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- W178765922 abstract "Proliferation of hematopoietic cells is governed by cytokine-regulated signaling pathways. We have previously shown that a cytokine-induced PI3K/AKT signaling pathway promotes CDK2 activation and overrides DNA damage-induced growth arrest in hematopoietic cells. In the present work, we have assessed the role of FOXO transcription factors as a potential intermediate in this signaling pathway. In this regard, overexpression of FOXO3a activity was found to reduce proliferation and CDK2 activity in cytokine-dependent hematopoietic cell lines. Moreover, enhanced FOXO activity potentiated the growth arrests that were induced by DNA damage and PI3K/AKT inhibition. By contrast, shRNA-knockdown of endogenous FOXO proteins attenuated the DNA damage-induced growth arrest in cells lacking PI3K/AKT activity. We also show that the ability of FOXO3a to inhibit cytokine-induced proliferation was dependent on expression of the CDK-inhibitor, p27. Together, these observations suggest that FOXO-mediated expression of p27 contributes to DNA damage-induced growth arrest, and that inhibition of this activity by cytokine-induced AKT can promote proliferation and override DNA damage checkpoints in hematopoietic cells. NIH Grant R01 CA79889" @default.
- W178765922 created "2016-06-24" @default.
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- W178765922 date "2008-03-01" @default.
- W178765922 modified "2023-09-27" @default.
- W178765922 title "FOXO transcription factors are required for DNA damage‐induced growth arrest checkpoints in hematopoietic cells" @default.
- W178765922 doi "https://doi.org/10.1096/fasebj.22.1_supplement.637.4" @default.
- W178765922 hasPublicationYear "2008" @default.
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