4.8 Article

Targeting Mitotic Exit Leads to Tumor Regression In Vivo: Modulation by Cdk1, Mastl, and the PP2A/B55α,δ Phosphatase

Journal

CANCER CELL
Volume 18, Issue 6, Pages 641-654

Publisher

CELL PRESS
DOI: 10.1016/j.ccr.2010.10.028

Keywords

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Funding

  1. Ministerio de Ciencia e Innovacion (MICINN) [SAF2009-07973, CSD2007-00017]
  2. Marie Curie Cancer Care
  3. Association for International Cancer Research (AICR)
  4. Fundacion Cientifica de la Asociacion Espanola contra el Cancer
  5. Junta de Castilla y Leon Grupo de Excelencia [GP 265]
  6. Comunidad de Madrid [S-BIO-0283-2006]
  7. Fundacion Ramon Areces, AICR [08-0188]
  8. European Union [HEALTH-F5-2010-241548]
  9. [BFU2008-01808]
  10. [CSD2007-00015]
  11. Worldwide Cancer Research [09-0658] Funding Source: researchfish

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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 progenitor/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 from mitosis upon inactivation of Cdk1 and the kinase Mastl (Greatwall). This mitotic exit depends on the activity of PP2A phosphatase complexes containing B55 alpha or B55 delta regulatory subunits. These data illustrate the relevance of critical players of mitotic exit in mammals and their implications in the balance between cell death and mitotic exit in tumor cells.

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