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Nucleophosmin sustains WNT-driven cell proliferation and tumor initiation in vivo

ABSTRACT: Nucleophosmin sustains WNT-driven cell proliferation and tumor initiation in vivo

PROVIDER: PRJNA1051495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27184613.fastq.gz	Fastqsanger.gz
	SRR27184614.fastq.gz	Fastqsanger.gz
	SRR27184615.fastq.gz	Fastqsanger.gz
	SRR27184616.fastq.gz	Fastqsanger.gz
	SRR27184617.fastq.gz	Fastqsanger.gz

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Nucleophosmin sustains WNT-driven cell proliferation and tumor initiation in vivo

Project description:Nucleophosmin (NPM1) is a nucleolar protein frequently overexpressed in many solid tumours with little known about its functional role to support carcinogenesis. Here, we identify Npm1 as a commonly upregulated gene following Apc loss in highly proliferative tissues, and high expression correlates with increased proliferation in CRC patients. We show that NPM1 is dispensable for adult epithelial tissue homeostasis, however, it has a profound effect on WNT-driven intestinal and liver tumourigenesis, leading to reduced proliferation and extension of survival. Mechanistically, NPM1 depletion triggers integrated stress response (ISR) and p53 pathway activation. P53 deletion, or inhibition of the ISR effects, rescue proliferation following NPM1 loss. Overall, our results demonstrate that NPM1 supports WNT-driven cell proliferation and tumour initiation by attenuating p53 pathway activation or induction of ISR. Being dispensable for homeostasis, NPM1 presents as a promising target for cancer therapy in WNT-driven tumours with functional p53, including difficult to treat KRAS-mutant CRC and hepatic cancers.

2024-02-15 | GSE249958 | GEO

Caspase-2 is essential for proliferation and self-renewal of nucleophosmin-mutated acute myeloid leukemia

Project description:Mutation in nucleophosmin (NPM1) causes relocalization of this normally nucleolar protein to the cytoplasm (NPM1c+). Despite NPM1 mutation being the most common driver mutation in cytogenetically normal adult acute myeloid leukemia (AML), the mechanisms of NPM1c+-induced leukemogenesis remain unclear. Caspase-2 is a pro-apoptotic protein activated by NPM1 in the nucleolus. Here, we show that caspase-2 is also activated by NPM1c+ in the cytoplasm and DNA damage-induced apoptosis is caspase-2-dependent in NPM1c+ but not in NPM1wt AML cells. Strikingly, in NPM1c+ cells, caspase-2 loss results in profound cell cycle arrest, differentiation, and down-regulation of stem cell pathways that regulate pluripotency including impairment in the AKT/mTORC1 and Wnt signaling pathways, and inhibition of Rictor cleavage. In contrast, there were minimal differences in proliferation, differentiation, or the transcriptional profile of NPM1wt cells lacking caspase-2. Our results show that caspase-2 is essential for proliferation and self-renewal of AML cells expressing mutated NPM1. This study demonstrates that caspase-2 is a major effector of NPM1c+ function.

2024-04-17 | GSE249545 | GEO

Non-canonical STAT3 activity sustains pathogenic Th17 proliferation and cytokine response to antigen

Project description:Non-canonical STAT3 activity sustains pathogenic Th17 proliferation and cytokine response to antigen

2020-07-01 | GSE151447 | GEO

CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [HiC]

Project description:CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [HiC]

| PRJNA1008732 | ENA

Caspase-2 is essential for proliferation and self-renewal of nucleophosmin-mutated acute myeloid leukemia

Project description:Caspase-2 is essential for proliferation and self-renewal of nucleophosmin-mutated acute myeloid leukemia

| PRJNA1049463 | ENA

Mutant nucleophosmin and cooperating pathways drive leukemia initiation and progression in mice

Project description:Comparison of gene expression profiles of mouse bone marrow nucleated cells. All comparisons are made between biological replicates (different mice) derived from animals carrying the Type A cytoplasmic Nucleophosmin mutation (Npm1c) found in human Acute Myeloid Leukaemia. Mice were culled 8 weeks after induction of the conditional Npm1c allele with Mx1-Cre. Whole bone marrow (BM, n=20: 11xNpm1c & 9xWildType) or antibody purified cell fractions (Lin minus, n=6: 4xNpm1c & 2xWildType; B220+, n=5: 3xNpm1c & 2xWildType and Gr1+/Mac1+, n=6: 4xNpm1c & 2xWildType) were studied. Files ("samples") include data from all samples in each comparison.<br>Global profiling was done using Illumina mouse-6 expression beadchip version 2. Data were quantile normalised and analysed using the bioconductor (http://www.bioconductor.org/), lumi (http://www.bioconductor.org/packages/2.0/bioc/html/lumi.html ) and limma packages, then p-value adjusted for multiple testing.

2011-03-15 | E-MEXP-3113 | biostudies-arrayexpress

CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [RNA-seq_CRISPR]

Project description:CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [RNA-seq_CRISPR]

| PRJNA1008731 | ENA

CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [ChIP-seq]

Project description:CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [ChIP-seq]

| PRJNA1008730 | ENA

CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [RNA-seq_dTAG]

Project description:CRL4-DCAF15 control of cohesin dynamics sustains cell proliferation [RNA-seq_dTAG]

| PRJNA1105321 | ENA

WNT ligands control initiation and progression of human papilloma-virus-driven squamous cell carcinoma

Project description:Human papilloma virus (HPV)-driven cutaneous squamous cell carcinoma (cSCC) is the most common cancer in immunosuppressed patients. Despite indications suggesting that HPV promotes genomic instability during cSCC development, the molecular pathways underpinning HPV-driven cSCC development remain unknown. We compared the transcriptome of HPV-driven mouse cSCC with normal skin and observed higher amounts of transcripts for Porcupine and WNT ligands in cSCC, suggesting a role for WNT-signaling in cSCC progression. We confirmed increased Porcupine expression in human cSCC samples. Blocking the secretion of WNT-ligands by the Porcupine inhibitor LGK974 significantly diminished initiation and progression of HPV-driven cSCC. Administration of LGK974 to mice with established cSCC resulted in differentiation of cancer cells and significant reduction of the cancer stem cell compartment. Thus, WNT/b-catenin signaling is essential for HPV-driven cSCC initiation and progression as well as for maintaining the cancer stem cell niche. Interference with WNT-secretion may thus represent a promising approach for therapeutic intervention.

2018-12-13 | GSE108454 | GEO

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