Gene Prioritization through Consensus Strategy, Enrichment Methodologies Analysis, and Networking for Osteosarcoma Pathogenesis
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Gene Prioritization through Consensus Strategy, Enrichment Methodologies Analysis, and Networking for Osteosarcoma PathogenesisAutor(es)
Fecha
2020-02-05Cita bibliográfica
Cabrera-Andrade A, López-Cortés A, Jaramillo-Koupermann G, Paz-y-Miño C, Pérez-Castillo Y, Munteanu CR, et al. Gene Prioritization through Consensus Strategy, Enrichment Methodologies Analysis, and Networking for Osteosarcoma Pathogenesis. Int. J. Mol. Sci. 2020; 21:1053.
Resumen
[Abstract] Osteosarcoma is the most common subtype of primary bone cancer, affecting mostly adolescents. In recent years, several studies have focused on elucidating the molecular mechanisms of this sarcoma; however, its molecular etiology has still not been determined with precision. Therefore, we applied a consensus strategy with the use of several bioinformatics tools to prioritize genes involved in its pathogenesis. Subsequently, we assessed the physical interactions of the previously selected genes and applied a communality analysis to this protein–protein interaction network. The consensus strategy prioritized a total list of 553 genes. Our enrichment analysis validates several studies that describe the signaling pathways PI3K/AKT and MAPK/ERK as pathogenic. The gene ontology described TP53 as a principal signal transducer that chiefly mediates processes associated with cell cycle and DNA damage response It is interesting to note that the communality analysis clusters several members involved in metastasis events, such as MMP2 and MMP9, and genes associated with DNA repair complexes, like ATM, ATR, CHEK1, and RAD51. In this study, we have identified well-known pathogenic genes for osteosarcoma and prioritized genes that need to be further explored.
Palabras clave
Gene prioritization
Osteosarcoma
Communality analysis
Pathogenesis
Early recognition
Osteosarcoma
Communality analysis
Pathogenesis
Early recognition
Versión del editor
Derechos
Atribución 3.0 España
ISSN
1422-0067
1661-6596
1424-6783
1661-6596
1424-6783