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Evolución selectiva del mesénquima estromal con pérdida de p53 en respuesta a la tumorigénesis epitelial
Reginald Hill1, Yurong Song, Robert D Cardiff
1Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Cell
|December 20, 2005
Resumen
La progresión del cáncer implica más que sólo las células tumorales. El estrés epitelial puede seleccionar de manera no autónoma las mutaciones de los fibroblastos, específicamente la pérdida de p53, en el microambiente tumoral.
Área de la Ciencia:
- Oncología Oncología.
- Biología del cáncer Biología del cáncer.
- Investigación del microambiente tumoral Investigación del microambiente tumoral
Sus antecedentes:
- La comprensión del cáncer tradicionalmente se centra en las aberraciones de las células tumorales.
- El microambiente tumoral, incluidos los fibroblastos, influye significativamente en la tumorigénesis.
- La evidencia sugiere una selección no autónoma de cambios genéticos / epigenéticos en las células estomales durante la progresión tumoral.
Objetivo del estudio:
- Para evaluar experimentalmente si los fibroblastos sufren cambios genéticos / epigenéticos debido al estrés oncogénico del epitelio.
- Investigar el papel de la comunicación intercelular en la conducción de las aberraciones de las células del estroma durante el desarrollo del cáncer.
Principales métodos:
- Utilizó un modelo de ratón de cáncer de próstata.
- Interrupción del ciclo celular epitelial inducida por la inhibición de la función de pRb.
- Analizó la respuesta de señalización paracrina en los fibroblastos asociados.
- Se evaluó la proliferación de fibroblastos y el estado de p53 bajo presión selectiva.
Principales resultados:
- La interrupción del ciclo celular epitelial desencadenó una respuesta paracrina p53 en los fibroblastos.
- Esta señalización paracrina suprimió la proliferación normal de los fibroblastos.
- Se ejerció una fuerte presión selectiva sobre el estroma.
- El mesenquima resultante exhibió una alta proliferación y pérdida de p53 adquirida.
Conclusiones:
- La comunicación intercelular dentro del microambiente tumoral impulsa la selección no autónoma de las aberraciones del estroma.
- El estrés oncogénico en el epitelio puede conducir a la selección de la pérdida de genes supresores de tumores (p53) en los fibroblastos.
- Este mecanismo contribuye a la progresión tumoral al alterar el compartimiento de los fibroblastos.
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