文章：

细菌脂多糖诱导口腔鳞状细胞癌细胞中PD-L1表达及侵袭性表型

Bacterial Lipopolysaccharide Induces PD-L1 Expression and an Invasive Phenotype of Oral Squamous Cell Carcinoma Cells

原文发布日期：13 January 2024

DOI: 10.3390/cancers16020343

类型: Article

开放获取: 是

英文摘要：

Background: Expression of programmed death ligand-1 (PD-L1) is related to the prognosis of many solid malignancies, including oral squamous cell carcinoma (OSCC), but the mechanism of PD-L1 induction remains obscure. In this study, we examined the expression of PD-L1 and partial epithelial–mesenchymal transition (pEMT) induced by bacterial lipopolysaccharide (LPS) in OSCC. Methods: The expression of Toll-like receptor 4 (TLR4) recognizing LPS in OSCC cell lines was analyzed. Moreover, the induction of PD-L1 expression byPorphyromonas gingivalis(P.g) orEscherichia coli(E. coli) LPS and EMT was analyzed by western blotting and RT-PCR. Morphology, proliferation, migration, and invasion capacities were examined upon addition of LPS. PD-L1 within EXOs was examined. Results: PD-L1 expression and pEMT induced by LPS ofP.gorE. coliin TLR4-expressing OSCC cell lines were observed. Addition of LPS did not change migration, proliferation, or cell morphology, but increased invasive ability. Moreover, higher expression of PD-L1 was observed in OSCC EXOs with LPS. Conclusion: Oral bacterial LPS is involved in enhanced invasive potential in OSCC cells, causing PD-L1 expression and induction of pEMT. The enhancement of PD-L1 expression after addition of LPS may be mediated by EXOs.

摘要翻译： 

背景：程序性死亡配体-1（PD-L1）的表达与包括口腔鳞状细胞癌（OSCC）在内的多种实体恶性肿瘤的预后相关，但PD-L1的诱导机制尚不明确。本研究探讨了细菌脂多糖（LPS）在OSCC中诱导PD-L1表达及部分上皮-间质转化（pEMT）的作用。方法：分析OSCC细胞系中识别LPS的Toll样受体4（TLR4）表达情况。通过蛋白质印迹和RT-PCR检测牙龈卟啉单胞菌（P.g）或大肠杆菌（E. coli）LPS对PD-L1表达及EMT的诱导作用。观察添加LPS后细胞的形态、增殖、迁移和侵袭能力变化，并检测外泌体（EXOs）中的PD-L1表达。结果：在表达TLR4的OSCC细胞系中观察到P.g或E. coli的LPS可诱导PD-L1表达和pEMT。添加LPS未改变细胞迁移、增殖或形态，但增强了侵袭能力。此外，在LPS处理的OSCC外泌体中观察到更高水平的PD-L1表达。结论：口腔细菌LPS通过诱导PD-L1表达和pEMT增强OSCC细胞的侵袭潜能，且LPS对PD-L1表达的促进作用可能通过外泌体介导。

原文链接：

Bacterial Lipopolysaccharide Induces PD-L1 Expression and an Invasive Phenotype of Oral Squamous Cell Carcinoma Cells