Santos Eliane Macedo Sobrinho, Santos Hércules Otacílio, Dos Santos Dias Ivoneth, Santos Sérgio Henrique, Batista de Paula Alfredo Maurício, Feltenberger John David, Sena Guimarães André Luiz, Farias Lucyana Conceição
Department of Dentistry, Universidade Estadual de Montes Claros, Minas Gerais, Brazil.; Instituto Federal do Norte de Minas Gerais-Campus Araçuaí, Minas Gerais, Brazil.
Instituto Federal do Norte de Minas Gerais-Campus Salinas, Minas Gerais, Brazil.
Int J Mol Cell Med. 2016 Fall;5(4):199-219. Epub 2016 Dec 6.
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 Kruskal-Wallis 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. was identified as leader gene for AM. In KCOT group, results show and . 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.
牙源性肿瘤的发病机制尚不清楚。识别基因失调和分子改变很重要。本研究旨在通过生物信息学分析,调查可能参与成釉细胞瘤(AM)和牙源性角化囊性瘤(KCOT)发病机制的基因。在GeneCards中识别参与AM和KCOT发病机制的基因。扩展基因列表,并使用STRING软件绘制基因相互作用网络。计算“加权链接数”(WNL)以识别“主导基因”(最高WNL)。通过K均值法对基因进行排名,并使用Kruskal-Wallis检验(P<0.001)。还使用STRING数据库生成的所有相互作用数据计算总相互作用得分(TIS),以实现每个基因的全局连通性。使用Cytoscape软件和BinGO插件进行拓扑和本体分析。文献综述数据用于证实生物信息学数据。被确定为AM的主导基因。在KCOT组中,结果显示和。两种肿瘤均表现出幂律行为。我们的拓扑分析通过计算两种牙源性肿瘤的聚类系数(AM为0.028,KCOT为零),提示主导基因可能在AM和KCOT的发病机制中起重要作用。散点图中获得的结果表明这些基因与AM和KCOT中涉及的分子过程有重要关系。对AM和KCOT的本体分析显示了不同的机制。通过文献综述证实了生物信息学分析。这些结果可能提示有前景的基因参与其中,有助于更好地理解AM和KCOT的发病机制。