Connexin43 functions as a non-canonical phenotypic stability factor in promoting hybrid Epithelial/Mesenchymal phenotype in glioblastoma cells.

ABSTRACT: Glioblastoma (GBM) is a highly malignant and aggressive brain tumor with patients typically experiencing a median survival of 15-18 months after diagnosis. Gap junction protein Connexin43 (Cx43) plays a crucial role in GBM by having both tumor-suppressing and tumor-promoting roles. Here, we identify a critical tumor-promoting role of Cx43 in GBM by functioning as a non-canonical phenotypic stability factor and driving partial EMT, which enhances the acquisition of stemness properties in the cells. Using high-grade mouse astrocytoma cell lines, we found that CT2A cells had higher Cx43 gap junction assembly as compared to KR158 cells. The increased Cx43 assembly in CT2A cells activates the NF-κB signaling pathway, promoting a hybrid E/M phenotype and thereby enhancing self-renewal properties

SUBMITTER: Mondal A 

PROVIDER: S-EPMC12269574 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature