GSE138010
Fosl1 regulates mesenchymal GBM plasticity
Despite recent advances in genomic profiling techniques, the precise mechanisms controlling GBM subtypes and their plasticity are not fully unraveled. Here,using transcriptomic data of patient derived stem cell lines we found that FOSL1 is a master regulator of the MES subtype. Depletion of FOSL1 resulted in loss of themesenchymal gene signature (MGS)  in mouse Kras-mutant neural stem cells and in human brain tumor stem cells. Overall design: Mouse neural stem cells (NSCs) from  GFAP-Tva, LSL_Cas9; Trp53 lox/lox; GFAP-Crep1 mice were transduced with a KrasG12V mutant and then with either Control or Fosl1 gRNAs