signaling pathway

ZBED6, a member of the zinc-finger protein superfamily, has incompletely defined biological functions in cancer. Previous studies suggest that ZBED6 may influence colorectal cancer growth and cell cycle regulation. This study aims to investigate the biological role and regulatory mechanisms of ZBED6 in glioblastoma. Bioinformatics analysis revealed abnormal activation of the Wnt/β-catenin signaling pathway in glioblastoma and a negative correlation between ZBED6 expression and Wnt/β-catenin signaling. Survival analysis further indicated that low ZBED6 expression is associated with poor prognosis in GBM patients. Through in vitro experiments, we demonstrated that ZBED6, as a transcription factor, regulates its downstream target TCF7L2, thereby modulating the Wnt/β-catenin signaling pathway. Additionally, we found that ZBED6 acts as a critical negative regulator of glioblastoma migration. Loss of ZBED6 expression may drive malignant progression by activating mesenchymal transition signaling, alleviating cell cycle arrest, and promoting oncogenic pathway activation. Collectively, these findings suggest that reduced ZBED6 expression in glioblastoma leads to aberrant TCF7L2 expression and dysregulated Wnt/β-catenin signaling activation, which is closely linked to poor clinical outcomes in GBM.