CHFR drives gastric cancer stemness and hepatic metastasis by suppressing ITCH-mediated ubiquitination and degradation of OCT4
In vivo xenograft assays demonstrated that CHFR overexpression significantly promoted GC liver metastasis, whereas simultaneous overexpression of CHFR and ITCH reversed this metastatic phenotype, highlighting the CHFR/ITCH/OCT4 axis as a therapeutic target for GC treatment.