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Un mecanismo de inmunovigilancia controla la ploidía de las células cancerosas
Laura Senovilla1, Ilio Vitale, Isabelle Martins
1INSERM, U848, Villejuif, France.
Science (New York, N.Y.)
|September 29, 2012
Resumen
Las células cancerosas con cromosomas adicionales (tetraploidización) se vuelven visibles para el sistema inmunológico debido al estrés del retículo endoplasmático y la exposición a la calreticulina. El sistema inmunológico luego elimina estas células hiperploides, impidiendo el crecimiento tumoral.
Área de la Ciencia:
- Oncología Oncología.
- Inmunología Inmunología.
- Biología celular Biología celular.
Sus antecedentes:
- Las células cancerosas acumulan alteraciones genéticas para evadir los mecanismos de supresión.
- La tetraploidización (células con cuatro conjuntos de cromosomas) contribuye a la oncogénesis debido a la inestabilidad genómica.
- Las células cancerosas hiperploides pueden convertirse en inmunogénicas a través del estrés del retículo endoplasmático y la exposición a la calreticulina.
Objetivo del estudio:
- Investigar el papel de la hiperploidía y la vigilancia inmune en el desarrollo del cáncer.
- Comprender los mecanismos por los cuales las células cancerosas hiperploides son reconocidas y eliminadas por el sistema inmunológico.
Principales métodos:
- Estudios in vivo con ratones inmunodeficientes y inmunocompetentes.
- Análisis del contenido de ADN, los marcadores de estrés del retículo endoplasmático y la exposición a la calreticulina en las células cancerosas.
- Ensayos de tumorigénesis con células cancerosas hiperploides.
Principales resultados:
- Las células cancerosas hiperploides con estrés en el retículo endoplasmático y exposición a la calreticulina proliferaron en ratones inmunodeficientes.
- En ratones inmunocompetentes, la formación de tumores a partir de células hiperploides se retrasó.
- Los tumores que se formaron en ratones inmunocompetentes mostraron un contenido reducido de ADN, estrés en el retículo endoplasmático y exposición a la calreticulina.
Conclusiones:
- Un nuevo mecanismo de inmunovigilancia se dirige y elimina las células cancerosas hiperploides.
- La selección inmune impone presión contra la inestabilidad genómica en el cáncer.
- Este hallazgo pone de relieve el potencial de dirigir las respuestas inmunes contra los tumores hiperploides.
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