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La inactivación irreversible de APC (Cdh1) subyace al punto de no retorno para la entrada en el ciclo celular

Steven D Cappell¹, Mingyu Chung¹, Ariel Jaimovich¹

¹Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.

|July 2, 2016

Resumen

El compromiso del ciclo celular, crucial para el cáncer, está determinado por la inactivación del complejo promotor de anafase/ciclosoma (APC/Cdh1). Este interruptor irreversible impide que las células vuelvan a la quiescencia después de que comience la replicación del ADN.

Área de la Ciencia:

Biología celular
Biología molecular
La bioquímica

Sus antecedentes:

La proliferación celular requiere un punto de compromiso antes de la replicación y división del ADN.
La fosforilación de la proteína del retinoblastoma (Rb) es un mediador propuesto de esta decisión.
La desregulación del ciclo celular contribuye al cáncer y las enfermedades degenerativas.

Objetivo del estudio:

Identificar el mecanismo molecular que actúa como punto de compromiso irreversible para la entrada en el ciclo celular.
Investigar el papel del complejo promotor de anafase/ciclosoma (APC/Cdh1) en el compromiso del ciclo celular.
Determinar el tiempo y la reversibilidad del punto de compromiso en respuesta al estrés celular.

Principales métodos:

Análisis del ciclo celular
Ensayos de fosforilación de las proteínas
Análisis de la actividad APC/Cdh1
Experimentos de inducción de la tensión celular

Principales resultados:

La inactivación de APC/Cdh1 funciona como el punto irreversible de no retorno para la entrada en el ciclo celular.
La inactivación de APC/Cdh1 es un cambio rápido y bistable iniciado por la ciclina E/Cdk2 y estabilizado por Emi1.
El estrés celular aplicado antes de la inactivación de APC / Cdh1 permite que las células vuelvan a la quiescencia; el estrés después no lo hace.

Conclusiones:

La inactivación de APC / Cdh1 es el punto crítico de compromiso, lo que hace que las células no puedan volver a la quiescencia.
Este hallazgo aclara la base molecular del compromiso del ciclo celular y sus implicaciones para la enfermedad.
Comprender este cambio proporciona información sobre posibles objetivos terapéuticos para el tratamiento del cáncer.

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