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Contributions of Rad9 to tumorigenesis.
Broustas, Constantinos G; Lieberman, Howard B.
Afiliación
  • Broustas CG; Center for Radiological Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
J Cell Biochem ; 113(3): 742-51, 2012 Mar.
Article en En | MEDLINE | ID: mdl-22034047
Rad9 plays a crucial role in maintaining genomic stability by regulating cell cycle checkpoints, DNA repair, telomere stability, and apoptosis. Rad9 controls these processes mainly as part of the heterotrimeric 9-1-1 (Rad9-Hus1-Rad1) complex. However, in recent years it has been demonstrated that Rad9 can also act independently of the 9-1-1 complex as a transcriptional factor, participate in immunoglobulin class switch recombination, and show 3'-5' exonuclease activity. Aberrant Rad9 expression has been associated with prostate, breast, lung, skin, thyroid, and gastric cancers. High expression of Rad9 is causally related to, at least, human prostate cancer growth. On the other hand, deletion of Mrad9, the mouse homolog, is responsible for increased skin cancer incidence. These results reveal that Rad9 can act as an oncogene or tumor suppressor. Which of the many functions of Rad9 are causally related to initiation and progression of tumorigenesis and the mechanistic details by which Rad9 induces or suppresses tumorigenesis are presently not known, but are crucial for the development of targeted therapeutic interventions.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transformación Celular Neoplásica / Proteínas de Ciclo Celular Límite: Animals / Humans Idioma: En Revista: J Cell Biochem Año: 2012 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transformación Celular Neoplásica / Proteínas de Ciclo Celular Límite: Animals / Humans Idioma: En Revista: J Cell Biochem Año: 2012 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos