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Microarray and bioinformatic analysis of conventional ameloblastoma: an observational analysis

Ameloblastoma is a highly aggressive odontogenic tumor, and its pathogenesis is associated with many participating genes. OBJECTIVE: We aimed to identify and validate new critical genes of conventional ameloblastoma using microarray and bioinformatics analysis. METHODOLOGY: Gene expression microarra...

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Detalles Bibliográficos
Autores principales: JACINTO-ALEMÁN, Luis Fernando, PORTILLA-ROBERTSON, Javier, LEYVA-HUERTA, Elba Rosa, RAMÍREZ-JARQUÍN, Josué Orlando, VILLANUEVA-SÁNCHEZ, Francisco Germán
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Faculdade De Odontologia De Bauru - USP 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9882959/
http://dx.doi.org/10.1590/1678-7757-2022-0308
Descripción
Sumario:Ameloblastoma is a highly aggressive odontogenic tumor, and its pathogenesis is associated with many participating genes. OBJECTIVE: We aimed to identify and validate new critical genes of conventional ameloblastoma using microarray and bioinformatics analysis. METHODOLOGY: Gene expression microarray and bioinformatic analysis were performed using CHIP H10KA and DAVID software for enrichment. Protein-protein interactions (PPI) were visualized using STRING-Cytoscape with MCODE plugin, followed by Kaplan-Meier and GEPIA analyses that were used for the candidate’s postulation. RT-qPCR and IHC assays were performed to validate the bioinformatic approach. RESULTS: 376 upregulated genes were identified. PPI analysis revealed 14 genes that were validated by Kaplan-Meier and GEPIA resulting in PDGFA and IL2RA as candidate genes. The RT-qPCR analysis confirmed their intense expression. Immunohistochemistry analysis showed that PDGFA expression is parenchyma located. CONCLUSION: With bioinformatics methods, we can identify upregulated genes in conventional ameloblastoma, and with RT-qPCR and immunoexpression analysis validate that PDGFA could be a more specific and localized therapeutic target.