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Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis

ABSTRACT: Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis

PROVIDER: PRJNA495837 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8033043.fastq.gz	Fastqsanger.gz
	SRR8033044.fastq.gz	Fastqsanger.gz
	SRR8033045.fastq.gz	Fastqsanger.gz
	SRR8033046.fastq.gz	Fastqsanger.gz
	SRR8033047.fastq.gz	Fastqsanger.gz

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Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (Illumina Beadchip)

Project description:Bcl9 and Pygo function within the Wnt enhanceosome to effect β-catenin-dependent transcription. Whether they also mediate β-catenin-dependent neoplasia is unclear. Here we assess their roles in intestinal tumorigenesis initiated by Apc loss-of-function (ApcMin). Gene expression profiling revealed that loss-of-Bcl9 synergizes with loss-of-Pygo to shift gene expression within Apc-mutant adenomas from stem cell-like to differentiation along Notch-regulated secretory lineages.

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Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (Illumina Beadchip)

Project description:Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (Illumina Beadchip)

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Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (RNA-Seq)

Project description:Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis (RNA-Seq)

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DNA methylation analysis in familial adenomatous polyposis

Project description:DNA methylation of 23 familial adenomatous polyposis tumors. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites.

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Pull down of full length and mutant BCL9 (deltaHD1) in mouse colorectal tumors and colonic epithelium

Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. Here we searched for BCL9 interacts that could explain the PYGO-independent phenotype induced be the loss of the HD1 (PYGO-binding) domain of BCL9

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Bcl9 and Pygo synergize downstream of Apc to effect intestinal neoplasia in mouse models recapitulating Familial Adenomatous Polyposis

Project description:This SuperSeries is composed of the SubSeries listed below.

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SNP data of Familial adenomatous polyposis (FAP) organoids

Project description:SNP data of Familial adenomatous polyposis (FAP) organoids

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Expression data of Familial adenomatous polyposis (FAP) organoids

Project description:Expression data of Familial adenomatous polyposis (FAP) organoids

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Single-cell transcriptomic survey of adenomatous polyposis patients with germline APC mutations

Project description:Patients with germline APC mutations are recognized by hundreds of adenoma polyps in colon, which will give rise to adenocarcinoma inevitably. Over 700 germline APC mutations have been reported to be the leading cause of adenomatous polyposis. However, the underlying mechanism of APC mutation triggered colonic cancer remains mysterious. Here, using a modified STRT-seq protocol, we analyzed over 4000 single cells from the four matching adenomatous polyposis, adenocarcinoma, adjacent normal colon tissue and one lymphatic metastasis from four adenomatous polyposis patients with APC mutations. We identified the main cell types existed in human intestine such as B cells, mast cells, T cells, macrophage cells, endothelial cells, stromal cells and epithelial cells. And the proportional changes of various cell types during the development of adenoma were showed. The transcriptomic similarities and differences between adenoma, adenocarcinoma and adjacent normal tissue were comprehensively investigated. For better understanding the tumor progression process, we also take advantage of other genomic signatures, such as SNV and CNV. We found that the gene expression signatures of adenoma and adenocarcinoma were largely similar when compared with adjacent normal tissue. But the mutation accumulation was indeed observed during the progression from adenoma to adenocarcinoma. To summarized, our work will help us accurately investigate the pathogenic mechanism and heterogeneity of APC inactive mutation triggered colonic cancer, which will also help us better understand the non-familial colorectal cancers

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