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. Author manuscript; available in PMC: 2020 Dec 9.
Published in final edited form as: Cell Rep. 2020 Mar 10;30(10):3383–3396.e7. doi: 10.1016/j.celrep.2020.02.014

Figure 7. ERK and SPRY2 Are at the Center of a Bypass Resistance Mechanism That Enables GBM Cells to Evade Treatment with EGFR and MET Inhibitors.

Figure 7.

In the model of signaling regulation proposed here, combined inhibition of EGFR and MET abrogates ERK and AKT activities, but the effect on ERK is short-lived. Activation of NF-κB promotes FGF1 and FGF2 production and autocrine activation of FGFR. The resultant reactivation of ERK drives SPRY2 expression and rescues GBM cells from death. The dashed boxes indicate proteins that, when targeted in combination with EGFR and MET, could be useful targets to pursue in future combinatorial strategies.