부산대학교 도서관

Simple Summary: There are many aspects of oral cancer invasion and metastasis that remain to be elucidated. It has been suggested that chronic inflammation caused by bacteria may be a cause of carcinogenesis, invasion, and metastasis. PD-L1 expression is associated with lymph node metastasis and poor prognosis in several cancers. Lipopolysaccharide (LPS) from Porphyromonas gingivalis, which is known to be the main cause of bacterial periodontitis, induced PD-L1 expression and partial epithelial–mesenchymal transition (pEMT) expression in oral cancer cells. Moreover, we identified PD-L1 expression within the exosomes of oral cancer cells. Exosomes may function as carriers of PD-L1. 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 by Porphyromonas gingivalis (P.g) or Escherichia 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 of P.g or E. coli in 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. [ABSTRACT FROM AUTHOR]