Figure 6.

MICAL‐L2 maintains EGFR content by Cdc42 in gastric cancer cells. A, BGC‐823 cells were transfected with siMICAL‐L2 and the activity of Cdc42 and Rac1 was measured by pulldown assays. **P < 0.01. B, SGC‐7901 cells were transfected with MICAL‐L2 plasmids and the activity of Cdc42 was measured by pulldown assays. *P < 0.05. C, MICAL‐L2‐overexpressed SGC‐7901 cells were transfected with Cdc42‐T17N (DN) plasmids and the total cellular proteins were extracted and analysed for EGFR level by Western blotting assays. D, Cells depleting MICAL‐L2 were transfected with Cdc42‐Q61L (CA) and the total cellular proteins were extracted and analysed for EGFR. E, A diagram about the mechanism. MICAL‐L2 potentiates gastric cancer cell migration via supporting EGFR stability and leading to the activation of EGFR downstream HSP27/Akt and Wnt/β‐catenin signalling pathways. MICAL‐L2 maintains EGFR stability, at least in part, through preventing EGFR degradation in lysosome by a Cdc42‐dependent manner