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La transcripción de Nrf2 inducida por oncogenes promueve la desintoxicación de las ROS y la tumorigénesis
Gina M DeNicola1, Florian A Karreth, Timothy J Humpton
1Li Ka Shing Centre, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge CB2 0RE, UK.
Nature
|July 8, 2011
Resumen
Los oncogenes como Kras, Braf y Myc suprimen las especies reactivas del oxígeno (ROS) aumentando la vía del antioxidante Nrf2, promoviendo el desarrollo del cáncer. Dirigirse a Nrf2 inhibe el crecimiento tumoral impulsado por oncogenes.
Área de la Ciencia:
- Biología celular Biología celular.
- Oncología Oncología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Las especies reactivas de oxígeno (ROS) son mutagénicas y pueden promover el cáncer.
- La vía Nrf2 (Factor 2 relacionado con el factor eritroide 2 del factor nuclear) regula las respuestas antioxidantes.
- Se observa un aumento de la activación de Nrf2 en la neoplasia, lo que sugiere un papel pro-tumorigénico.
Objetivo del estudio:
- Investigar el metabolismo de los ROS en las células que expresan oncogenes.
- Determinar el papel de los oncogenes (Kras, Braf, Myc) en la regulación de la vía Nrf2.
- Explorar el potencial terapéutico de dirigirse a Nrf2 en la oncogénesis.
Principales métodos:
- Utilizó células murinas primarias que expresan los alelos oncogénicos Kras, Braf y Myc.
- Evaluación de los niveles de ROS y la transcripción de Nrf2.
- Genéticamente dirigido a la vía Nrf2 in vivo.
Principales resultados:
- Los oncogenes Kras, Braf y Myc suprimieron activamente las ROS.
- Los oncogenes aumentaron la transcripción de Nrf2, elevando el programa antioxidante basal.
- La orientación genética de Nrf2 alteró la proliferación inducida por K-Ras ((G12D) y la tumorigénesis.
Conclusiones:
- La activación de Nrf2 inducida por oncogenes es un nuevo mecanismo que promueve el cáncer.
- El programa antioxidante Nrf2 es un mediador no reconocido previamente de la oncogénesis.
- Dirigirse a Nrf2 puede ser una estrategia viable para la terapia del cáncer.
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