Autonomous rhythmic activity in glioma networks drives brain tumor growth

Glioblastoma cell networks harbor a plastic population of highly active glioblastoma cells that display rhythmic Ca2+ oscillations and are particularly connected to others. Targeting the autonomous rhythmic activity of periodic tumor cells by pharmacological interference with the potassium channel KCa3.1 strongly compromised global network communication. This led to a marked reduction of tumor cell viability within the entire network, reduced tumor growth in mice, and prolonged animal survival. The dependency of glioblastoma networks on periodic Ca2+ activity generates a vulnerability that can be exploited for the development of novel therapies, with KCa3.1 inhibiting drugs as one example. To investigate the molecular mechanism of KCa3.1 blockade, we exposed glioblastoma cells to Senicapoc, a selective inhinitor of the KCa3.1 channel, and performed gene expression profiling analysis using data obtained from RNA-Seq. Overall design: Comparative gene expression profiling analysis of RNA-seq data for S24 cells and its Senicapoc treated derivates.