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La señalización de la quinasa oncogénica
1The Salk Institute, Molecular and Cell Biology Laboratory, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. blume@salk.edu
Nature
|May 18, 2001
Resumen
Las kinasas de proteína-tirosina (PTK) regulan la señalización celular, pero su desregulación impulsa el cáncer. Esta revisión detalla cómo las vías aberrantes PI(3)K/Akt y mTOR/p70S6K contribuyen a las malignidades humanas.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- La señalización celular de las células.
- Oncología Oncología.
Sus antecedentes:
- Las kinasas de proteína-tirosina (PTK) son críticas para la comunicación y el desarrollo celular.
- La actividad de la PTK está normalmente estrictamente regulada; la desregulación conduce a la transformación maligna.
- Los principales efectores aguas abajo incluyen la fosfoinositida 3-OH quinasa (PI(3) K) y Akt/p70S6K.
Objetivo del estudio:
- Revisar cómo surgen las PTK oncogénicas a partir de controles autoinhibidores interrumpidos.
- Para actualizar el conocimiento sobre la señalización desregulada de PI(3)K/Akt y mTOR/p70S6K en cánceres humanos.
Principales métodos:
- Revisión de la literatura sobre las vías de señalización de PTK.
- Análisis de las alteraciones genéticas que afectan la actividad de la quinasa.
- Centrarse en las vías PI(3)K/Akt y mTOR/p70S6K en el cáncer.
Principales resultados:
- Las PTK oncogénicas resultan de la pérdida de la autoinhibición normal.
- La señalización desregulada de PI(3)K/Akt es un mecanismo común en el cáncer.
- La señalización aberrante mTOR/p70S6K también contribuye significativamente a las neoplasias malignas.
Conclusiones:
- Comprender la desregulación de PTK es crucial para la terapia del cáncer.
- Dirigirse a las vías PI(3)K/Akt y mTOR/p70S6K ofrece un potencial terapéutico.
- Se necesita más investigación sobre la regulación de la quinasa para el tratamiento del cáncer.
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