Fig. 7: A proposed model depicts how VASH2 promotes chemoresistance and the malignant biological behaviors of LUSC cells by increasing the detyrosination of α-tubulin.

VASH2-induced increase in tubulin detyrosination boosts the binding of KIF3C to microtubules and enhances KIF3C-dependent endosomal recycling of EGFR, contributing to the prolonged activation of downstream PI3K/Akt/mTOR signaling and LUSC progression.