FSTL3-Driven Cuproptosis Resistance and EPCs Promote OSCC Metastasis

depletion in immunotherapy-resistant tumors unleashed potent antitumor immunity and synergized with immunotherapy. Our findings establish FSTL3 as a pivotal node coordinating dual metastasis mechanisms: cuproptosis resistance and immune evasion. Targeting FSTL3 disrupts both adaptive programs, effectively inhibiting lymph node metastasis. This work nominates FSTL3 as a therapeutic target; combining FSTL3 inhibition with immunotherapy represents a promising dual-targeting strategy to improve OSCC outcomes by simultaneously disabling cancer cell survival and immune escape.