Glioma cell infiltration remains a major cause of tumour relapse and we have previously demonstrated that SFK signalling mediates basal glioma invasion by activating MMP9 (ref. 25). Two-chamber migration assays demonstrated enhanced migratory properties in transformed iNPCs (Supplementary Fig. 9a,b). RNA profiling demonstrated the significant upregulation of MMP9 in Ras/EGFR/SrciNPCs and p53KD-Ras/EGFR/SrciNPCs (Supplementary Fig. 9c) and MMP9 inhibition significantly hampered migration (Supplementary Fig. 9b). In addition, all identified anti-cancer compounds and two metabolic inhibitors (2-DG and Rot/AA) hampered the migration of primary GTICs and transformed iNPCs (Fig. 4b). Differentiation of cancer stem cells is thought to give rise to less malignant populations that are presumably more sensitive to chemotherapy, whereas the self-renewing stem cell compartment is thought to contribute to resistance and recurrence2389353637. Self-renewal assays indicated that Ras/EGFR/SrciNPCs and p53KD-Ras/EGFR/SrciNPCs possessed the highest self-renewal potential, whereas p53KDiNPCs were more similar to WTiNPCs (Supplementary Fig. 9d,e). Treatment with the identified compounds significantly compromised the self-renewal properties of Ras/EGFR/SrciNPCs and p53KD-Ras/EGFR/SrciNPCs (Fig. 4c). In addition, iNPC-differentiated neural cells demonstrated higher susceptibility to chemical treatments (Supplementary Fig. 10a). Next, we investigated the effect
