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El andamio del complejo SMAD3 y p300 por el ARN largo no codificante LIMD1-AS1 promueve la plasticidad de las células
Chuannan Fan1, Davy Cats2, Miriam Selle3
1Oncode Institute and Department of Cell and Chemical Biology, Leiden University Medical Center,Leiden, 2300 RC, the Netherlands.
Nucleic acids research
|September 1, 2025
Resumen
Un ARN largo no codificante recién descubierto, LIMD1-AS1, amplifica la señalización de TGF-β en el cáncer de mama. Esta molécula promueve la plasticidad de las células tumorales y un mal pronóstico, ofreciendo un potencial objetivo terapéutico.
Área de la Ciencia:
- Biología molecular
- Investigación del cáncer
- La epigenética
Sus antecedentes:
- La señalización del factor de crecimiento transformador (TGF) -β impulsa la plasticidad de las células cancerosas a través de la transición epitelial a mesenquimal (EMT).
- La comprensión de los mecanismos reguladores de la señalización de TGF-β es crucial para el desarrollo de terapias dirigidas al cáncer.
Objetivo del estudio:
- Identificar y caracterizar nuevos reguladores de la señalización del TGF-β en el cáncer de mama.
- Investigar el papel de LIMD1 Antisense RNA 1 (LIMD1-AS1) en la EMT inducida por TGF-β y la progresión del cáncer de mama.
Principales métodos:
- PCR cuantitativa en tiempo real para evaluar la expresión de LIMD1-AS1.
- Pruebas celulares para evaluar la EMT, la migración y la extravasación.
- Ensayos de unión al ARN y co-inmunoprecipitación para determinar las interacciones moleculares.
- Inhibición farmacológica de la actividad de la acetiltransferasa p300.
Principales resultados:
- La expresión de LIMD1-AS1 está regulada al alza en el cáncer de mama y se correlaciona con un mal pronóstico.
- El agotamiento de LIMD1-AS1 inhibe la EMT inducida por TGF-β, la migración y la extravasación.
- LIMD1-AS1 mejora la actividad transcripcional de SMAD3 promoviendo su interacción con p300.
- La inhibición de p300 o el desplazamiento de LIMD1-AS1 interrumpe la señalización de TGF-β/SMAD y la EMT.
Conclusiones:
- LIMD1-AS1 actúa como un regulador positivo de la señalización TGF-β/SMAD, creando un circuito de retroalimentación que mejora la plasticidad de las células de cáncer de mama.
- LIMD1-AS1 representa un objetivo terapéutico potencial para el tratamiento del cáncer de mama.
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