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DCAF7 recluta USP2 para facilitar la progresión del carcinoma hepatocelular al suprimir la ferroptosis inducida por

Honglv Jiang¹, Xiaohui Wang¹, Zhenhua Zhu²

¹Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, Suzhou, Jiangsu, China.

Cell death & disease

|August 28, 2025

Resumen

El factor asociado DDB1- y CUL4 7 (DCAF7) y USP2 suprimen la ferroptosis en el cáncer de hígado. Dirigirse a estas proteínas inhibe el crecimiento del tumor promoviendo un tipo específico de muerte celular llamada clockophagy.

Área de la Ciencia:

En el campo de la oncología
Biología celular
Mecanismos moleculares

Sus antecedentes:

El factor 7 asociado a DDB1 y CUL7 (DCAF7) está implicado en la tumorigénesis y la ferroptosis.
No se comprende completamente el papel de DCAF7 en la progresión de la ferroptosis del carcinoma hepatocelular (HCC).
La ferroptosis es una forma de muerte celular regulada dependiente del hierro con implicaciones en el cáncer.

Objetivo del estudio:

Investigar la función de DCAF7 en la regulación de la ferroptosis del carcinoma hepatocelular (HCC).
Para explorar la relación entre DCAF7, USP2 y la clockophagy en HCC.
Identificar DCAF7 y USP2 como objetivos terapéuticos potenciales para el tratamiento del CHC.

Principales métodos:

Se ha evaluado la expresión de DCAF7 y USP2 en tejidos de HCC.
Se utilizó la ablación genética de DCAF7 y la inhibición farmacológica de USP2 en modelos de HCC.
Investigó el mecanismo que involucra DCAF7, USP2, ubiquitinación de BMAL1, clockophagy y el eje HIF1α-SLC7A11.

Principales resultados:

DCAF7 y USP2 están muy expresados en HCC.
La inhibición de DCAF7 o USP2 sensibiliza las células de HCC a la ferroptosis y reduce la progresión tumoral in vitro e in vivo.
DCAF7 recluta USP2 para reducir la ubiquitinación de BMAL1, inhibiendo así la clockophagy.

Conclusiones:

DCAF7 y USP2 actúan como nuevos supresores de la ferroptosis inducida por la clockophagy en el HCC.
La orientación hacia DCAF7 o USP2 promueve la ferroposis a través de la vía HIF1α-SLC7A11.
DCAF7 y USP2 representan objetivos terapéuticos potenciales para el carcinoma hepatocelular.

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