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Represión del gen del factor de crecimiento II parecido a la insulina por el supresor del tumor de Wilms WT1
I A Drummond1, S L Madden, P Rohwer-Nutter
1Howard Hughes Medical Institute, University of Chicago, IL 60637.
Science (New York, N.Y.)
|July 31, 1992
Resumen
El gen supresor del tumor de Wilms WT1 actúa como un represor, controlando la transcripción del factor de crecimiento similar a la insulina II (IGF-II). Este hallazgo explica la sobreexpresión de IGF-II en los tumores de Wilms y el papel de WT1 en el desarrollo renal.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología del desarrollo Biología del desarrollo.
- Genética del cáncer Genética del cáncer.
Sus antecedentes:
- El tumor de Wilms es un cáncer de riñón pediátrico a menudo asociado con la sobreexpresión del factor de crecimiento similar a la insulina II (IGF-II), un mitógeno fetal.
- El gen supresor del tumor de Wilms (WT1) codifica un factor de transcripción que por lo general actúa como un represor.
Objetivo del estudio:
- Investigar el mecanismo molecular por el cual WT1 regula la transcripción de IGF-II.
- Para determinar si WT1 reprime directamente el promotor de IGF-II y su papel en la patogénesis del tumor de Wilms.
Principales métodos:
- Se utilizaron ensayos de transfección transitoria para definir la principal región promotora fetal de IGF-II.
- La unión de WT1 al promotor de IGF-II se evaluó in vivo.
- Se emplearon ensayos de genes reporteros para medir la actividad represiva de WT1 en la transcripción de IGF-II.
Principales resultados:
- El principal promotor fetal de IGF-II fue mapeado a una región de nucleótidos de -295 a +135.
- Se encontró que WT1 se une a múltiples sitios dentro de esta región promotora.
- WT1 demostró una potente represión de la transcripción de IGF-II in vivo, con una represión máxima dependiente de los sitios de unión de WT1 que flanquean el sitio de inicio de la transcripción.
Conclusiones:
- WT1 reprime directamente el principal promotor fetal de IGF-II, proporcionando una explicación molecular para la sobreexpresión de IGF-II en los tumores de Wilms.
- WT1 regula negativamente la proliferación de células blastemales al limitar la producción de IGF-II durante el desarrollo renal.
- Estos hallazgos destacan un eje regulador crítico en el desarrollo renal y la tumorigénesis de Wilms.
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