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Los defectos de la barrera asociados al adenoma y los productos microbianos impulsan el crecimiento tumoral mediado
Sergei I Grivennikov1, Kepeng Wang, Daniel Mucida
1Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, California 92093-0723, USA.
Nature
|October 5, 2012
Resumen
El crecimiento del cáncer colorrectal es impulsado por la inflamación. Los cambios genéticos en los tumores permiten que los productos microbianos entren, lo que desencadena una inflamación que promueve la progresión del tumor, incluso sin enfermedad inflamatoria intestinal.
Área de la Ciencia:
- Oncología Oncología.
- Inmunología Inmunología.
- Gastroenterología y Gastroenterología.
Sus antecedentes:
- El cáncer colorrectal (CRC) a menudo se desarrolla sin enfermedad inflamatoria intestinal, pero exhibe firmas genéticas inflamatorias y se infiltra.
- La inflamación provocada por el tumor, en particular la que involucra a las células T-helper interleucina-17 (T(H) 17 , está relacionada con una pobre supervivencia de la CCR.
- Los mecanismos que impulsan la inflamación provocada por el tumor en el CCR siguen siendo poco conocidos.
Objetivo del estudio:
- Investigar los mecanismos que impulsan la inflamación provocada por el tumor en el cáncer colorrectal.
- Para aclarar el papel de la interleucina-23 (IL-23) y la interleucina-17 (IL-17) en la tumorigénesis del CCR.
- Explorar el impacto de la integridad de la barrera epitelial en el desarrollo de la CRC.
Principales métodos:
- Utilizó un modelo de ratón de tumorigénesis colorrectal.
- Expresión génica analizada, incluyendo firmas inflamatorias y proteínas de barrera.
- Investigó el papel de las vías de señalización IL-23/IL-17.
- Examinó las infiltraciones de células inmunes y su activación.
Principales resultados:
- La señalización de IL-23 promueve significativamente el crecimiento, la progresión y el desarrollo de una respuesta tumoral a IL-17.
- Las células mieloides asociadas al tumor, activadas por productos microbianos que penetran en el tumor, son la fuente principal de IL-23.
- Se observó una expresión defectuosa de las proteínas de barrera en las neoplasias colorrectales tempranas y tardías, lo que facilita la invasión microbiana.
Conclusiones:
- El deterioro de la barrera epitelial, inducido por lesiones genéticas que inician el cáncer, permite que los productos microbianos invadan los tumores.
- Esta invasión desencadena una inflamación provocada por el tumor, mediada por IL-23 e IL-17, que posteriormente impulsa el crecimiento y la progresión del tumor.
- La comprensión de estos mecanismos ofrece objetivos terapéuticos potenciales para el CCR.
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