Bioinformatics Analysis Reveals Genes Involved in the Pathogenesis of Ameloblastoma and Keratocystic Odontogenic Tumor

Document Type : Original Article

Authors
1 Department of Dentistry, Universidade Estadual de Montes Claros, Minas Gerais, Brazil
2 Instituto Federal do Norte de Minas Gerais-Campus Araçuaí, Minas Gerais, Brazil
3 Instituto Federal do Norte de Minas Gerais-Campus Salinas, Minas Gerais, Brazil
4 Department of Biology, Universidade Estadual de Montes Claros, Minas Gerais, Brazil
5 Department of Pharmacology, Universidade Federal de Minas Gerais, Brazil
6 Texas Tech University Health Science Center, Lubbock, TX, USA
Abstract
Pathogenesis of odontogenic tumors is not well known. It is important to identify genetic deregulations and
molecular alterations. This study aimed to investigate, through bioinformatic analysis, the possible genes
involved in the pathogenesis of ameloblastoma (AM) and keratocystic odontogenic tumor (KCOT). Genes
involved in the pathogenesis of AM and KCOT were identified in GeneCards. Gene list was expanded, and the
gene interactions network was mapped using the STRING software. “Weighted number of links” (WNL) was
calculated to identify “leader genes” (highest WNL). Genes were ranked by K-means method and KruskalWallis test was used (P<0.001). Total interactions score (TIS) was also calculated using all interaction data
generated by the STRING database, in order to achieve global connectivity for each gene. The topological and
ontological analyses were performed using Cytoscape software and BinGO plugin. Literature review data was
used to corroborate the bioinformatics data. CDK1 was identified as leader gene for AM. In KCOT group, results
show PCNA and TP53. Both tumors exhibit a power law behavior. Our topological analysis suggested leader
genes possibly important in the pathogenesis of AM and KCOT, by clustering coefficient calculated for both
odontogenic tumors (0.028 for AM, zero for KCOT). The results obtained in the scatter diagram suggest an
important relationship of these genes with the molecular processes involved in AM and KCOT. Ontological
analysis for both AM and KCOT demonstrated different mechanisms. Bioinformatics analyzes were confirmed
through literature review. These results may suggest the involvement of promising genes for a better
understanding of the pathogenesis of AM and KCOT.
Keywords