N-3-(oxododecanoyl)-L-homoserine lactone (3-O-C12-HSL), a small bacterial signaling molecule secreted byPseudomonas aeruginosa (P. aeruginosa), can block dendritic cell (DC) maturation and participate in immuneescape, but the underlying mechanism is unclear. We speculate that regulation of DC maturation and functionby lncRNAs may be the mechanism by which 3-O-C12-HSL inhibits the immune response. We found that3-O-C12-HSL increased the expression level of the lncRNA NRIR, impeding monocyte-derived dendritic cell(Mo-DC) maturation. In addition, we observed the effect of NRIR on the expression of CD40, CD80, HLA-DRand IL-6. NRIR overexpression significantly reduced the expression of Mo-DC surface markers, while 3-OC12-HSL did not significantly reduce the expression of Mo-DC surface markers after NRIR knockdown.These results indicate that 3-O-C12-HSL indeed affects the differentiation and maturation of Mo-DCs throughNRIR. IL-6 stimulates T cell proliferation and activation, and we found that high NRIR expression reduced IL-6 levels. However, under NRIR knockdown, 3-O-C12-HSL did not decrease IL-6 expression, suggesting that3-O-C12-HSL may affect T cell activation through NRIR. This study is the first to elucidate the important roleof a lncRNA in the mechanism of 3-O-C12-HSL activity. It also provides new ideas regarding P. aeruginosainfection pathogenesis.

TEAD4 has been reported to act as an oncogenic gene in various types of cancer. This study intends to investigate the role and regulatory mechanism of TEAD4 in thyroid cancer (TC). GEPIA was used to predict the expression pattern of TEAD4 in TC. Expressions of TEAD4 and wnt3a in TC tissues and cells were analyzed by qRT-PCR and Western blot. TC cells were transfected with TEAD4 overexpression plasmids and treated with or without IWR-1-endo (a Wnt signaling inhibitor), and then TC cell viability, migration and invasion were assessed by MTT and Transwell assay. Expressions of E-cadherin, N-cadherin and Vimentin in cells were analyzed by Western blot. TEAD4 was low-expressed in TC tissues and cells. TEAD4 overexpression inhibited the viability, inhibited migration and invasion of TC cells, and downregulated N-cadherin and Vimentin expression, while promoted E-cadherin and wnt3a expression. The wnt3a expression was positively correlated with TEAD4 expression in TC. IWR-1-endo treatment reversed the effect of TEAD4 in TC cells. TEAD4 overexpression suppresses TC progression and metastasis in vitro through modulating Wnt signaling.