Programmed death-ligand 1 (PD-L1) is a critical regulator to defend tumor cells against immune surveillance. Thyroid hormone has been shown to induce PD-L1 expression in cancer cells. Its nano-particulated analogue, nano-diamino-tetrac (NDAT; Nanotetrac) is an anticancer/anti-angiogenic agent. In the current study, the inhibitory mechanism by which NDAT inhibited PD-L1 mRNA abundance and PD-L1 protein content in oral cancer cells was investigated. NDAT inhibited inducible PD-L1 expression and protein accumulation by the inhibition of activated ERK1/2 and PI3K. Knockdown PD-L1 also inhibited the proliferation of oral cancer cells which suggests that the inhibitory effect of NDAT on PD-L1 expression maybe is one of the critical mechanisms for NDAT-induced anti-proliferative effect in oral cancer cells.

程序性死亡配体1（PD-L1）是保护肿瘤细胞免受免疫监视的重要调节剂。甲状腺激素已显示出可诱导癌细胞中PD-L1的表达。它的纳米颗粒类似物，纳米二氨基-丁酸（NDAT； Nanotetrac）是一种抗癌/抗血管生成剂。在当前的研究中，研究了NDAT抑制口腔癌细胞中PD-L1 mRNA丰度和PD-L1蛋白含量的抑制机制。NDAT通过抑制活化的ERK1 / 2和PI3K来抑制可诱导的PD-L1表达和蛋白质积累。敲低PD-L1也抑制口腔癌的细胞，这表明NDAT对抑制作用增殖PD-L1 表达可能是NDAT诱导的口腔癌细胞抗增殖作用的关键机制之一。