Epigenetic regulation by CBX7 in glioblastoma: molecular mechanisms and translational perspectives

CBX7, a member of the Chromobox protein family and a core subunit of Polycomb Repressive Complex 1 (PRC1), has recently gained attention as an important regulator of chromatin organization and gene expression. In tumorigenesis, CBX7 can act as an oncogene or tumor suppressor highlighting a complex role to be investigated. In glioblastoma multiforme (GBM), CBX7 acts primarily as a tumor suppressor. Reduced CBX7 activity is related to poor patient survival by inducing glioblastoma cell hyperproliferation and invasiveness. Several molecular studies have highlighted the direct involvement of CBX7 in fundamental processes such as cell cycle regulation and the maintenance of stem-like characteristics. In GBM, epigenetic phenomena (such as hypermethylation of the CBX7 promoter region), regulation mediated by specific miRNAs, and protein-protein interactions are responsible for CBX7 downregulation. Restoring CBX7 expression in GBM reduced cell invasiveness and migration, highlighting its importance as a prognostic indicator and potential therapeutic target. Overall, current data support a model in which CBX7 operates as a crucial epigenetic regulator in glioblastoma, and its modulation may offer new opportunities for the development of targeted treatment strategies.