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Mus musculus

ABSTRACT: Intestinal IKKa is required for tumor initiation in APC mutant mice

PROVIDER: PRJNA394141 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5824340.fastq.gz	Fastqsanger.gz
	SRR5824341.fastq.gz	Fastqsanger.gz
	SRR5824342.fastq.gz	Fastqsanger.gz
	SRR5824343.fastq.gz	Fastqsanger.gz
	SRR5824344.fastq.gz	Fastqsanger.gz

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Project description:Mouse intestinal crypt epithelial cells: Apc+/Δ716 mice vs. Apc+/Δ716 Id2-/- compound mutant mice

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Mutant p53 R270H induces invasion and metastasis of mouse intestinal tumor organoids through gain-of-function mechanism

Project description:Apc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set.

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Effects of mitochondrial stress on intestinal tumor development depends on Apc status

Project description:Mitochondrial stress triggers both metabolic and transcriptomic reprogramming but its effects on tumor development remains unclear. It is also unknown whether the genetic status has any influence on the capacity of mitochondrial stress to control tumor development. To explore these issues, we generated a mouse model lacking the lipid transfer protein Stard7 in intestinal epithelial cells (IECs) and assessed tumor development in both Wnt-dependent tumor initiation and in inflammation-driven tumor development. The loss of Stard7 in both models of intestinal tumors impaired mitochondrial Complex I activity, led to a severe metabolic and lipidomic reprogramming and potentiated mTORC1 activation. As a result, levels of enzymes involved in serine biosynthesis were enhanced in Stard7-deficient IECs showing or not constitutive Wnt signaling. Strikingly, despite similar molecular signatures upon Stard7 deficiency in intestinal crypts showing or not constitutive Wnt signaling, Stard7 contributed to tumor development in AOM/DSS-treated mice but inhibits Wnt-driven cancer initiation in the intestine. Apc+/min mice lacking Stard7 in IECs developed more tumors in the distal colon as well as a specific microbiota signature. Collectively, our results suggest that the Apc genetic status critically controls the effects of mitochondrial stress on intestinal tumor development.

2026-02-19 | PXD046922 | Pride

Mus musculus

Project description:Non-tumor/tumor intestinal tissue of control or intestine-specific HAI-1 deficient Apc(Min/+) mice

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Bidirectional Introgression between Mus musculus domesticus and Mus spretus.

Project description: Not available

| S-EPMC8784167 | biostudies-literature

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Project description:DNA microarray analysis of colorectal tissue from Apc mutant mice

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The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

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Testis expression in Mus musculus domesticus x Mus musculus musculus hybrid zone mice

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Non-tumor/tumor intestinal tissue of control or intestine-specific HAI-1 deficient Apc(Min/+) mice

Project description:To analyse roles of HAI-1/Spint1 in intestinal tumorigenesis, we examined the effect of intestine-specific deletion of Spint1 gene on Apc(Min/+) mice. The loss of Hai-1/Spint1 significantly accelerated tumor formation in ApcMin/+ mice and shortened their survival periods. Mouse small intestine tumor tissue or background mucosa lacking macroscopically visible tumors were proceeded to RNA extraction and hybridization on microarrays (Affymetrix Mouse Genome 430 2.0 Array). Non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox) mice and non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox)/Vil-Cre mice were analysed. The experiment was repeated respectively.

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