PD-1 Carried on Small Extracellular Vesicles Leads to OSCC Metastasis

癌症研究 转移 上皮-间质转换 癌变 MAPK/ERK通路 生物 体外 免疫组织化学 细胞凋亡 免疫系统 细胞 激酶 化学 细胞生物学 免疫学 癌症 生物化学 遗传学
作者
Longting Zhang,Jie Yang,Huaiping Xia,Jing Huang,Hon‐Man Liu,Min Wu,Bingya Liu,Weihua Wang,Gang Chen
出处
期刊:Journal of Dental Research [SAGE Publishing]
卷期号:102 (7): 795-805 被引量:4
标识
DOI:10.1177/00220345231165209
摘要

Immune checkpoint molecule PD-1, expressed on the cell surface, impairs antigen-driven activation of T cells and thus plays a critical role in tumorigenesis, progression, and the poor prognosis of oral squamous cell carcinoma (OSCC). In addition, increasing evidence indicates that PD-1 carried on small extracellular vesicles (sEVs) also mediates tumor immunity, although their contributions to OSCC are yet unclear. Here, we investigated the biological functions of sEV PD-1 in patients with OSCC. The cell cycle, proliferation, apoptosis, migration, and invasion of CAL27 cell lines treated with or without sEV PD-1 were examined in vitro. We performed mass spectrometry to investigate the underlying biological process, combined with an immunohistochemical study of SCC7-bearing mice models and OSCC patient samples. In vitro data demonstrated that sEV PD-1 induced senescence and subsequent epithelial-mesenchymal transition (EMT) in CAL27 cells by ligating with tumor cell surface PD-L1 and activating the p38 mitogen-activated protein kinase (MAPK) pathway. Comprehensive immunohistochemical analysis of the xenograft mice models and OSCC patient samples revealed a very close correlation between the level of circulating sEV PD-1 and lymph node metastasis. These results demonstrate that circulating sEV PD-1 triggers senescence-initiated EMT in a PD-L1-p38 MAPK-dependent manner, contributing to tumor metastasis. It also suggests that the inhibition of sEV PD-1 may be a promising therapeutic target for the treatment of OSCC.
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