Abstract
Programmed death-ligand 1 (PD-L1), a critical immune checkpoint ligand, is commonly overexpressed on the surface of many tumor types including lung and prostate cancer. PD-L1 can exert cancerpromoting activity through either suppressing T cell-mediated immune response or activating tumor-intrinsic signaling. Here, we demonstrated that β-tocotrienol (P-T3), an isomer of vitamin E, effectively inhibited PD-L1 expression both in vitro and in vivo, which was mechanistically associated inactivating JAK2/STAT3 pathway. Down-regulating PD-L1 expression by P-T3 led to enhanced immune response and inactivation of PD-L1-induced tumor-intrinsic signaling, which in turn contributed to its anticancer activity. This study uncovered a novel mechanism involved in the anticancer effect of P-T3.
NSTL