Nanostring data Robertson et al. re interaction between FOXG1 and Wnt/ß-catenin signalling

GBM stem cells (GSCs) display phenotypic and molecular features reminiscent of normal neural stem cells, and exhibit a spectrum of cell cycle states (dormant, quiescent, proliferative). However, mechanisms controlling the transition from quiescence to proliferation in both NSCs and GSCs are poorly understood. Elevated expression of the forebrain transcription factor FOXG1 is often observed in GBM. Here, using small molecule modulators and genetic perturbations, we identify a synergistic interaction between FOXG1 and Wnt/ß-catenin signalling. Increased FOXG1 enhances Wnt-driven transcriptional targets enabling highly efficient cell-cycle re-entry from quiescence; however, neither FOXG1 nor Wnt is essential in rapidly proliferating cells. We demonstrate that FOXG1 overexpression supports gliomagenesis in vivo and that additional ß-catenin induction drives accelerated tumour growth. These data indicate that elevated FOXG1 cooperates with Wnt signalling to support the transition from quiescence to proliferation in GSCs.