Suppr超能文献

程序性死亡配体在人类头颈部鳞状细胞癌微环境中的调节是通过基质金属蛋白酶介导的蛋白水解切割来实现的。

Regulation of programmed-death ligand in the human head and neck squamous cell carcinoma microenvironment is mediated through matrix metalloproteinase-mediated proteolytic cleavage.

机构信息

Department of Oral and Maxillofacial Surgery, Division of Cancer Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa 920-8640, Japan.

Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool L7 8TX, UK.

出版信息

Int J Oncol. 2018 Feb;52(2):379-388. doi: 10.3892/ijo.2017.4221. Epub 2017 Dec 11.

Abstract

Recurrent and/or metastatic head and neck squamous cell carcinoma (R/M HNSCC) is a devastating malignancy with a poor prognosis. According to recent clinical studies, tumour growth can be effectively reduced and survival can be improved by blocking the programmed death receptor-1 (PD-1)/programmed death-ligand 1 (PD‑L1) pathway. PD-L1 expression has been proposed as a potential causative mechanism, as HNSCC is highly immunosuppressive. However, anti-PD-1 treatment is beneficial only for certain patients. Therefore, the mechanisms controlling PD-L1 expression warrant further investigation in order to provide a better understanding of the predicting efficacy of and optimising anti-PD-1 therapy, alone or in combination. In this study, PD-L1 protein extracted from the cell membrane was found to be downregulated in OSC-20 cells compared with OSC-19 cells, despite a higher PD-L1 expression in the total cell lysate of the OSC-20 compared with the OSC-19 cells. Several matrix metalloproteinases (MMPs) were found to be upregulated in HNSCC; in particular, MMP-7 and -13 were upregulated in the OSC-20 compared with the OSC-19 cells. Purified PD-L1 was degraded by recombinant MMP-13 and -7. The expression of PD-L1 was significantly restored by a specific inhibitor of MMP-13 (CL82198), which suggested the involvement of MMP-13 in the shedding/cleavage of PD-L1 in the OSC-20 cells. Among the anticancer drugs conventionally used in the treatment of patients with HNSCC, paclitaxel increased MMP-13 expression in R/M HNSCC cells (HOC313 cells) co-cultured without/with dendritic cells (DCs). These results suggest that the shedding/cleavage of PD-L1 by MMP-13 is one of the mechanisms behind the protective effect against invasion and metastasis. Thus, MMP-13 has potential value as a marker predictive of the decreased efficacy of anti-PD-1 therapy. In addition, paclitaxel is a particularly promising candidate for combination therapy in R/M HNSCC with anti-PD-1 therapy.

摘要

复发性和/或转移性头颈部鳞状细胞癌(R/M HNSCC)是一种预后不良的破坏性恶性肿瘤。根据最近的临床研究,通过阻断程序性死亡受体 1(PD-1)/程序性死亡配体 1(PD-L1)通路,可以有效减少肿瘤生长并提高生存率。PD-L1 表达已被提出是一种潜在的致病机制,因为 HNSCC 具有高度免疫抑制性。然而,抗 PD-1 治疗仅对某些患者有益。因此,控制 PD-L1 表达的机制需要进一步研究,以便更好地了解单独或联合使用抗 PD-1 治疗的预测疗效并进行优化。在这项研究中,与 OSC-19 细胞相比,从细胞膜中提取的 PD-L1 蛋白在 OSC-20 细胞中下调,尽管 OSC-20 细胞的总细胞裂解物中的 PD-L1 表达高于 OSC-19 细胞。几种基质金属蛋白酶(MMPs)在 HNSCC 中上调;特别是,与 OSC-19 细胞相比,MMP-7 和 -13 在 OSC-20 细胞中上调。重组 MMP-13 和 -7 降解纯化的 PD-L1。MMP-13 的特异性抑制剂(CL82198)显著恢复了 PD-L1 的表达,这表明 MMP-13 参与了 OSC-20 细胞中 PD-L1 的脱落/裂解。在传统上用于治疗 HNSCC 患者的抗癌药物中,紫杉醇增加了 R/M HNSCC 细胞(HOC313 细胞)与树突状细胞(DCs)共培养时 MMP-13 的表达。这些结果表明,MMP-13 介导的 PD-L1 的脱落/裂解是侵袭和转移保护作用的机制之一。因此,MMP-13 作为预测抗 PD-1 治疗疗效降低的标志物具有潜在价值。此外,紫杉醇与抗 PD-1 治疗联合用于 R/M HNSCC 具有特别有前途的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c8/5741372/ec90bb80952c/IJO-52-02-0379-g00.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验