Hec1 overexpression hyperactivates the mitotic checkpoint and induces tumor formation in vivo
[EN]Hec1 (Highly Expressed in Cancer 1) is one of four proteins of the outer kinetochore Ndc80 complex involved in the dynamic interface between centromeres and spindle microtubules. Its overexpression is seen in a variety of human tumors and correlates with tumor grade and prognosis. We show here t...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2008 |
| País: | España |
| Institución: | Universidad de Salamanca (USAL) |
| Repositorio: | GREDOS. Repositorio Institucional de la Universidad de Salamanca |
| OAI Identifier: | oai:gredos.usal.es:10366/167952 |
| Acceso en línea: | http://hdl.handle.net/10366/167952 |
| Access Level: | acceso abierto |
| Palabra clave: | Aneuploidy Cancer Chromosome instability Kinetochores Mitosis Chromosomal Instability Doxycycline Microtubule-Associated Proteins Gene Expression Regulation Neoplasms Nuclear Proteins Tissue Distribution Animals Cell Cycle Proteins Mice 2302 Bioquímica inestabilidad cromosómica proteínas asociadas a microtúbulos neoplasias mitosis ratones proteínas nucleares aneuploidía cinetocoros regulación de la expresión génica animales distribución tisular doxiciclina proteínas del ciclo celular |
| Sumario: | [EN]Hec1 (Highly Expressed in Cancer 1) is one of four proteins of the outer kinetochore Ndc80 complex involved in the dynamic interface between centromeres and spindle microtubules. Its overexpression is seen in a variety of human tumors and correlates with tumor grade and prognosis. We show here that the overexpression of Hec1 in an inducible mouse model results in mitotic checkpoint hyperactivation. As previously observed with overexpression of the Mad2 gene, hyperactivation of the mitotic checkpoint leads to aneuploidy in vitro and is sufficient to generate tumors in vivo that harbor significant levels of aneuploidy. These results underscore the role of chromosomal instability as a result of mitotic checkpoint hyperactivation in the initiation of tumorigenesis. |
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