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Las células tumorales exhiben desregulación del factor promotor del gen histona del ciclo celular HiNF-D
J Holthuis1, T A Owen, A J van Wijnen
1Department of Cell Biology, University of Massachusetts Medical School, Worcester 01655.
Science (New York, N.Y.)
|March 23, 1990
Resumen
La regulación del ciclo celular de la transcripción del gen de la histona es crucial para el crecimiento celular normal. La actividad de unión aberrante de HiNF-D en las células cancerosas contribuye a la proliferación incontrolada y la pérdida de la regulación del crecimiento.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología celular Biología celular.
- Investigación del cáncer Investigación del cáncer.
Sus antecedentes:
- La expresión génica regulada por el ciclo celular es vital para el crecimiento y desarrollo celular normal.
- La pérdida del estricto control del crecimiento celular es un sello distintivo del fenotipo neoplásico transformado.
- La síntesis de la proteína histona durante la fase S es esencial para la replicación del ADN y el empaque de la cromatina.
Objetivo del estudio:
- Para investigar el papel de la actividad de unión HiNF-D en la transcripción del gen de la histona regulada por el ciclo celular.
- Para comparar la actividad de HiNF-D en células normales frente a células transformadas.
- Para dilucidar el vínculo potencial entre la actividad alterada de HiNF-D y la transformación neoplásica.
Principales métodos:
- Análisis de extractos de proteínas nucleares de las células en diferentes fases del ciclo celular.
- Análisis de la actividad de unión de HiNF-D al promotor del gen de la histona H4.
- Comparación de la actividad de HiNF-D en células diploides normales frente a líneas celulares derivadas de tumores o transformadas.
Principales resultados:
- Las células normales exhiben una actividad de unión HiNF-D dependiente del ciclo celular, que alcanza su punto máximo en la fase S.
- Las células transformadas muestran una actividad de unión HiNF-D constitutivamente elevada a lo largo del ciclo celular.
- La actividad de HiNF-D en las células transformadas solo disminuye con la diferenciación.
Conclusiones:
- La unión constitutiva alterada de HiNF-D al promotor del gen de la histona H4 se correlaciona con la pérdida de la regulación del crecimiento celular en el cáncer.
- Esta desregulación del HiNF-D puede ser un mecanismo clave que contribuye a la transformación neoplásica.
- Dirigir la actividad de HiNF-D podría ofrecer estrategias terapéuticas para el tratamiento del cáncer.
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