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Objective: The aim of this study was to investigate the role and related mechanism of chordin‐like 1 (CHRDL1) in oral squamous cell carcinoma (OSCC). Methods: The expressions of CHRDL1 were analyzed in both mRNA and protein levels by bioinformatics analysis, immunohistochemistry, and fluorescence in situ hybridization in OSCC. Survival analysis was used to determine the relationship between CHRDL1 and prognosis. In addition, enrichment analysis was used to suggest signal pathways involved in CHRDL1. Besides, the relationships between CHRDL1 and miRNAs, hypoxia, and immune infiltration were explored. Results: The mRNA level of CHRDL1 in OSCC was significantly lower than that in normal tissues, while the protein level was significantly higher than that in normal tissues. The high mRNA levels of CHRDL1 suggested a poor prognosis in patients with OSCC. The enrichment results showed that CHRDL1 might be involved in the Calcium signaling pathway, dilated cardiomyopathy, and focal adhesion. 7 immune cells were positively correlated with CHRDL1, while Tgd was negatively correlated with CHRDL1. In addition, we also found that hsa‐miR‐455‐3p directly targeted CHRDL1 and reduced the mRNA levels of CHRDL1. Conclusion: CHRDL1 plays a vital role in promoting cancer in OSCC and is down‐regulated at the mRNA levels by hsa‐miR‐455‐3p. [ABSTRACT FROM AUTHOR]

Aim: To ascertain the anti‐inflammation mechanism of catechins in lipopolysaccharide‐treated human dental pulp cells (HDPCs). Methods: Expression of tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, and IL‐6 was measured using quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assays. The anti‐inflammatory mechanism was explored by examining activation of nuclear factor‐kappa B (NF‐κB) signaling using qPCR, Western blotting, and immunofluorescence staining. Results: Human dental pulp cells proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3‐gallate (EGCG). mRNA expression of the pro‐inflammatory cytokines TNF‐α, IL‐1β, and IL‐6 was decreased significantly in ECG‐ and EGCG‐treated HDPCs. Subsequently, the effects of ECG and EGCG upon activation of NF‐κB signaling were evaluated by Western blotting and immunofluorescence staining. Expression of p‐p65 protein in HDPCs treated with ECG, EGCG, or an NF‐κB inhibitor (Bay 11‐7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining. Conclusions: Catechin could reduce lipopolysaccharide‐stimulated inflammation in HDPCs by inhibiting activation of the NF‐κB pathway. [ABSTRACT FROM AUTHOR]