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Background: Reports on the proteomic studies of ameloblastoma and other common odontogenic lesions are limited. We thus explored the differential proteins among ameloblastoma, odontogenic keratocyst, dentigerous cyst, and normal gingival tissue using proteomics and identified hub proteins involved in the local aggressiveness and recurrence of ameloblastoma. Methods: Samples were obtained from 14 patients with ameloblastoma, 6 with odontogenic keratocyst, 9 with a dentigerous cyst, and 5 with normal gingival tissue. Proteins were then extracted, purified, quantified, and analysed using Easy‐nLC chromatography and mass spectrometry. Further functional annotation and enrichment analyses were performed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes on the target protein collection. Protein clustering and protein–protein interaction network analyses were used to screen the hub proteins. Proteins with significant interactions were screened according to their degree index. These results were verified by immunohistochemical staining. Proteins meeting the screening criteria of expression difference ploidy >1.2‐fold (upregulation and downregulation) and p < 0.05 were considered differential proteins. Results: In ameloblastoma, 808 differential proteins were upregulated and 505 were downregulated compared with those in odontogenic keratocyst; 309 were upregulated and 453 were downregulated compared with those in dentigerous cyst; and 2210 were upregulated and 829 were downregulated compared with those in normal gingival tissue. The three groups of differential proteins were associated with cellular exosomes, antigen binding, complement activation, human papillomavirus infection, focal adhesion, cell adhesion molecules, and metabolic pathways. Conclusion: CDH3 is associated with the local aggressiveness and recurrence of ameloblastoma and is a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Oral squamous cell carcinoma (OSCC) is a highly malignant tumour, and the prediction of its prognosis remains challenging. The prognostic value of T-lymphocyte proliferation regulators in OSCC remains to be explored. We integrated mRNA expression profiles and relevant clinical information of OSCC patients from The Cancer Genome Atlas database. The expression and function of T-lymphocyte proliferation regulators and their relationship with overall survival (OS) were analysed. The T-lymphocyte proliferation regulator signature was screened using univariate Cox regression and least absolute shrinkage and selection operator coefficients and used to construct models for prognosis and staging prediction as well as for immune infiltration analysis. Final validation was performed using single-cell sequencing database and immunohistochemical staining. Most T-lymphocyte proliferation regulators in the TCGA cohort exhibited different expression levels between OSCC and paracancerous tissues. A prognostic model constructed using the T-lymphocyte proliferation regulator signature (RAN , CDK1 , and CDK2) was used to categorise patients into high- and low-risk groups. The OS was significantly lower in the high-risk group than the low-risk group (p < 0.01). The predictive ability of the T-lymphocyte proliferation regulator signature was validated by receiver operating characteristic curve analysis. Immune infiltration analysis revealed different immune statuses in both groups. We established a new T-lymphocyte proliferation regulator signature that can predict the prognosis of OSCC. The results of this study will contribute to studies of T-cell proliferation and the immune microenvironment in OSCC to improve prognosis and immunotherapeutic response. • TCGA RNA-seq data was used to assess the prognostic value of TCRs in OSCC. • A prognostic model was created using the RAN-CDK1-CDK2 TCR signature. • Overall survival was significantly lower in the high-risk group. • Immune infiltration and TCR gene expression differed between risk groups. • Immunohistochemical staining for RAN-CDK1-CDK2 TCR signature in OSCC tissues and precancerous tissues. [ABSTRACT FROM AUTHOR]

To perform an integrated analysis in identifying novel hub genes that could facilitate the diagnosis and targeted therapy of ameloblastoma. The expression profiling dataset, GSE38494, was obtained from the Gene Expression Omnibus database. Differentially expressed genes were identified through GEO2R online tool and characterised via Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The protein-protein interaction network and hub genes were screened using the STRING database and Cytoscape software. Subsequently, an upregulated gene was selected for further validation using the GSE132472 dataset. Further, immunohistochemistry was performed to assess the expression of the selected gene in ameloblastomas, odontogenic keratocysts, dentigerous cysts, and gingival tissues. The diagnostic and therapeutic utility of the selected hub genes were further verified by receiver operating characteristic analysis and the DGIdb database. We identified six hub genes in ameloblastoma, among which the upregulated gene PKD2 and its related gene PKD1 were further validated. GO functional annotation revealed that PKD2 is involved in cell-cell junction, extracellular exosome, cytoplasm, endoplasmic reticulum, and calcium ion transport. The immunohistochemical analysis showed that the expression of polycystin-1 and polycystin-2, encoded by the PKD1 and PKD2 genes, respectively, was upregulated in ameloblastoma. PKD1 and PKD2 had a high diagnostic utility for ameloblastoma, and allopurinol interacted with the PKD2 gene. Our research indicates that polycystins are highly expressed in ameloblastoma and might be involved in the oncogenesis of ameloblastoma, thus offering a new perspective on the molecular mechanisms and targeted therapies on ameloblastoma. • Polycystin-1 and polycystin-2 had higher expression in ameloblastoma. • PKD1 and PKD2 genes had a high diagnostic utility for ameloblastoma. • Allopurinol interacts with PKD2 gene and could be a potential drug candidate. • Polycystins offer a new perspective on the targeted therapies of ameloblastoma. [ABSTRACT FROM AUTHOR]