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Foxa1 y Foxa2 son esenciales para el dimorfismo sexual en el cáncer de hígado
Zhaoyu Li1, Geetu Tuteja, Jonathan Schug
1Department of Genetics and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Cell
|January 24, 2012
Resumen
El carcinoma hepatocelular (HCC) muestra diferencias sexuales, con los hombres más afectados. Los factores Foxa1/2 son cruciales para los efectos de las hormonas sexuales en el desarrollo del cáncer de hígado en ratones y humanos.
Área de la Ciencia:
- Hepatología Hepatología.
- Biología Molecular Biología Molecular
- Endocrinología Endocrinología.
Sus antecedentes:
- El carcinoma hepatocelular (HCC) exhibe un dimorfismo sexual significativo, con una mayor incidencia en los hombres.
- Los mecanismos moleculares subyacentes que involucran a las hormonas sexuales siguen siendo en gran medida desconocidos.
Objetivo del estudio:
- Investigar el papel de los factores de transcripción Foxa1 y Foxa2 en la regulación dependiente de las hormonas sexuales del carcinoma hepatocelular (HCC).
Principales métodos:
- Utilizó la hepatocarcinogénesis inducida por dietilnitrosamina en ratones de tipo salvaje y ratones con deficiencia de Foxa1/a2.
- Análisis de la corregulación de genes diana por Foxa1/a2 con el receptor de estrógenos (ERα) y el receptor de andrógenos (AR).
- Examinó los polimorfismos de un solo nucleótido (SNPs) en los sitios de unión a FOXA2 en muestras de hígado humano.
Principales resultados:
- El HCC sexualmente dimórfico se revirtió en ratones con deficiencia de Foxa1/a2.
- La corregulación de los genes diana por Foxa1/a2 y ERα/AR se perdió en ratones con deficiencia.
- Los SNPs en los sitios de unión a FOXA2 redujeron la unión a FOXA2 y ERα en el hígado humano y se correlacionaron con HCC en mujeres.
Conclusiones:
- Los factores Foxa1/a2 son esenciales tanto para la resistencia mediada por estrógenos como para la facilitación mediada por andrógenos del CHC.
- Los factores foxa y sus dianas juegan un papel central en el dimorfismo sexual del carcinoma hepatocelular.
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