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La proteína supresora de menino tumoral es un cofactor oncogénico esencial para la leucemogénesis asociada a MLL
Akihiko Yokoyama1, Tim C P Somervaille, Kevin S Smith
1Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
Cell
|October 22, 2005
Resumen
Las proteínas de fusión de la leucemia oncogénica de linaje mixto (MLL) requieren interacción con el supresor tumoral menin para la leucemogénesis. La menina es esencial para la transformación mieloide impulsada por MLL y las alteraciones epigenéticas, validándola como un objetivo terapéutico potencial.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología del cáncer Biología del cáncer.
- La epigenética es la epigenética.
Sus antecedentes:
- La proteína de leucemia de linaje mixto (MLL) es una histona metiltransferasa implicada en la leucemia aguda.
- La MLL funciona dentro de un complejo que incluye el menin, un producto del gen supresor de tumores MEN1.
- Las mutaciones de MEN1 están relacionadas con tumores endocrinos.
Objetivo del estudio:
- Para investigar el papel de la interacción MLL-menina en la leucemogénesis mediada por MLL.
- Para determinar si el menin es esencial para el mantenimiento de la transformación mieloide impulsada por MLL.
- Explorar el papel de la menina en la desregulación epigenética en los cánceres asociados a la LLM.
Principales métodos:
- Demostración de una asociación estable entre las proteínas de fusión oncogénicas de MLL y el meningo.
- Evaluación de la necesidad de la interacción MLL-menina en la iniciación de la leucemogénesis.
- La ablación genética aguda del menino para observar los efectos en las células transformadas por MLL.
Principales resultados:
- Las proteínas de fusión oncogénicas de MLL se unen al menín a través de un motivo conservado, esencial para la leucemogénesis.
- La menina es crítica para mantener la transformación mieloide asociada a la MLL, pero no para otras transformaciones inducidas por oncogenes.
- La ablación de menina invierte la expresión aberrante del gen Hox y deroga las propiedades oncogénicas de los blastos transformados en MLL.
Conclusiones:
- Una oncoproteína humana (proteína de fusión MLL) depende críticamente de la interacción directa con un supresor tumoral (menina) para su actividad oncogénica.
- Menin es un objetivo potencial validado para la terapia molecular en leucemias impulsadas por MLL.
- Menin juega un papel central en las funciones epigenéticas alteradas subyacentes a la patogénesis del cáncer hematopoyético.
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