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Expression data from U2OS ER-E2F1 cells after FOXO knockdown and E2F1 activation

ABSTRACT: Effect of FOXO knockdown on E2F1-mediated transcription

ORGANISM(S): Homo sapiens

PROVIDER: GSE39136 | GEO | 2012/07/06

SECONDARY ACCESSION(S): PRJNA170072

REPOSITORIES: GEO

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Expression data from U2OS ER-E2F1 cells after FOXO knockdown and E2F1 activation

Project description:Effect of FOXO knockdown on E2F1-mediated transcription U2OS cells stably expressing ER-E2F1 were infected with two different lentiviruses both targeting FOXO1 and FOXO3 or control virus encoding scrambled sequence. Twenty four hours post infection medium was replaced to serum-free DMEM for 24 hours. Then medium was replaced to serum-free DMEM with or without 20 nM 4-hydroxy tamoxifen for 6 hours.

2012-07-05 | E-GEOD-39136 | biostudies-arrayexpress

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Foxo signaling declines with age

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Expression data from MxCre;E2F1-/-2-/-3f/f Cd11B myeloid cells

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Project description:Activity of Forkhead box O (FOXO) transcription factors is inhibited by PI3K-PKB/Akt signalling to control a variety of cellular processes including cell cycle progression. Through comparative analysis of a number of microarray datasets, we identified a set of genes commonly regulated by FOXO and PI3K/PKB, which includes Carboxyl-Terminal Domain Small Phosphatase 2 (CTDSP2). We validated CTDSP2 as a genuine FOXO target gene and show that ectopic CTDSP2 can induce cell cycle arrest. We analysed transcriptional regulation after CTDSP2 expression and identified extensive regulation of genes involved in cell cycle progression, which depends on the phosphatase activity of CTDSP2. Most notably regulated genes are p21Cip1/Waf1 and E2F1, both implicated in S-phase entry. We show that p21Cip1/Waf1 is regulated by CTDSP2 in a p53-independent manner and that p21Cip1/Waf1 upregulation results in decreased cyclin/CDK2 and cyclin/CDK6 activity. Thus, we identify FOXO-dependent CTDSP2 regulation as a novel regulatory mechanism for inhibiting proliferation in the absence of growth factor/PI3K signalling.

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