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La supresión tumoral en ausencia de detención del ciclo celular mediada por p53, apoptosis y senescencia

Tongyuan Li¹, Ning Kon, Le Jiang

¹Institute for Cancer Genetics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

|June 12, 2012

Resumen

La proteína supresora de tumores p53 normalmente detiene la formación de tumores a través de la detención del ciclo celular, la apoptosis y la senescencia. Sin embargo, este estudio revela que la p53

Área de la Ciencia:

Biología Molecular Biología Molecular
Investigación del cáncer Investigación del cáncer.
La tumorigénesis es la tumorigénesis.

Sus antecedentes:

La proteína supresora de tumores p53 es crucial para prevenir el cáncer.
Las funciones canónicas de p53 incluyen la detención del ciclo celular, la apoptosis y la senescencia.
El papel de la acetilación de p53 en estos mecanismos de supresión tumoral no se entiende completamente.

Objetivo del estudio:

Para investigar el papel de la acetilación de p53 en la supresión tumoral.
Para determinar si las funciones canónicas de p53 son limitantes de velocidad para la supresión tumoral.
Explorar funciones alternativas del p53 en la prevención de la tumorigénesis espontánea.

Principales métodos:

Se generaron ratones con mutaciones específicas en los sitios de acetilación de p53 (p53 (((K117R) y p53 ((3KR)).
Se evaluó la detención del ciclo celular mediada por p53, la apoptosis y la senescencia en células mutantes.
Monitoreo de la formación de tumores y supervivencia en ratones mutantes.
Se evaluó la regulación de p53 del metabolismo energético y las especies reactivas de oxígeno (ROS).

Principales resultados:

Las células p53 ((K117R/K117R) mantuvieron la detención del ciclo celular y la senescencia, pero perdieron la apoptosis.
Las células p53 ((3KR/3KR) perdieron las tres funciones canónicas de p53 (arrestamiento, apoptosis, senescencia).
Ni los ratones p53 ((K117R / K117R) ni los ratones p53 ((3KR / 3KR) desarrollaron tumores de inicio temprano.
p53(3KR) mantuvo la regulación metabólica y las funciones de eliminación de ROS.

Conclusiones:

La acetilación p53 modula diferencialmente sus funciones.
Las funciones canónicas de p53 no son limitantes de velocidad para la supresión espontánea del tumor.
Las actividades no canónicas de p53, como la regulación metabólica y la función antioxidante, son críticas para prevenir tumores de aparición temprana.

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