Fig. 9
From: EMP3 sustains oncogenic EGFR/CDK2 signaling by restricting receptor degradation in glioblastoma
Proposed model of EMP3 function in GBM. EMP3 interacts with TBC1D5, and the resulting complex inactivates RAB7 in late endosomes. Inactive RAB7 is unable to facilitate EGFR degradation, and EGFR is stabilized. EMP3-dependent stabilization of EGFR sustains downstream signaling via the EGFR effector CDK2. This cascade culminates in the transcription of EGFR-responsive genes involved in cell cycle progression. Ultimately, these mechanisms ensure sustained proliferation, apoptosis resistance, and reduced susceptibility to targeted kinase inhibitors. Figure created with BioRender