Decoding the role and regulation of Wnt/STOP in drug-resistant cancer cells for personalized treatment strategies

Abstract

This project addresses a critical gap in understanding how nutrient stress, specifically an amino acid downshift, intersects with Wnt/STOP and influences response to chemotherapy in drug resistant cancer cells. We will mechanistically define how GSK3-dependent proteasomal degradation is coupled to amino acid availability, and will decipher how Wnt/STOP dependency varies across cancer types. Ultimately, we will leverage these insights to develop targeted therapeutic strategies to overcome drug resistance.