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The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

ABSTRACT: The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

PROVIDER: PRJNA609747 | ENA |

REPOSITORIES: ENA

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The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

Project description:The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

| PRJNA610426 | ENA

The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

Project description:Integrative analysis of colorectal cancer (CRC) whole genomes and matched transcriptomes revealed that somatic promoter mutations are associated with increased Chromodomain helicase DNA-binding protein 2 (CHD2) levels. In both primary and metastatic CRC patients, elevated CHD2 levels are associated with worse prognosis and overall survival. We find that CHD2 increases promoter-transcription start site-chromatin accessibility and transcriptional upregulation of multiple oncogenes. In vitro, elevated CHD2 promoted CRC cell proliferation, migration and growth. In orthotopic xenografts, CHD2 promoted higher tumor burden and abdominal metastases, most prominently to the liver. FTD/TPI is an FDA approved chemotherapy for advanced chemo-refractory CRC. In orthotopic CRC models, FTD/TPI was highly effective in reducing metastases and prolonging survival for CHD2 high expressing CRCs. Thus, high CHD2 expression may be a potential CRC chemopredictive biomarker for FTD/TPI. Overall, these results provide new insights into the role of non-coding mutations and CHD2 levels to promote CRC growth and metastasis.

2025-02-19 | GSE146232 | GEO

The Chromatin Remodeler Chromodomain Helicase DNA Binding Protein 2 Promotes Colorectal Cancer Progression

2021-02-12 | GSE146398 | GEO

Chromodomain Helicase DNA-binding 4 (CHD4) is required for B cell identity and lineage progression

Project description:B cell specification and identity are controlled by transcription factors and cytokine receptors that drive the expression of stage-specific transcriptomes during lineage progression. A key feature of these mechanisms is the repression of inappropriate transcription. Here, we utilized RNA-seq to demonstrate that chromodomain helicase DNA-binding protein 4 (CHD4), an ATPase/helicase subunit of Mi-2/NuRD chromatin remodeling complexes, is essential for B cell identity. In mice that lack CHD4 selectively in the B lineage, defects include developmental arrest at the early pro-B cell stage. While many pro-B-specific genes are expressed in the mutant cells, transcripts that are normally restricted to other tissues including pancreas and bone are expressed out of context. Moreover, CHD4-deficient pro-B cells do not proliferate in response to IL-7, exhibit greatly decreased utilization of distal VH segments and accumulate DNA damage. Together, our data confirm the importance of CHD4 and NuRD complexes for the generation of functional B cells.

2019-05-22 | GSE84806 | GEO

Gene expression regulation by the Chromodomain Helicase DNA-binding protein 9 (CHD9) chromatin remodeler is dispensable for murine development

Project description:Gene expression regulation by the Chromodomain Helicase DNA-binding protein 9 (CHD9) chromatin remodeler is dispensable for murine development

| PRJNA625751 | ENA

Mice lacking the chromodomain helicase DNA-binding 5 chromatin remodeler display autism-like characteristics.

Project description:Although autism spectrum disorders (ASDs) share a core set of nosological features, they exhibit substantial genetic heterogeneity. A parsimonious hypothesis posits that dysregulated epigenetic mechanisms represent common pathways in the etiology of ASDs. To investigate this hypothesis, we generated a novel mouse model resulting from brain-specific deletion of chromodomain helicase DNA-binding 5 (Chd5), a chromatin remodeling protein known to regulate neuronal differentiation and a member of a gene family strongly implicated in ASDs. RNA sequencing of Chd5-/- mouse forebrain tissue revealed a preponderance of changes in expression of genes important in cellular development and signaling, sociocommunicative behavior and ASDs. Pyramidal neurons cultured from Chd5-/- cortex displayed alterations in dendritic morphology. Paralleling ASD nosology, Chd5-/- mice exhibited abnormal sociocommunicative behavior and a strong preference for familiarity. Chd5-/- mice further showed deficits in responding to the distress of a conspecific, a mouse homolog of empathy. Thus, dysregulated chromatin remodeling produces a pattern of transcriptional, neuronal and behavioral effects consistent with the presentation of ASDs.

| S-EPMC5537637 | biostudies-literature

Intrinsically Disordered Regions in Chromodomain Helicase DNA-binding (CHD) Proteins Shape Distinct Protein Interaction Networks

Project description:Intrinsically Disordered Regions in Chromodomain Helicase DNA-binding (CHD) Proteins Shape Distinct Protein Interaction Networks

| PRJNA1151020 | ENA

Gene expression profiling on heads of Drosophila chromodomain helicase DNA binding protein 1 (CHD1) deletion mutants

Project description:Gene expression profiling on heads of Drosophila chromodomain helicase DNA binding protein 1 (CHD1) deletion mutants

| PRJNA610298 | ENA

Notch signaling suppresses the progression of colorectal tumorigenesis

Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.

2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress

Chromatin remodeler CHD8 in CNS myelination and remyelination

Project description:Mutations in CHD8, an ATP-dependent chromodomain-helicase-DNA-binding protein 8, are known to cause a set of Autism Spectrum Disorders (ASD). We found that CHD8 is highly expressed in myelinating oligodendrocytes (OL) and their progenitors in the developing central nervous system (CNS). We performed CHD8 chIP-seq analysis in cultured oligodendrocytes.

2018-06-20 | GSE107919 | GEO

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