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AFX-like Forkhead transcription factors mediate cell-cycle regulation by Ras and PKB through p27kip1

Author

Listed:
  • René H. Medema

    (Jordan Laboratory G03-647)

  • Geert J. P. L. Kops

    (University Medical Center)

  • Johannes L. Bos

    (University Medical Center)

  • Boudewijn M. T. Burgering

    (University Medical Center)

Abstract

The Forkhead transcription factors AFX, FKHR and FKHR-L1 are orthologues of DAF-16, a Forkhead factor that regulates longevity in Caenorhabditis elegans1,2,3. Here we show that overexpression of these Forkhead transcription factors causes growth suppression in a variety of cell lines, including a Ras-transformed cell line and a cell line lacking the tumour suppressor PTEN. Expression of AFX blocks cell-cycle progression at phase G1, independent of functional retinoblastoma protein (pRb) but dependent on the cell-cycle inhibitor p27kip1. Indeed, AFX transcriptionally activates p27kip1, resulting in increased protein levels. We conclude that AFX-like proteins are involved in cell-cycle regulation and that inactivation of these proteins is an important step in oncogenic transformation.

Suggested Citation

  • René H. Medema & Geert J. P. L. Kops & Johannes L. Bos & Boudewijn M. T. Burgering, 2000. "AFX-like Forkhead transcription factors mediate cell-cycle regulation by Ras and PKB through p27kip1," Nature, Nature, vol. 404(6779), pages 782-787, April.
    • Handle: RePEc:nat:nature:v:404:y:2000:i:6779:d:10.1038_35008115
    DOI: 10.1038/35008115
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    Cited by:

    1. Alison E. Smith & Emanuela Ferraro & Anton Safonov & Cristina Bernado Morales & Enrique J. Arenas Lahuerta & Qing Li & Amanda Kulick & Dara Ross & David B. Solit & Elisa Stanchina & Jorge Reis-Filho &, 2021. "HER2 + breast cancers evade anti-HER2 therapy via a switch in driver pathway," Nature Communications, Nature, vol. 12(1), pages 1-10, December.
    2. Veronica Ulici & Claudine G James & Katie D Hoenselaar & Frank Beier, 2010. "Regulation of Gene Expression by PI3K in Mouse Growth Plate Chondrocytes," PLOS ONE, Public Library of Science, vol. 5(1), pages 1-11, January.

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