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纳米二氨基四嗪(NDAT)抑制 PD-L1 表达,这对于口腔癌细胞的增殖是必不可少的。

Nano-diamino-tetrac (NDAT) inhibits PD-L1 expression which is essential for proliferation in oral cancer cells.

机构信息

Department of Dentistry, Hsinchu MacKay Memorial Hospital, Hsinchu City, Taiwan.

Taipei Cancer Center, Taipei Medical University, Taiwan; PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taiwan.

出版信息

Food Chem Toxicol. 2018 Oct;120:1-11. doi: 10.1016/j.fct.2018.06.058. Epub 2018 Jun 28.

Abstract

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.

摘要

程序性死亡配体 1(PD-L1)是一种关键的调节剂,可防止肿瘤细胞免受免疫监视。已经表明甲状腺激素可诱导癌细胞中 PD-L1 的表达。其纳米颗粒类似物,纳米二氨基四(NDAT;Nanotetrac)是一种抗癌/抗血管生成剂。在本研究中,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 通过抑制激活的 ERK1/2 和 PI3K 来抑制诱导型 PD-L1 的表达和蛋白积累。敲低 PD-L1 也抑制了口腔癌细胞的增殖,这表明 NDAT 对 PD-L1 表达的抑制作用可能是 NDAT 诱导口腔癌细胞抗增殖作用的关键机制之一。

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