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The binding sites of Foxp4 on genome in the early stage of SVF cells differentiating to beige adipocytes

ABSTRACT: We found deletion of Foxp4 in SVF cells would inhibit beige adipocyte differentiation and thermogenesis.In order to investage the binding sites of Foxp4 on genome of SVF cells, we isolated SVF cells from ingunal adipose tissues and did Foxp4 and H3K27ac ChIP-Seqs after two days' browning differentiaion.

ORGANISM(S): Mus musculus

PROVIDER: GSE199567 | GEO | 2022/04/06

REPOSITORIES: GEO

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Genome-wide binding sites of Foxp4 in beige adipocyte

Project description:We found deletion of Foxp4 in mature adipocytes would augment juvenile and mature beige adipocyte thermogenesis.In order to investage the binding site of Foxp4 in the genome of beige adipocytes, we did Foxp4 ChIP-Seq with differentiated SVF cells derived from ingunal adipose tissues.

2022-04-06 | GSE199559 | GEO

The binding sites of Foxp4 on genome in the early stage of SVF cells differentiating to beige adipocytes

Project description:The binding sites of Foxp4 on genome in the early stage of SVF cells differentiating to beige adipocytes

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3' RNA-seq of differentiating (brown) mouse subcutaneous SVF cells upon knockdown of Zfp521, Fhl1, or Mxd1

Project description:White fat browning is a highly variable genetic trait in mice (Guerra et al., 1998). To gain an overview of strain variations in browning capacities, we performed transcriptome analysis of white fat browning in (1) 5 inbred mouse strains (C57BL/6J, 129S6sv/ev, A/J, AKR/J, and SWR/J) with distinct browning propensities in WAT, and (2) F1 hybrids derived from a high (129S6sv/ev) and low browning strain (C57BL/6J) cross. From our analyses, several transcription factors emerged as novel regulators of white fat browning, including the TFs Zfp521, Fhl1, and Mxd1. We further validated the role of these TFs and performed 3' RNA-seq experiments upon their knockdown, in order to characterize their mechanism of action.

2019-11-01 | E-MTAB-8343 | biostudies-arrayexpress

Effect of knocking down FOXP4 and YAP1 in gastric cancer cells

Project description:The Hippo-YAP1 pathway is an evolutionally conserved signaling cascade that controls organ size and tissue regeneration. Its dysregulation has been well-studied to promote tumor initiation and progression, including gastric cancer (GC). Although the Hippo-YAP1 signaling pathway regulates the expression of thousands of target genes, how these target genes contribute to the oncogenic program driven by YAP1 remains unknown. Here we identified the vital role of FOXP4 in YAP1-driven gastric carcinogenesis by maintaining stemness and promoting peritoneal metastasis. Knocking down FOXP4 impairs GC spheroid formation and inhibits stemness marker expression, while its upregulation potentiates the cancer cells with more stemness. RNA-seq analysis revealed SOX12 as functional downstream of FOXP4 in the YAP1-induced carcinogenesis. Targeting FOXP4 by 42-(2-Tetrazolyl) rapamycin in GC cells enhanced the 5-FU efficacies. Our findings have unveiled FOXP4 as a novel stemness marker that promotes tumorigenesis by upregulating SOX12. Additionally, we have identified FOXP4 as a direct target for modulating YAP1 signaling in GC. Therefore, the YAP1-FOXP4-SOX12 axis presents a promising therapeutic target for GC.

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A non-cell autonomous mechanism of beige adipocyte renaissance in subcutaneous adipose tissue

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FOXP4-mediated induction of PTK7 activates the Wnt/β-catenin pathway and promotes ovarian cancer development

Project description:Ovarian cancer (OC) presents a significant challenge in clinical settings due to its difficulty in early diagnosis and its resistance to treatment. FOXP4 is a member of the FOXP subfamily and is involved in various biological processes including embryonic development, cell cycle regulation, and tumorigenesis. Despite its potential role in cancer, the exact function and significance of FOXP4 in OC remain uncertain. Here we showed that FOXP4 was expressed at high levels in OC, and its high expression was associated with poor prognosis. Furthermore, RNA sequencing and functional analysis of cells lacking FOXP4 suggest that FOXP4 contributes to the activation of the Wnt signaling pathway, leading to the amplification of the malignant phenotype in OV. Mechanistically, FOXP4 directly induces the expression of protein tyrosine kinase 7 (PTK7), a Wnt-binding receptor tyrosine pseudokinase, leading to abnormal activation of the Wnt signaling pathway. Disrupting the FOXP4-Wnt feedback loop by inactivating the Wnt signaling pathway or reducing FOXP4 expression resulted in the reduction of the malignant phenotype of OC cells, while restoring PTK7 expression reversed this effect. In conclusion, our findings highlight the importance of FOXP4 in the activation of the Wnt signaling pathway in OC and provide evidence for the potential therapeutic value of targeting this pathway in the treatment of the disease.

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M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

Project description:Beige adipocytes accumulates mitochondria and alleviates metabolic disorder via activating energy expenditure. Whether the opposing process of mitochondrial biogenesis and clearance are integrated regulated in beige adipocytes is beyond known. Here we show that DNA binding protein Ets1 suppresses beige adipocyte formation via bidirectional regulation of mitochondrial biogenesis and clearance. The expression level of Ets1 was down-regulated in browning adipocytes, and up-regulated in the subcutaneous fat of obese mice. Adipocyte Ets1 heterozygous knock-in mice showed suppressed beige adipocytes formation under cold stress, while the homozygous knock-in mice are cold intolerance. On the other hand, knocking out Ets1 in adipocytes enhanced energy expenditure and protect the mice from high fat diet induced metabolic disorders. Mechanical assay suggests Ets1 binds to the promoter region of mitochondria complex coding genes and autophagy related genes, transcriptionally suppresses mitochondrial biogenesis and activates its clearance. Our results indicate that Ets1 integrally regulates the balance of mitochondria generation and degradation, hence acts as a pivotal governor of mitochondria content and negatively regulates beige adipocyte formation.

2023-07-01 | GSE234879 | GEO

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