The NRF2 transcription factor plays a dual role in colorectal cancer: A systematic review

[EN] Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is import...

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Detalles Bibliográficos
Autores: Gonzalez Donquiles, C., Alonso Molero, J, Fernández Villa, Tania, Vilorio Marques, L., Molina de la Torre, Antonio José, Martín Sánchez, Vicente
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Institución:Universidad de León
Repositorio:BULERIA. Repositorio Institucional de la Universidad de León
OAI Identifier:oai:buleria.unileon.es:10612/22359
Acceso en línea:https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0177549
https://hdl.handle.net/10612/22359
Access Level:acceso abierto
Palabra clave:Medicina. Salud
colorectal cancer
Descripción
Sumario:[EN] Colorectal cancer is one of the most common cancers worldwide, and is influenced by the interplay of various factors, including a very strong genetic component. For instance, incorrect mitochondrial biogenesis is correlated with increased risk of developing colorectal cancer. Thus, it is important to understand the consequences of changes in both the expression and the correct function of the transcription factors that regulate mitochondrial biogenesis, namely NRF2.The main objective of this paper is to characterise the relationship between NRF2 and colorectal cancer by compiling data from an exhaustive literature search. Information was obtained by defining specific search terms and searching in several databases. After a strict selection procedure, data were tabulated and the relationships between articles were assessed by measuring heterogeneity and by constructing conceptual maps.The proper basal function of NRF2 and Keap1 are essential for preventing oncogenic processes in the colon. Consequently, any disruption to the expression of these genes can promote the genesis and progression of colon cancer.