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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: PRJNA610426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11241256_1.fastq.gz	Fastqsanger.gz
	SRR11241256_2.fastq.gz	Fastqsanger.gz
	SRR11241257_1.fastq.gz	Fastqsanger.gz
	SRR11241257_2.fastq.gz	Fastqsanger.gz
	SRR11241258_1.fastq.gz	Fastqsanger.gz

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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.

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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.

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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

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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.

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

Project description:Chromodomain helicase DNA-binding (CHD) chromatin remodelers regulate transcription and DNA repair. They govern cell-fate decisions during embryonic development and are often deregulated in human pathologies. Chd1-8 show upon germline disruption pronounced, often developmental lethal phenotypes. Here we show that contrary to Chd1-8 disruption, Chd9-/-animals are viable, fertile and display no developmental defects or disease predisposition. Germline deletion of Chd9 only moderately affects gene expression in tissues and derived cells, whereas acute depletion in human cancer cells elicits more robust changes suggesting that CHD9 is a highly context-dependent chromatin regulator that, surprisingly, is dispensable for mouse development.

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RNA helicase DDX5-induced circPHF14 promotes gastric cancer cell progression

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Regulation network of colorectal cancer specific enhancers in progression of colorectal cancer

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2021-05-03 | GSE173699 | GEO

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