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SOX4 is an upstream transcriptional regulator of FOXC1 in acute myeloid leukemia [4C-seq]

ABSTRACT: SOX4 is an upstream transcriptional regulator of FOXC1 in acute myeloid leukemia [4C-seq]

PROVIDER: PRJNA729509 | ENA |

REPOSITORIES: ENA

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SOX4 is an upstream transcriptional regulator of FOXC1 in acute myeloid leukemia [ATAC-seq]

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Proteomic Analysis of Foxc1-interacting proteins in HEK293T cells

Project description:Foxc1 has been identified to participate in regulating genes expression directly by binding their promoters as well as playing various roles in signal transduction within the cells. In this study, we found that, in F9 Embryonal Carcinoma cells, Foxc1 repressed the promoter’s transcription activity by binding the region of 1Kb upstream of Transcription Start Site within Nanog promoter.To understand more functions of Foxc1, streptavidin-biotin affinity purification combined with Liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) analysis was carried out.Bioinformatic analysis identified 360 proteins which may act as Foxc1 interactors.

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Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFÎ²-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2. Our Dataset comprises of 12 ChIP-seq samples using chromatin from NMuMG cells which was immunoprecipitated using H3K27me3-specific antibody during TGFÎ²-induced EMT (2ng/ml) at 6 different stages (day 0, 1, 4, 7, 10, 20).

2013-06-20 | E-GEOD-45579 | biostudies-arrayexpress

SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice [ChIP-Seq]

Project description:Brown adipose tissue (BAT) is critical for non-shivering thermogenesis making it a promising therapeutical strategy to combat obesity and metabolic disease. However, the regulatory mechanisms underlying brown fat formation remain incompletely understood. Here, we found SOX4 is required for BAT development and thermogenic program. Depletion of SOX4 in BAT progenitors (Sox4-MKO) or brown adipocytes (Sox4-BKO) resulted in whitened BAT and hypothermia upon acute cold exposure. The reduced thermogenic capacity observed in Sox4-MKO mice increases their susceptibility to diet-induced obesity. Overexpression of SOX4 enhances BAT thermogenesis counteracting diet-induced obesity. Mechanistically, SOX4 activates transcription of EBF2 which determines brown fat fate. Moreover, phosphorylation of SOX4 at S235 by PKA facilitates its nuclear translocation and EBF2 transcription. Further, SOX4 cooperates with EBF2 to activate transcriptional programs governing thermogenic gene expression. These results demonstrate that SOX4 serves as an upstream regulator of EBF2 providing valuable insights into BAT development and thermogenic function maintenance.

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SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice [RNA-Seq]

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An intronic region within FTO confers differentiation block in acute myeloid leukaemia through regulation of IRX3 and HOX [ChIP-seq re-analysis]

Project description:Transcription factors are key determinants in myeloid identity and differentiation fates and when mis- expressed or mutated, they cause a differentiation block, the cardinal feature of acute myeloid leukaemia (AML). The Forkhead family transcription factor FOXC1, is de-repressed in a lineage- inappropriate manner in approximately 30% of cases of HOXAhigh AML with functional consequences and prognostic significance. The mechanisms by which FOXC1 is mis-expressed remain to be determined and they presumably belong to a network of transcription factors and chromatin proteins that represent attractive therapeutic targets in AML. We performed an integrative omics analysis using AML primary samples and discovered an active distal enhancer at the FOXC1 topologically associated domain (TAD) that is more acetylated, accessible and differentially interacts with FOXC1, positively regulating its expression in FOXC1high AML. Moreover, through integrated next generation sequencing and functional analysis, we identified SOX4 as one of the upstream regulators of FOXC1 in leukaemia, where it is broadly expressed and associated with a high level of differentiation block. SOX4 binds at multiple sites across the FOXC1 TAD and directly controls its expression. Genome wide, SOX4 is preferentially bound at sites of accessible and acetylated chromatin at both promoter regions and active enhancers of transcription factors genes that include FOXC1, where it acts as a transcription activator. Our studies reveal a set of regulatory elements that control FOXC1 expression and highlight the role of SOX4 as a transcriptional activator that promotes differentiation block in AML.

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Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFβ-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2.

2013-06-20 | GSE45579 | GEO

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