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USF2 regula la vía JAK2/STAT3 a través de la regulación al alza de SLC25A17 mediada por PEX3 para afectar el
Huifeng Wang1, Yanyan Sun2, Rui Zi1
1The First Department of Oncology, Tumor Hospital, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, Yinchuan 750003, PR China.
Toxicology and applied pharmacology
|August 30, 2025
Resumen
El Factor estimulador aguas arriba 2 (USF2) impulsa el cáncer de pulmón promoviendo el metabolismo lipídico anormal a través de PEX3 y SLC25A17, activando la vía JAK2 / STAT3 y aumentando el crecimiento tumoral.
Área de la Ciencia:
- En el campo de la oncología
- Biología molecular
- La bioquímica
Sus antecedentes:
- El factor estimulador aguas arriba 2 (USF2) está implicado en el cáncer, pero su papel en la patogénesis del adenocarcinoma pulmonar (LUAD) no está claro.
- Comprender los mecanismos moleculares de USF2 es crucial para desarrollar terapias dirigidas a LUAD.
Objetivo del estudio:
- Para aclarar la función y los mecanismos moleculares de USF2 en el adenocarcinoma pulmonar (LUAD).
- Investigar el papel de USF2 en la regulación del metabolismo de los lípidos y la progresión del cáncer en las células LUAD.
Principales métodos:
- Se analizó la expresión de USF2 en tejidos y células LUAD.
- Realizó experimentos de eliminación de genes y sobreexpresión en células A549.
- Se investigó la interacción de USF2 con el promotor de PEX3 y el papel de PEX3 en el metabolismo de los lípidos.
- Se examinó la participación de SLC25A17 y la vía JAK2/STAT3.
- Se utilizó un modelo de ratón xenograft para evaluar el crecimiento tumoral y el metabolismo lipídico in vivo.
Principales resultados:
- USF2 fue regulado al alza en LUAD y su knockdown inhibió la proliferación, la invasión y la apoptosis inducida en las células A549.
- La sobreexpresión de USF2 condujo a un metabolismo lipídico anormal mediante la regulación al alza de PEX3 y posteriormente de SLC25A17.
- SLC25A17 activó la vía JAK2/ STAT3, promoviendo la acumulación de lípidos y el crecimiento tumoral.
- La eliminación de USF2 suprimió el crecimiento tumoral y el metabolismo lipídico anormal en un modelo de xenotransplante.
Conclusiones:
- USF2 promueve la progresión de la LUAD al mejorar la señalización JAK2/ STAT3 mediada por SLC25A17 a través de la activación transcripcional de PEX3.
- Este mecanismo exacerba el metabolismo lipídico anormal, contribuyendo al desarrollo de la LUAD.
- USF2 representa un objetivo terapéutico potencial para el adenocarcinoma pulmonar.
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