Background. Aim of this bioinformatics study based on transcriptomic analysis was to reveal the cross-talk between periodontitis (PD) and hypothyroidism (HT). Methods. The gene expression datasets GSE18152 and GSE176153 of HT and GSE10334, GSE16134, and GSE173078 of PD were downloaded through the Gene Expression Omnibus (GEO) database. Differential Expression Genes (DEG) between cases and controls in each microarray were assessed by using the “limma” (linear models for microarray data) R package (|log2 fold change (FC)| >0 and P -value <0.05). To analyze the cross-talk effect between HT and PD, the intersection of DEG of HT and PD was selected. To investigate the biological function of cross-talk genes, the gene ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were applied. Protein-Protein Interaction (PPI) network was constructed using Cytoscape software. Top 10 cross-talk genes were screened, and the expression values of these 10 genes were extracted. ROC analysis was performed by using the pROC package and GGplot2 package of R language to predict the classification accuracy. Results. The overlapping DEG between HT and PD were 107 cross-talk genes. The results revealed that developmental process ( P -value =1.06E-21) was the most significantly enriched biological process, followed by cell differentiation ( P -value =8.49E-18) and immune system process ( P -value =6.78E-11). KEGG analysis showed that Complement and coagulation cascades ( P -value =2.29E-05), Hematopoietic cell lineage ( P -value =2.66E-05), Phospholipase D signaling pathway ( P -value =0.034367878) and Chemokine signaling pathway ( P -value =0.04946333) were significantly enriched. The top 10 genes with most connections were LCE1B, LCE2B, LCE2A, LCE2C, LCE1C, LCE1F, ITGAM, C1QB, TREM2, and CD19. The AUC values of the two datasets of HT were both greater than 65% (GSE18152 = 81.42%, GSE176153 = 68.75%). AUC values of three datasets of PD were all greater than 60% (GSE10334 = 69.23%, GSE16134 = 73.72%, GSE173078 = 81.6%). Conclusions. A genetic cross-talk between HT and PD was detected, whereby LCE family genes appeared to play the most important role.

Background. The human tyrosine kinase 2 (TYK2) has been found to be associated with at least 20 autoimmune diseases; however, its tumor-regulating role in head and neck squamous cell carcinoma (HNSC) has not been researched by using an integrative bioinformatics approach, yet. Objective. To investigate the regulating mechanisms of the TYK2 gene in HNSC in terms of its expression pattern, prognostic values, involved biological functions, and implication of tumor immunity. Methods. The TYK2 gene expression pattern and regulatory involvement in HNSC were investigated using publically accessible data from TCGA database. R software tools and public web servers were utilized to conduct statistical analysis on cancer and noncancerous samples. Results. TYK2 was found to be significantly upregulated in HNSC samples compared with healthy control samples. The expression of TYK2 gene was shown to be associated with the prognosis of HNSC by showing its upregulation represented better survival outcome. The regulating role of TYK2 in HNSC was found mainly in several pathways including DNA replication, base excision repair, apoptosis, p53 signaling pathway, and NF-kappa B signaling pathway. The gene set enrichment analysis (GSEA) results showed that TYK2-significantly correlated genes were mainly enriched in several biological functional terms including cell cycle, DNA replication, PLK1 pathway, ATR pathway, and Rho GTPase pathway. In addition, TYK2 was found to be involved in tumor immunity, showing positive correlation with the majority of tumor infiltrating immune cells, immune checkpoint genes, and significant representative components of tumor microenvironment, according to the ESTIMATE-Stromal-Immune score. Conclusions. Given the dysregulation, prognostic values, regulating tumor progression-related pathways, and the tumor immune-modulatory role of TYK2 in HNSC, the TYK2 gene should be regarded as a potential therapeutic target in treating head and neck cancer.