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Targeting mitotic exit leads to tumor regression in vivo: Modulation by Cdk1, Mastl, and the PP2A/B55α,δ phosphatase

Reference: Cancer Cell. 2010 Dec 14;18(6):641-54. Targeting mitotic exit leads to tumor regression in vivo: Modulation by Cdk1, Mastl, and the PP2A/B55α,δ phosphatase
Authors: Manchado E, Guillamot M, de Cárcer G, Eguren M, Trickey M, García-Higuera I, Moreno S, Yamano H, Cañamero M, Malumbres M.
Summary: Targeting mitotic exit has been recently proposed as a relevant therapeutic approach against cancer. By using genetically engineered mice we show that the APC/C cofactor Cdc20 is essential for anaphase onset in vivo in embryonic or adult cells, including progenitors/stem cells. Ablation of Cdc20 results in efficient regression of aggressive tumors whereas current mitotic drugs display limited effects. Yet, Cdc20-null cells can exit upon concomitant inactivation of Cdk1 and the kinase Mastl (Greatwall). This mitotic exit depends on the activity of PP2A phosphatase complexes containing B55α or B55δ regulatory subunits. These data reveal critical players of mitotic exit in mammals and provide new avenues for manipulating the balance between apoptotic cell death and mitotic exit in tumor cells.
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REFERENCIA DEL GRUPO E INVESTIGADOR
Eusebio Manchado está realizando la Tesis Doctoral en el grupo de División Celular y Cáncer dirigido por el Dr. Marcos Malumbres en el Centro Nacional de Investigaciones Oncológicas (CNIO). En la actualidad el trabajo del grupo se centra fundamentalmente en el estudio de los principales reguladores mitóticos y su posible implicación en cáncer mediante el desarrollo de modelos de ratón modificados genéticamente.

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