Fig. 8: Time-resolved proteome/phosphoproteome of the angiocrine-induced VC-Resist state transition unveils partial proneural-to-mesenchymal transition.

A Upregulated proteins in common between the patient-derived PN-MGG4 and the mouse MES-GL261 GBM cells treated for 6 or 72 h with control or blood vessel conditioned media (CM-BV) (n = 5 independent experiments). (Top) Venn graph of the common genes. (Middle) Kinase enrichment analysis (KEA) of the common proteins using the KEA3 web-based platform. Lower is the combined score, more probable is the activity of the kinase. (Bottom) Network among the top proteins in the KEA. Volcano plots are in Supplementary Fig. 14A. B Temporal proteomic profiling of cell plasticity in GBM exposed to blood vessel conditioned media (CM-BV). Y-axes are means of all log2(fold change) between CT and CM-BV for Neftel’ cell states (20–30 markers per GBM classifier) or VC-Resist (32 proteins), excluding the infinite values. C More phosphorylated proteins in common between the patient-derived PN-MGG4 and the mouse MES-GL261 GBM cells treated for 6 or 72 h with control (CT-CM) or blood vessel conditioned media (BV-CM). (Top) Venn graph of the common genes. (Bottom) Word cloud plot for the commonly hyper-phosphorylated proteins. The largest fonts represent proteins that are present in all four datasets, while the smallest fonts are for proteins shared in just 2 datasets (from different cell lines). Volcano plots are in Supplementary Fig. 14C. D Kinase enrichment analysis (KEA) on phosphoproteome in the patient-derived PN-MGG4 and the mouse MES-GL261 GBM cells treated for 72 h with control (CT-CM) or blood vessel conditioned media (BV-CM) (n = 5 independent experiments; z-score is indicator of the kinase activity estimated; significant in black and not-significant in gray).