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Molecular and Cellular Biology, December 2000, p. 8969-8982, Vol. 20, No. 23
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Forkhead Transcription Factors Are Critical Effectors of Cell Death and Cell Cycle Arrest Downstream of PTEN

Noriaki Nakamura,1,2 Shivapriya Ramaswamy,1,2 Francisca Vazquez,1,2 Sabina Signoretti,1,3 Massimo Loda,1,3 and William R. Sellers1,2,*

Department of Adult Oncology, Dana-Farber Cancer Institute,1 and Departments of Internal Medicine2 and Pathology,3 Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115

Received 24 April 2000/Returned for modification 13 June 2000/Accepted 21 August 2000

PTEN acts as a tumor suppressor, at least in part, by antagonizing phosphoinositide 3-kinase (PI3K)/Akt signaling. Here we show that Forkhead transcription factors FKHRL1 and FKHR, substrates of the Akt kinase, are aberrantly localized to the cytoplasm and cannot activate transcription in PTEN-deficient cells. Restoration of PTEN function restores FKHR to the nucleus and restores transcriptional activation. Expression of a constitutively active form of FKHR that cannot be phosphorylated by Akt produces the same effect as reconstitution of PTEN on PTEN-deficient tumor cells. Specifically, activated FKHR induces apoptosis in cells that undergo PTEN-mediated cell death and induces G1 arrest in cells that undergo PTEN-mediated cell cycle arrest. Furthermore, both PTEN and constitutively active FKHR induce p27KIP1 protein but not p21. These data suggest that Forkhead transcription factors are critical effectors of PTEN-mediated tumor suppression.

* Corresponding author. Mailing address: Dana-Farber Cancer Institute, D720C, 44 Binney St., Boston, MA 02115. Phone: (617) 632-5261. Fax: (617) 632-5417. E-mail: William_Sellers{at}dfci.harvard.edu.

Molecular and Cellular Biology, December 2000, p. 8969-8982, Vol. 20, No. 23
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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