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Intrinsic WNT pathway hyperactivation dictates metastasis in mesenchymal colorectal cancer

ABSTRACT: Intrinsic WNT pathway hyperactivation dictates metastasis in mesenchymal colorectal cancer

PROVIDER: PRJNA1163318 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30735200.fastq.gz	Fastqsanger.gz
	SRR30735201.fastq.gz	Fastqsanger.gz
	SRR30735202.fastq.gz	Fastqsanger.gz
	SRR30735203.fastq.gz	Fastqsanger.gz
	SRR30735204.fastq.gz	Fastqsanger.gz

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Intrinsic WNT pathway hyperactivation dictates metastasis in mesenchymal colorectal cancer

Project description:Colorectal cancer (CRC) can be divided into 4 distinct subtypes of which consensus molecular subtype 4 (CMS4) is most aggressive and associated with metastasis and poor survival. Previously, we reported that the KPN mouse model, containing a Kras mutation, Trp53 deletion and Notch1 intracellular domain overexpression, resembles human CMS4. Strikingly, although tumor formation in this model is slow and limited in number, effective metastasis is observed pointing to in vivo selection. To understand this aggressive behavior, we compared two distinct in vitro KPN models, organoids and tumoroids. The organoid model represents a system driven by its original mutations, while the tumoroids were derived from in vivo grown tumors that allowed for selection during their development. Here, we reveal that tumoroids harbor endogenous WNT pathway activity driven by tankyrase activity and Cdx2 downregulation. The importance of this WNT pathway activation was evident for metastasis development, but less so for primary tumor growth. Intriguingly, these findings reflect a specific subset of aggressive human CMS4 cancers that display low CDX2 expression and lack of classical WNT pathway mutations, that have a higher tendency to metastasize. Together, these data propose a novel mechanism for WNT pathway hyperactivation that drives metastasis formation in an aggressive CRC model.

2025-02-03 | GSE277663 | GEO

Loss of p53 dictates Wnt-dependent systemic inflammation in breast cancer

Project description:Cancer-associated inflammatory processes in the tumour microenvironment, as well as systemically, are strongly linked with poor disease outcome in cancer patients. For most human solid tumour types, high systemic neutrophil-to-lymphocyte ratios (NLR) are associated with increased metastasis and poor overall survival and recent experimental studies have demonstrated a causal relationship between neutrophils and metastasis formation. However, to date, the cancer cell-intrinsic mechanisms dictating the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Using a panel of 16 distinct genetically engineered mouse models (GEMMs) for breast cancer, we demonstrate that tumour cell-intrinsic loss of p53 changes the phenotype and function of macrophages in the microenvironment, leading to activation of a systemic inflammatory cascade that drives neutrophil expansion. Mechanistically, p53 loss in cancer cells induces secretion of Wnt ligands that act in a paracrine fashion to stimulate IL-1b production from tumour-associated macrophages. Intratumoural IL-1β production stimulates an inflammatory cascade leading to the systemic accumulation of neutrophils. Pharmacological and genetic blockade of cancer cell-derived Wnt secretion reverses IL-1β expression by macrophages and subsequent systemic neutrophilic inflammation. Collectively, using pre-clinical mouse models for breast cancer, we demonstrate a novel mechanistic link between loss of p53 in cancer cells, Wnt ligand secretion and systemic immune activation. This illustrates the importance of cancer cell-intrinsic genetic aberrations in dictating cancer-associated inflammation. These insights set the stage for personalized immune intervention strategies for cancer patients.

2019-05-20 | GSE112665 | GEO

Effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression in HT29 cells

Project description:To investigate effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression and probe possible mechanism of cell viability effect, we overexpressed GFP/CTNNB1, or induce knockdown of APC by shNT1 (non-targeting) and shAPC

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RNA sequencing of circulating tumour cells implicates WNT signaling in pancreatic cancer metastasis

Project description:This SuperSeries is composed of the following subset Series: GSE40171: RNA sequencing of circulating tumour cells implicates WNT signaling in pancreatic cancer metastasis (mouse data) GSE40174: RNA sequencing of circulating tumour cells implicates WNT signaling in pancreatic cancer metastasis (human data) Refer to individual Series

2012-08-17 | E-GEOD-40176 | biostudies-arrayexpress

Intrinsic epigenetic state of primary osteosarcoma drives metastasis.

Project description:Intrinsic epigenetic state of primary osteosarcoma drives metastasis.

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Loss of p53 dictates Wnt-dependent systemic inflammation in breast cancer

Project description:Loss of p53 dictates Wnt-dependent systemic inflammation in breast cancer

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Intrinsic epigenetic state of primary osteosarcoma drives metastasis [ATAC-seq]

Project description:Intrinsic epigenetic state of primary osteosarcoma drives metastasis [ATAC-seq]

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Intrinsic epigenetic state of primary osteosarcoma drives metastasis [RNA-seq]

Project description:Intrinsic epigenetic state of primary osteosarcoma drives metastasis [RNA-seq]

| PRJNA983857 | ENA

Intrinsic epigenetic state of primary osteosarcoma drives metastasis [ChIP-seq]

Project description:Intrinsic epigenetic state of primary osteosarcoma drives metastasis [ChIP-seq]

| PRJNA983858 | ENA

90 min Met4 hyperactivation ChIP-chip

Project description:Identification of in vivo binding targets of Met4 and Met32 by conducting chromatin immunoprecipitation studies using genomic tiling arrays (ChIP-on-chip 4X44K whole yeast genome arrays by Agilent) following 90 minutes Met4 hyperactivation.

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