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La ciclosporina induce la progresión del cáncer por un mecanismo celular autónomo
M Hojo1, T Morimoto, M Maluccio
1Department of Transplantation Medicine and Extracorporeal Therapy, Weill Medical College of Cornell University, New York, New York 10021, USA.
Nature
|February 24, 1999
Resumen
La ciclosporina, un inmunosupresor, aumenta directamente la invasividad de las células cancerosas a través de un mecanismo celular autónomo, independiente de la inmunidad del huésped. Este proceso implica la transformación del factor de crecimiento beta (TGF-beta) y contribuye al aumento de la malignidad después del trasplante.
Área de la Ciencia:
- Oncología Oncología.
- Inmunología Inmunología.
- Biología celular Biología celular.
Sus antecedentes:
- La malignidad es un riesgo significativo después del trasplante de órganos, a menudo relacionado con la terapia inmunosupresora que afecta la inmunidad del huésped.
- Los mecanismos exactos por los cuales los inmunosupresores promueven la progresión del cáncer requieren una mayor aclaración.
Objetivo del estudio:
- Investigar un mecanismo potencial independiente de la inmunidad del huésped por el cual los inmunosupresores mejoran la malignidad.
- Explorar el papel de la ciclosporina en la inducción de cambios celulares que promueven la progresión del cáncer.
Principales métodos:
- Tratamiento de células de adenocarcinoma con ciclosporina (ciclosporina A) y análisis de cambios fenotípicos (morfología, motilidad, crecimiento independiente del anclaje).
- Evaluación del efecto de los anticuerpos monoclonales contra el factor de crecimiento transformador-beta (TGF-beta) en los cambios inducidos por la ciclosporina.
- Estudios in vivo con ratones beige SCID inmunodeficientes para evaluar el crecimiento tumoral y la metástasis después del tratamiento con ciclosporina, con o sin anticuerpos anti-TGF-beta.
Principales resultados:
- La ciclosporina indujo alteraciones morfológicas significativas, aumento de la motilidad y crecimiento independiente del anclaje en las células de adenocarcinoma, lo que indica una mayor invasividad.
- Estos cambios inducidos por ciclosporina fueron anulados por anticuerpos monoclonales anti-TGF-beta.
- In vivo, la ciclosporina promovió el crecimiento tumoral y la metástasis en ratones inmunodeficientes, un efecto evitado por los anticuerpos anti-TGF-beta.
Conclusiones:
- La ciclosporina promueve la progresión del cáncer a través de un mecanismo celular autónomo, independiente de la supresión inmunológica del huésped.
- La producción de factor de crecimiento transformador-beta (TGF-beta) inducida por ciclosporina juega un papel crítico en la mediación de este efecto pro-maligno.
- Estos hallazgos sugieren nuevas estrategias terapéuticas dirigidas al TGF-beta para mitigar el riesgo de cáncer asociado con los medicamentos inmunosupresores.
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