Targeting PDPN enhances antitumor T-cell activity by disrupting β-catenin-mediated PD-L1 expression in melanoma

These findings identify PDPN as a critical driver of immune evasion in melanoma via b-catenin-mediated PD-L1 upregulation. Inhibitory targeting of PDPN with CY12-RP2 represents a promising therapeutic approach capable of disrupting this immunosuppressive pathway and reversing tumor immune escape.