HSPA8 Activates Wnt/β‐Catenin Signaling to Facilitate BRAF V600E Colorectal Cancer Progression by CMA‐Mediated CAV1 Degradation (Adv. Sci. 3/2024)

BRAF V600E BRAF V600E mutation in colorectal cancer results in failure of standard chemotherapy and low response rate to BRAF targeted drugs, but the underlying molecular mechanism is still unclear. In article number 2306535, Bowen Li, Jingwen Jiang, Canhua Huang, and co-workers have discovered that upregulated HSPA8 predicts poor prognosis of BRAF V600E colorectal cancer, which leads to CAV1 degradation via chaperone-mediated autophagy and subsequent β-catenin nuclear translocation. Notably, the HSPA8 inhibitor VER155008 sensitizes BRAF V600E colorectal cancer to targeted drugs, which offers potential therapeutic strategies.