Quimbaya Gómez, Mauricio AlbertoCuevas Osorio, María José2025-09-182025-09-182024http://hdl.handle.net/11522/4867Every cancer cell has fundamental properties that confers them the ability of growing uncontrollably and adapt to their environment. Genomic instability (GI) is one of these characteristics and chromosomal instability is one of its main forms. Instability is reached because there are altered mechanisms that causes chromosome missegregation resulting in changes of chromosomes number and structure. The main mechanisms by which chromosomes are affected are by dysregulation of cell cycle checkpoint pathways. Certain genes are altered by this instability, impacting the cell cycle progression. Various circuits are proposed in Suescum and collaborators instability model, that represents the interactions between these proteins. In this study, the expression of two regulatory genes [INCENP and PLK1], present in the model, and linked with chromosomal instability is measured by qPCR analysis in HEK293 [embryonic kidney line] and HT-29 [colon adenocarcinoma model]. Additionally, the expression of key cell cycle genes [CDK1, CDC20, AURKB] is measured in the same cell lines to compare their expression regarding the dysregulation of PLK1 and INCENP genes. The results showed a decrease in the expression of studied genes in HT29 cell line in comparison to HEK293. Suggesting that evaluated cancer cells have reduced levels of expression in important mitotic genes.9 p.application/pdfspaCancerCell cycleGenetic instabilityCrhomosome missegregationGene expressionHEK293HT29bachelor thesishttps://creativecommons.org/licenses/by-nc-sa/4.0/http://purl.org/coar/access_right/c_abf2