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Chromatin Remodeling of Colorectal Cancer Liver Metastasis is Mediated by an HGF-PU.1-DPP4 Axis

ABSTRACT: Chromatin Remodeling of Colorectal Cancer Liver Metastasis is Mediated by an HGF-PU.1-DPP4 Axis

PROVIDER: PRJNA641206 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12072422.fastq.gz	Fastqsanger.gz
	SRR12072423.fastq.gz	Fastqsanger.gz
	SRR12072424.fastq.gz	Fastqsanger.gz
	SRR12072425.fastq.gz	Fastqsanger.gz
	SRR12072426.fastq.gz	Fastqsanger.gz

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Similar Datasets

Chromatin Remodeling of Colorectal Cancer Liver Metastasis is Mediated by an HGF-PU.1-DPP4 Axis.

Project description:Colorectal cancer (CRC) metastasizes mainly to the liver, which accounts for the majority of CRC-related deaths. Here it is shown that metastatic cells undergo specific chromatin remodeling in the liver. Hepatic growth factor (HGF) induces phosphorylation of PU.1, a pioneer factor, which in turn binds and opens chromatin regions of downstream effector genes. PU.1 increases histone acetylation at the DPP4 locus. Precise epigenetic silencing by CRISPR/dCas9KRAB or CRISPR/dCas9HDAC revealed that individual PU.1-remodeled regulatory elements collectively modulate DPP4 expression and liver metastasis growth. Genetic silencing or pharmacological inhibition of each factor along this chromatin remodeling axis strongly suppressed liver metastasis. Therefore, microenvironment-induced epimutation is an important mechanism for metastatic tumor cells to grow in their new niche. This study presents a potential strategy to target chromatin remodeling in metastatic cancer and the promise of repurposing drugs to treat metastasis.

| S-EPMC8498885 | biostudies-literature

Chromatin Remodeling of Colorectal Cancer Liver Metastasis is Mediated by an HGF-PU.1-DPP4 Axis

Project description:Integrative analysis of colorectal cancer (CRC) ATAC-seq and RNA-seq revealed an epigenomic and transcriptomic remodeling during liver metastasis.

2021-06-17 | GSE153016 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

Project description:The physiological adaptation to cold environmental temperatures involves the remodeling of energy-storing white adipose tissue (WAT) into an energy-burning thermogenic phenotype, characterized by the emergence of multi-locular beige adipocytes. To date, the full array of cold-responsive cells within WAT that mediate thermogenic remodeling remain undefined. Here, we demonstrate that distinct perivascular PDGFRb+ adipocyte precursor cell (APC) subpopulations are differentially sensitive to cold temperatures in vivo. One day of cold exposure elicits striking transcriptional changes in DPP4+ PDGFRb+ APCs, whereas committed DPP4- PDGFRb+ preadipocytes appear comparatively much less responsive. This adaptation includes beta-adrenergic receptor mediated induction in the expression of the pro-thermogenic cytokine, IL-33. DPP4+ PDGFRb+ cells represent the sole source of IL-33 within inguinal WAT of adult mice. Doxycycline-inducible deletion of Il33 in PDGFRb+ cells at the onset of cold exposure significantly compromises the thermogenic remodeling of WAT without directly impacting the differentiation capacity of APCs per se. Together, these studies reveal the presence of a cold-responsive progenitor cell subpopulation in adult WAT and highlight their ability to regulate tissue plasticity through the production of immunological factors.

2021-11-09 | GSE165974 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

2021-11-09 | GSE169672 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_p-CREB ChIP seq

2021-11-09 | GSE169669 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

Project description:Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

| PRJNA698817 | ENA

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing PU.1 mutants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

2019-11-20 | PXD013167 | Pride

The Bap1-SMN axis in Dpp4+ skeletal muscle mesenchymal cells regulates survival of motor neurons

Project description:Spinal muscular atrophy (SMA) is a neuromuscular disease caused by mutations in the survival of motor neuron (SMN) gene. Although the primary manifestation of SMA is degeneration of motor neurons in a dying-back manner, deficient SMN intrinsic to motor neurons does not cause severe motor neuron loss, as is the case in SMA mouse models. Thus, the involvement of non-neuronal cells in the pathogenesis of SMA has been suggested. Here, we report that a novel subset of fibro-adipogenic progenitors expressing Dpp4 (Dpp4+ FAPs) is required for the survival of motor neurons, in which BRCA1-associating protein 1 (Bap1) is crucial for the stabilization of SMN by preventing its ubiquitination-dependent degradation. Inactivation of Bap1 in FAPs decreased SMN levels and accompanied degeneration of the neuromuscular junction, leading to dying-back loss of motor neurons and muscle atrophy, reminiscent of SMA pathogenesis. Overexpression of ubiquitination-resistant SMN variant, SMNK186R, in Bap1-null FAPs completely prevented neuromuscular degenerations. In addition, transplantation of Dpp4+ FAPs, but not Dpp4- FAPs, completely rescued neuromuscular defects in the mutant mice. Our data revealed that Bap1-mediated stabilization of SMN in Dpp4+ FAPs is crucial for the survival of motor neurons and provided a new therapeutic approach to treat SMA.

2022-06-30 | GSE190426 | GEO

Changes in gene expression in primary human white preadipocytes in response to knockdown of DPP4

Project description:Transcriptional profiling of primary human white preadipocytes after infection with lentiviral vector either containing shRNA directed against dipeptidypeptidase 4 (DPP4) or unspecific shRNA as negative control Treatment of cells with DPP4 shRNA or control shRNA was done in 4 biological replicates, the first sample of DPP4 KD was hybridized against the first sh-control sample, the second DPP4 smple against the second control sample and so on

2015-11-24 | E-GEOD-75328 | biostudies-arrayexpress

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

Project description:Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

| PRJNA717303 | ENA

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